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Chris M Wood - One of the best experts on this subject based on the ideXlab platform.
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internal spatial and temporal co2 dynamics fasting feeding drinking and the Alkaline Tide
2019Co-Authors: Chris M WoodAbstract:The gastrointestinal tract of fish contains powerful transport mechanisms for HCO 3 − and H+, and is a site of temporal and spatial variations in pH, HCO 3 − , and PCO2 (CO2 dynamics) that are far greater than those in the systemic circulation. Most research to date has focused on fasted marine animals, and the HCO 3 − -related transport mechanisms required to deal with the consequences of drinking sea water, which are critical for osmoregulation. Far less is known about freshwater fish, and about the consequences of ingesting food, which appear to intensify the changes in gastrointestinal CO2 dynamics in both freshwater and marine fish. CO2 recycling from the chyme to the secretory cells, through the hydration reaction catalyzed by intracellular carbonic anhydrase, may play a key role in refueling H+ and HCO 3 − transport in the stomach and intestine, respectively. These events in the tract result in postprandial “Alkaline” or “acidic Tides” in the systemic circulation, the mechanistic details of which need much further study. Current understanding of these areas in marine and freshwater teleosts, both fasted and fed, as well as in marine elasmobranchs, is synthesized, and key areas for future investigation are highlighted.
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acid base responses to feeding and intestinal cl uptake in freshwater and seawater acclimated killifish fundulus heteroclitus an agastric euryhaline teleost
The Journal of Experimental Biology, 2010Co-Authors: Chris M Wood, Carol Bucking, Martin GrosellAbstract:Marine teleosts generally secrete basic equivalents (HCO(3)(-)) and take up Na(+) and Cl(-) in the intestine so as to promote absorption of H(2)O. However, neither the integration of these functions with feeding nor the potential role of the gut in ionoregulation and acid-base balance in freshwater have been well studied. The euryhaline killifish (Fundulus heteroclitus) is unusual in lacking both an acid-secreting stomach and a mechanism for Cl(-) uptake at the gills in freshwater. Responses to a satiation meal were evaluated in both freshwater- and seawater-acclimated killifish. In intact animals, there was no change in acid or base flux to the external water after the meal, in accord with the absence of any post-prandial Alkaline Tide in the blood. Indeed, freshwater animals exhibited a post-prandial metabolic acidosis ('acidic Tide'), whereas seawater animals showed no change in blood acid-base status. In vitro gut sac experiments revealed a substantially higher rate of Cl(-) absorption by the intestine in freshwater killifish, which was greatest at 1-3 h after feeding. The Cl(-) concentration of the absorbate was higher in preparations from freshwater animals than from seawater killifish and increased with fasting. Surprisingly, net basic equivalent secretion rates were also much higher in preparations from freshwater animals, in accord with the 'acidic Tide'; in seawater preparations, they were lowest after feeding and increased with fasting. Bafilomycin (1 micromol l(-1)) promoted an 80% increase in net base secretion rates, as well as in Cl(-) and fluid absorption, at 1-3 h post-feeding in seawater preparations only, explaining the difference between freshwater and seawater fish. Preparations from seawater animals at 1-3 h post-feeding also acidified the mucosal saline, and this effect was associated with a marked rise in P(CO(2)), which was attenuated by bafilomycin. Measurements of chyme pH from intact animals confirmed that intestinal fluid (chyme) pH and basic equivalent concentration were lowest after feeding in seawater killifish, whereas P(CO(2)) was greatly elevated (80-95 Torr) in chyme from both seawater and freshwater animals but declined to lower levels (13 Torr) after 1-2 weeks fasting. There were no differences in pH, P(CO(2)) or the concentrations of basic equivalents in intestinal fluid from seawater versus freshwater animals at 12-24 h or 1-2 weeks post-feeding. The results are interpreted in terms of the absence of gastric HCl secretion, the limitations of the gills for acid-base balance and Cl(-) transport, and therefore the need for intestinal Cl(-) uptake in freshwater killifish, and the potential for O(2) release from the mucosal blood flow by the high P(CO(2)) in the intestinal fluids. At least in seawater killifish, H(+)-ATPase running in parallel to HCO(3)(-):Cl(-) exchange in the apical membranes of teleost enterocytes might reduce net base secretion and explain the high P(CO(2)) in the chyme after feeding.
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the role of the kidney in compensating the Alkaline Tide electrolyte load and fluid balance disturbance associated with feeding in the freshwater rainbow trout oncorhynchus mykiss
Comparative Biochemistry and Physiology A-molecular & Integrative Physiology, 2010Co-Authors: Michael J Landman, Carol Bucking, Chris M WoodAbstract:The effect in freshwater rainbow trout of digesting a commercial pellet meal on the renal handling of water, ions and acid-base equivalents was investigated through urine collection over a 48 h period following meal ingestion. The glomerular filtration rate (GFR) and urine flow rate (UFR) were reduced in fed fish between 12 and 24h following the meal, likely reflecting a loss of endogenous water across the gastric epithelium as a result of ingesting dry, ion-rich food pellets. The kidney was also responsible for the excretion of some excess dietary Ca(2+), and, to a much lesser extent, Na(+) and Cl(-), while the urinary excretion of K(+) was unaffected. The most dramatic effect of feeding was the elevation of renal Mg(2+) excretion, with the kidney transitioning from net Mg(2+) reabsorption to net Mg(2+) secretion during digestion. The renal handling of dietary ions accounted for 3-27% of the total ions absorbed from the diet, indicating that a majority of the ions are excreted extra-renally or incorporated into growth. However this does highlight the underestimation of renal ion handling when using unfed fish models. The metabolic alkalosis created by digestion (the Alkaline Tide) resulted in an increase in urine pH as well as a transition from net acidic equivalent excretion in the urine to net basic equivalent excretion. This was due to a decrease in the titratable acidity minus bicarbonate component of urine as well as a decrease in ammonia secretion. Additionally, the experimental separation of the urinary component of acid-base excretion from that of the gills highlighted the substantially larger contribution of the latter. During the Alkaline Tide, renal excretion accounted for approximately 5% of the total basic equivalent excretion to the external water.
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post prandial metabolic alkalosis in the seawater acclimated trout the Alkaline Tide comes in
The Journal of Experimental Biology, 2009Co-Authors: Carol Bucking, John L Fitzpatrick, Sunita R Nadella, Chris M WoodAbstract:The consequences of feeding and digestion on acid-base balance and regulation in a marine teleost (seawater-acclimated steelhead trout; Oncorhynchus mykiss) were investigated by tracking changes in blood pH and [HCO3-], as well as alterations in net acid or base excretion to the water following feeding. Additionally the role of the intestine in the regulation of acid-base balance during feeding was investigated with an in vitro gut sac technique. Feeding did not affect plasma glucose or urea concentrations, however, total plasma ammonia rose during feeding, peaking between 3 and 24 h following the ingestion of a meal, three-fold above resting control values (approximately 300 micromol ml(-1)). This increase in plasma ammonia was accompanied by an increase in net ammonia flux to the water (approximately twofold higher in fed fish versus unfed fish). The arterial blood also became Alkaline with increases in pH and plasma [HCO3-] between 3 and 12 h following feeding, representing the first measurement of an Alkaline Tide in a marine teleost. There was no evidence of respiratory compensation for the measured metabolic alkalosis, as Pa CO2 remained unchanged throughout the post-feeding period. However, in contrast to an earlier study on freshwater-acclimated trout, fed fish did not exhibit a compensating increase in net base excretion, but rather took in additional base from the external seawater, amounting to approximately 8490 micromol kg(-1) over 48 h. In vitro experiments suggest that at least a portion of the Alkaline Tide was eliminated through increased HCO3- secretion coupled to Cl- absorption in the intestinal tract. This did not occur in the intestine of freshwater-acclimated trout. The marked effects of the external salinity (seawater versus freshwater) on different post-feeding patterns of acid-base balance are discussed.
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using omeprazole to link the components of the post prandial Alkaline Tide in the spiny dogfish squalus acanthias
The Journal of Experimental Biology, 2009Co-Authors: Chris M Wood, Patrick J Walsh, Aaron G Schultz, Stephen R MungerAbstract:After a meal, dogfish exhibit a metabolic alkalosis in the bloodstream and a marked excretion of basic equivalents across the gills to the external seawater. We used the H(+), K(+)-ATPase pump inhibitor omeprazole to determine whether these post-prandial Alkaline Tide events were linked to secretion of H(+) (accompanied by Cl(-)) in the stomach. Sharks were fitted with indwelling stomach tubes for pretreatment with omeprazole (five doses of 5 mg omeprazole per kilogram over 48 h) or comparable volumes of vehicle (saline containing 2% DMSO) and for sampling of gastric chyme. Fish were then fed an involuntary meal by means of the stomach tube consisting of minced flatfish muscle (2% of body mass) suspended in saline (4% of body mass total volume). Omeprazole pre-treatment delayed the post-prandial acidification of the gastric chyme, slowed the rise in Cl(-) concentration of the chyme and altered the patterns of other ions, indicating inhibition of H(+) and accompanying Cl(-) secretion. Omeprazole also greatly attenuated the rise in arterial pH and bicarbonate concentrations and reduced the net excretion of basic equivalents to the water by 56% over 48 h. Arterial blood CO(2) pressure (Pa(CO(2))) and plasma ions were not substantially altered. These results indicate that elevated gastric H(+) secretion (as HCl) in the digestive process is the major cause of the systemic metabolic alkalosis and the accompanying rise in base excretion across the gills that constitute the Alkaline Tide in the dogfish.
Patrick J Walsh - One of the best experts on this subject based on the ideXlab platform.
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using omeprazole to link the components of the post prandial Alkaline Tide in the spiny dogfish squalus acanthias
The Journal of Experimental Biology, 2009Co-Authors: Chris M Wood, Patrick J Walsh, Aaron G Schultz, Stephen R MungerAbstract:After a meal, dogfish exhibit a metabolic alkalosis in the bloodstream and a marked excretion of basic equivalents across the gills to the external seawater. We used the H(+), K(+)-ATPase pump inhibitor omeprazole to determine whether these post-prandial Alkaline Tide events were linked to secretion of H(+) (accompanied by Cl(-)) in the stomach. Sharks were fitted with indwelling stomach tubes for pretreatment with omeprazole (five doses of 5 mg omeprazole per kilogram over 48 h) or comparable volumes of vehicle (saline containing 2% DMSO) and for sampling of gastric chyme. Fish were then fed an involuntary meal by means of the stomach tube consisting of minced flatfish muscle (2% of body mass) suspended in saline (4% of body mass total volume). Omeprazole pre-treatment delayed the post-prandial acidification of the gastric chyme, slowed the rise in Cl(-) concentration of the chyme and altered the patterns of other ions, indicating inhibition of H(+) and accompanying Cl(-) secretion. Omeprazole also greatly attenuated the rise in arterial pH and bicarbonate concentrations and reduced the net excretion of basic equivalents to the water by 56% over 48 h. Arterial blood CO(2) pressure (Pa(CO(2))) and plasma ions were not substantially altered. These results indicate that elevated gastric H(+) secretion (as HCl) in the digestive process is the major cause of the systemic metabolic alkalosis and the accompanying rise in base excretion across the gills that constitute the Alkaline Tide in the dogfish.
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is the Alkaline Tide a signal to activate metabolic or ionoregulatory enzymes in the dogfish shark squalus acanthias
Physiological and Biochemical Zoology, 2008Co-Authors: Chris M Wood, Makiko Kajimura, Thomas P Mommsen, Patrick J WalshAbstract:Abstract Experimental metabolic alkalosis is known to stimulate whole‐animal urea production and active ion secretion by the rectal gland in the dogfish shark. Furthermore, recent evidence indicates that a marked Alkaline Tide (systemic metabolic alkalosis) follows feeding in this species and that the activities of the enzymes of the ornithine‐urea cycle (OUC) for urea synthesis in skeletal muscle and liver and of energy metabolism and ion transport in the rectal gland are increased at this time. We therefore evaluated whether alkalosis and/or NaCl/volume loading (which also occurs with feeding) could serve as a signal for activation of these enzymes independent of nutrient loading. Fasted dogfish were infused for 20 h with either 500 mmol L−1 NaHCO3 (alkalosis + volume expansion) or 500 mmol L−1 NaCl (volume expansion alone), both isosmotic to dogfish plasma, at a rate of 3 mL kg−1 h−1. NaHCO3 infusion progressively raised arterial pH to 8.28 ( \documentclass{aastex} \usepackage{amsbsy} \usepackage{amsfo...
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osmoregulation ionoregulation and acid base regulation by the gastrointestinal tract after feeding in the elasmobranch squalus acanthias
The Journal of Experimental Biology, 2007Co-Authors: Chris M Wood, Makiko Kajimura, Patrick J Walsh, Carol BuckingAbstract:In order to study the physiological consequences of voluntary feeding in the gastrointestinal tract of a ureotelic marine elasmobranch, dogfish (fasted for 96 h) were sampled at various times up to 360 h after consuming a 5-6% ration of teleost fish (hake) under natural feeding conditions. Digestion and absorption were completed between 120 and 360 h post-feeding. The tissue masses of different segments of the gastrointestinal tract increased and decreased markedly as the chyme moved through, mainly because of fluid engorgement rather than hyperplasia. In fasted dogfish, the cardiac and pyloric stomachs contained only small volumes of highly acidic fluid (pH 1.77+/-1.12, 2.05+/-0.08) similar in composition to seawater. Feeding resulted in gastric pHs of 3.20+/-0.31 and 3.95+/-0.40 at 6 h, followed by slow declines through 60 h. An Alkaline Tide in the blood also occurred at 6 h. In the face of large changing masses of highly acidic chyme in the stomachs, the pH (6.50+/-0.10), ionic composition and volume of chyme in the intestine (spiral valve) were precisely regulated from 6 to 60 h post-feeding at very different values from those in the stomachs, and intestinal HCO3(-) remained low (5.12+/-0.83 mmol l(-1)). The colon was usually empty and its pH constant at 7.20+/-0.16 at all times. Despite the ingestion of strongly hypo-osmotic teleost tissue, the osmolality of the chyme remained in equilibrium with that of the blood plasma in all segments at all times after feeding. Much of the osmotic equilibration was because of the secretion of urea into the chyme, particularly in the intestine. After feeding, gastric fluid concentrations of Na(+) and Mg(2+) declined, K(+) and Ca(2+) increased, whereas Cl(-) exhibited little change, indicating that additional drinking of seawater was minimal. Na(+), K(+), water and especially Cl(-) were absorbed in the intestine, whereas Mg(2+) and Ca(2+) were largely excluded. Our results illustrate the complex integration of digestive and ionoregulatory function in the elasmobranch digestive tract, and marked differences from the teleost pattern.
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Alkaline Tide and nitrogen conservation after feeding in an elasmobranch squalus acanthias
The Journal of Experimental Biology, 2005Co-Authors: Chris M Wood, Makiko Kajimura, Thomas P Mommsen, Patrick J WalshAbstract:SUMMARY We investigated the consequences of feeding for acid–base balance, nitrogen excretion, blood metabolites and osmoregulation in the Pacific spiny dogfish. Sharks that had been starved for 7 days were surgically fitted with indwelling stomach tubes for gastric feeding and blood catheters for repetitive blood sampling and were confined in chambers, allowing measurement of ammonia-N and urea-N fluxes. The experimental meal infused via the stomach tube consisted of flatfish muscle (2% of body mass) suspended in saline (4% of body mass total volume). Control animals received only saline (4% of body mass). Feeding resulted in a marked rise in both arterial and venous pH and HCO 3 – concentrations at 3–9 h after the meal, with attenuation by 17 h. Venous Ṗ O2 also fell. As there were negligible changes in Ṗ CO2 , the response was interpreted as an Alkaline Tide without respiratory compensation, associated with elevated gastric acid secretion. Urea-N excretion, which comprised >90% of the total, was unaffected, while ammonia-N excretion was very slightly elevated, amounting to <3% of the total-N in the meal over 45 h. Plasma ammonia-N rose slightly. Plasma urea-N, TMAO-N and glucose concentrations remained unchanged, while free amino acid and β-hydroxybutyrate levels exhibited modest declines. Plasma osmolality was persistently elevated after the meal relative to controls, partially explained by a significant rise in plasma Cl – . This marked post-prandial conservation of nitrogen is interpreted as reflecting the needs for urea synthesis for osmoregulation and protein growth in animals that are severely N-limited due to their sporadic and opportunistic feeding lifestyle in nature.
Carol Bucking - One of the best experts on this subject based on the ideXlab platform.
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acid base responses to feeding and intestinal cl uptake in freshwater and seawater acclimated killifish fundulus heteroclitus an agastric euryhaline teleost
The Journal of Experimental Biology, 2010Co-Authors: Chris M Wood, Carol Bucking, Martin GrosellAbstract:Marine teleosts generally secrete basic equivalents (HCO(3)(-)) and take up Na(+) and Cl(-) in the intestine so as to promote absorption of H(2)O. However, neither the integration of these functions with feeding nor the potential role of the gut in ionoregulation and acid-base balance in freshwater have been well studied. The euryhaline killifish (Fundulus heteroclitus) is unusual in lacking both an acid-secreting stomach and a mechanism for Cl(-) uptake at the gills in freshwater. Responses to a satiation meal were evaluated in both freshwater- and seawater-acclimated killifish. In intact animals, there was no change in acid or base flux to the external water after the meal, in accord with the absence of any post-prandial Alkaline Tide in the blood. Indeed, freshwater animals exhibited a post-prandial metabolic acidosis ('acidic Tide'), whereas seawater animals showed no change in blood acid-base status. In vitro gut sac experiments revealed a substantially higher rate of Cl(-) absorption by the intestine in freshwater killifish, which was greatest at 1-3 h after feeding. The Cl(-) concentration of the absorbate was higher in preparations from freshwater animals than from seawater killifish and increased with fasting. Surprisingly, net basic equivalent secretion rates were also much higher in preparations from freshwater animals, in accord with the 'acidic Tide'; in seawater preparations, they were lowest after feeding and increased with fasting. Bafilomycin (1 micromol l(-1)) promoted an 80% increase in net base secretion rates, as well as in Cl(-) and fluid absorption, at 1-3 h post-feeding in seawater preparations only, explaining the difference between freshwater and seawater fish. Preparations from seawater animals at 1-3 h post-feeding also acidified the mucosal saline, and this effect was associated with a marked rise in P(CO(2)), which was attenuated by bafilomycin. Measurements of chyme pH from intact animals confirmed that intestinal fluid (chyme) pH and basic equivalent concentration were lowest after feeding in seawater killifish, whereas P(CO(2)) was greatly elevated (80-95 Torr) in chyme from both seawater and freshwater animals but declined to lower levels (13 Torr) after 1-2 weeks fasting. There were no differences in pH, P(CO(2)) or the concentrations of basic equivalents in intestinal fluid from seawater versus freshwater animals at 12-24 h or 1-2 weeks post-feeding. The results are interpreted in terms of the absence of gastric HCl secretion, the limitations of the gills for acid-base balance and Cl(-) transport, and therefore the need for intestinal Cl(-) uptake in freshwater killifish, and the potential for O(2) release from the mucosal blood flow by the high P(CO(2)) in the intestinal fluids. At least in seawater killifish, H(+)-ATPase running in parallel to HCO(3)(-):Cl(-) exchange in the apical membranes of teleost enterocytes might reduce net base secretion and explain the high P(CO(2)) in the chyme after feeding.
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the role of the kidney in compensating the Alkaline Tide electrolyte load and fluid balance disturbance associated with feeding in the freshwater rainbow trout oncorhynchus mykiss
Comparative Biochemistry and Physiology A-molecular & Integrative Physiology, 2010Co-Authors: Michael J Landman, Carol Bucking, Chris M WoodAbstract:The effect in freshwater rainbow trout of digesting a commercial pellet meal on the renal handling of water, ions and acid-base equivalents was investigated through urine collection over a 48 h period following meal ingestion. The glomerular filtration rate (GFR) and urine flow rate (UFR) were reduced in fed fish between 12 and 24h following the meal, likely reflecting a loss of endogenous water across the gastric epithelium as a result of ingesting dry, ion-rich food pellets. The kidney was also responsible for the excretion of some excess dietary Ca(2+), and, to a much lesser extent, Na(+) and Cl(-), while the urinary excretion of K(+) was unaffected. The most dramatic effect of feeding was the elevation of renal Mg(2+) excretion, with the kidney transitioning from net Mg(2+) reabsorption to net Mg(2+) secretion during digestion. The renal handling of dietary ions accounted for 3-27% of the total ions absorbed from the diet, indicating that a majority of the ions are excreted extra-renally or incorporated into growth. However this does highlight the underestimation of renal ion handling when using unfed fish models. The metabolic alkalosis created by digestion (the Alkaline Tide) resulted in an increase in urine pH as well as a transition from net acidic equivalent excretion in the urine to net basic equivalent excretion. This was due to a decrease in the titratable acidity minus bicarbonate component of urine as well as a decrease in ammonia secretion. Additionally, the experimental separation of the urinary component of acid-base excretion from that of the gills highlighted the substantially larger contribution of the latter. During the Alkaline Tide, renal excretion accounted for approximately 5% of the total basic equivalent excretion to the external water.
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post prandial metabolic alkalosis in the seawater acclimated trout the Alkaline Tide comes in
The Journal of Experimental Biology, 2009Co-Authors: Carol Bucking, John L Fitzpatrick, Sunita R Nadella, Chris M WoodAbstract:The consequences of feeding and digestion on acid-base balance and regulation in a marine teleost (seawater-acclimated steelhead trout; Oncorhynchus mykiss) were investigated by tracking changes in blood pH and [HCO3-], as well as alterations in net acid or base excretion to the water following feeding. Additionally the role of the intestine in the regulation of acid-base balance during feeding was investigated with an in vitro gut sac technique. Feeding did not affect plasma glucose or urea concentrations, however, total plasma ammonia rose during feeding, peaking between 3 and 24 h following the ingestion of a meal, three-fold above resting control values (approximately 300 micromol ml(-1)). This increase in plasma ammonia was accompanied by an increase in net ammonia flux to the water (approximately twofold higher in fed fish versus unfed fish). The arterial blood also became Alkaline with increases in pH and plasma [HCO3-] between 3 and 12 h following feeding, representing the first measurement of an Alkaline Tide in a marine teleost. There was no evidence of respiratory compensation for the measured metabolic alkalosis, as Pa CO2 remained unchanged throughout the post-feeding period. However, in contrast to an earlier study on freshwater-acclimated trout, fed fish did not exhibit a compensating increase in net base excretion, but rather took in additional base from the external seawater, amounting to approximately 8490 micromol kg(-1) over 48 h. In vitro experiments suggest that at least a portion of the Alkaline Tide was eliminated through increased HCO3- secretion coupled to Cl- absorption in the intestinal tract. This did not occur in the intestine of freshwater-acclimated trout. The marked effects of the external salinity (seawater versus freshwater) on different post-feeding patterns of acid-base balance are discussed.
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the Alkaline Tide and ammonia excretion after voluntary feeding in freshwater rainbow trout
The Journal of Experimental Biology, 2008Co-Authors: Carol Bucking, Chris M WoodAbstract:We investigated the potential acid-base and nitrogenous waste excretion challenges created by voluntary feeding in freshwater rainbow trout, with particular focus on the possible occurrence of an Alkaline Tide (a metabolic alkalosis created by gastric HCl secretion during digestion). Plasma metabolites (glucose, urea and ammonia) were measured at various time points before and after voluntary feeding to satiation (approximately 5% body mass meal of dry commercial pellets), as was the net flux of ammonia and titratable alkalinity to the water from unfed and fed fish. Arterial blood, sampled by indwelling catheter, was examined for post-prandial effects on pH, plasma bicarbonate and plasma CO2 tension. There was no significant change in plasma glucose or urea concentrations following feeding, whereas plasma ammonia transiently increased, peaking at threefold above resting values at 12 h after the meal and remaining elevated for 24 h. The increased plasma ammonia was correlated with an increase in net ammonia excretion to the water, with fed fish significantly elevating their net ammonia excretion two- to threefold between 12 and 48 h post feeding. These parameters did not change in unfed control fish. Fed fish likewise increased the net titratable base flux to the water by approximately threefold, which resulted in a transition from a small net acid flux seen in unfed fish to a large net base flux in fed fish. Over 48 h, this resulted in a net excretion of 13 867 micromol kg(-1) more base to the external water than in unfed fish. The arterial blood exhibited a corresponding rise in pH (between 6 and 12 h) and plasma bicarbonate (between 3 and 12 h) following feeding; however, no respiratory compensation was observed, as PaCO2 remained constant. Overall, there was evidence of numerous challenges created by feeding in a freshwater teleost fish, including the occurrence of an Alkaline Tide, and its compensation by excretion of base to the external water. The possible influence of feeding ecology and environmental salinity on these challenges, as well as discrepancies in the literature, are discussed.
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the Alkaline Tide goes out and the nitrogen stays in after feeding in the dogfish shark squalus acanthias
Respiratory Physiology & Neurobiology, 2007Co-Authors: Chris M Wood, Carol Bucking, John L Fitzpatrick, Sunita R NadellaAbstract:In light of previous work showing a marked metabolic alkalosis ("Alkaline Tide") in the bloodstream after feeding in the dogfish shark (Squalus acanthias), we evaluated whether there was a corresponding net base excretion to the water at this time. In the 48 h after a natural voluntary meal (teleost tissue, averaging 5.5% of body weight), dogfish excreted 10,470 micromol kg(-1) more base (i.e. HCO3- equivalents) than the fasted control animals (which exhibited a negative base excretion of -2160 micromol kg(-1)). This large activation of branchial base excretion after feeding thereby prevented a potentially fatal alkalinization of the body fluids by the Alkaline Tide. The rate peaked at 330 micromol kg(-1) h(-1) at 12.5-24 h after the meal. Despite a prolonged 1.7-fold elevation in MO2 after feeding ("specific dynamic action"), urea-N excretion decreased by 39% in the same 48 h period relative to fasted controls. In contrast, ammonia-N excretion did not change appreciably. The N/O2 ratio declined from 0.51 in fasted animals to 0.19 in fed sharks, indicating a stimulation of N-anabolic processes at this time. These results, which differ greatly from those in teleost fish, are interpreted in terms of the fundamentally different ureotelic osmoregulatory strategy of elasmobranchs, and recent discoveries on base excretion and urea-retention mechanisms in elasmobranch gills.
Denis V Andrade - One of the best experts on this subject based on the ideXlab platform.
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blood oxygen affinity increases during digestion in the south american rattlesnake crotalus durissus terrificus
Comparative Biochemistry and Physiology A-molecular & Integrative Physiology, 2015Co-Authors: Rafael P Bovo, Adriana Fuga, Mariana A Michelicampbell, Jose Eduardo De Carvalho, Denis V AndradeAbstract:Abstract Digesting snakes experience massive increases in metabolism that can last for many days and are accompanied by adjustments in the oxygen transport cascade. Accordingly, we examined the oxygen-binding properties of the blood in the South American rattlesnake ( Crotalus durissus terrificus ) during fasting and 24 and 48 h after the snakes have ingested a rodent meal corresponding to 15% (± 2%) of its own body mass. In general, oxygen–hemoglobin (Hb–O 2 ) affinity was significantly increased 24 h post-feeding, and then returned toward fasting values within 48 h post-feeding. Content of organic phosphates ([NTP] and [NTP]/[Hb]), hemoglobin cooperativity (Hill's n), and Bohr Effect (ΔlogP 50 /ΔpH) were not affected by feeding. The postprandial increase in Hb–O 2 affinity in the South American rattlesnake can be almost entirely ascribed by the moderate Alkaline Tide that follows meal ingestion. In general, digesting snakes were able to regulate blood metabolites at quite constant levels (e.g., plasma osmolality, lactate, glucose, and total protein levels). The level of circulating lipids, however, was considerably increased, which may be related to their mobilization, since lipids are known to be incorporated by the enterocytes after snakes have fed. In conclusion, our results indicate that the exceptional metabolic increment exhibited by C. d. terrificus during meal digestion is entirely supported by the aerobic pathways and that among the attending cardiorespiratory adjustments, pulmonary Hb–O 2 loading is likely improved due to the increment in blood O 2 affinity.
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ventilatory compensation of the Alkaline Tide during digestion in the snake boa constrictor
The Journal of Experimental Biology, 2004Co-Authors: Denis V Andrade, Luis Felipe Toledo, Augusto Shinya Abe, Tobias WangAbstract:SUMMARY The increased metabolic rate during digestion is associated with changes in arterial acid–base parameters that are caused by gastric acid secretion (the `Alkaline Tide9). Net transfer of HCl to the stomach lumen causes an increase in plasma HCO 3 – levels, but arterial pH does not change because of a ventilatory compensation that counters the metabolic alkalosis. It seems, therefore, that ventilation is controlled to preserve pH and not P CO 2 during the postprandial period. To investigate this possibility, we determined arterial acid–base parameters and the metabolic response to digestion in the snake Boa constrictor , where gastric acid secretion was inhibited pharmacologically by oral administration of omeprazole. The increase in oxygen consumption of omeprazole-treated snakes after ingestion of 30% of their own body mass was quantitatively similar to the response in untreated snakes, although the peak of the metabolic response occurred later (36 h versus 24 h). Untreated control animals exhibited a large increase in arterial plasma HCO 3 – concentration of approximately 12 mmol l –1 , but arterial pH only increased by 0.12 pH units because of a simultaneous increase in arterial P CO 2 by about 10 mmHg. Omeprazole virtually abolished the changes in arterial pH and plasma HCO 3 – concentration during digestion and there was no increase in arterial P CO 2 . The increased arterial P CO 2 during digestion is not caused, therefore, by the increased metabolism during digestion or a lower ventilatory responsiveness to ventilatory stimuli during a presumably relaxed state in digestion. Furthermore, the constant arterial P CO 2 , in the absence of an Alkaline Tide, of omeprazole-treated snakes strongly suggests that pH rather than P CO 2 normally affects chemoreceptor activity and ventilatory drive.
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effects of inhibition gastric acid secretion on arterial acid base status during digestion in the toad bufo marinus
Comparative Biochemistry and Physiology A-molecular & Integrative Physiology, 2003Co-Authors: Johnnie B Andersen, Denis V Andrade, Tobias WangAbstract:Digestion affects acid–base status, because the net transfer of HCl from the blood to the stomach lumen leads to an increase in levels in both extra- and intracellular compartments. The increase in plasma wx , the Alkaline y y HCO HCO 3 3 Tide, is particularly pronounced in amphibians and reptiles, but is not associated with an increased arterial pH, because of a concomitant rise in arterial PCO caused by a relative hypoventilation. In this study, we investigate whether the 2 postprandial increase in PaCO of the toad Bufo marinus represents a compensatory response to the increased plasma 2 wx or a state-dependent change in the control of pulmonary ventilation. To this end, we successfully prevented the y HCO3 Alkaline Tide, by inhibiting gastric acid secretion with omeprazole, and compared the response to that of untreated toads determined in our laboratory during the same period. In addition, we used vascular infusions of bicarbonate to mimic the Alkaline Tide in fasting animals. Omeprazole did not affect blood gases, acid–base and haematological parameters in fasting toads, but abolished the postprandial increase in plasma wx and the rise in arterial PCO that normally y HCO 32 peaks 48 h into the digestive period. Vascular infusion of , that mimicked the postprandial rise in plasma y HCO3 wx , led to a progressive respiratory compensation of arterial pH through increased arterial PCO . Thus, irrespective y HCO3 2
Tobias Wang - One of the best experts on this subject based on the ideXlab platform.
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ventilatory compensation of the Alkaline Tide during digestion in the snake boa constrictor
The Journal of Experimental Biology, 2004Co-Authors: Denis V Andrade, Luis Felipe Toledo, Augusto Shinya Abe, Tobias WangAbstract:SUMMARY The increased metabolic rate during digestion is associated with changes in arterial acid–base parameters that are caused by gastric acid secretion (the `Alkaline Tide9). Net transfer of HCl to the stomach lumen causes an increase in plasma HCO 3 – levels, but arterial pH does not change because of a ventilatory compensation that counters the metabolic alkalosis. It seems, therefore, that ventilation is controlled to preserve pH and not P CO 2 during the postprandial period. To investigate this possibility, we determined arterial acid–base parameters and the metabolic response to digestion in the snake Boa constrictor , where gastric acid secretion was inhibited pharmacologically by oral administration of omeprazole. The increase in oxygen consumption of omeprazole-treated snakes after ingestion of 30% of their own body mass was quantitatively similar to the response in untreated snakes, although the peak of the metabolic response occurred later (36 h versus 24 h). Untreated control animals exhibited a large increase in arterial plasma HCO 3 – concentration of approximately 12 mmol l –1 , but arterial pH only increased by 0.12 pH units because of a simultaneous increase in arterial P CO 2 by about 10 mmHg. Omeprazole virtually abolished the changes in arterial pH and plasma HCO 3 – concentration during digestion and there was no increase in arterial P CO 2 . The increased arterial P CO 2 during digestion is not caused, therefore, by the increased metabolism during digestion or a lower ventilatory responsiveness to ventilatory stimuli during a presumably relaxed state in digestion. Furthermore, the constant arterial P CO 2 , in the absence of an Alkaline Tide, of omeprazole-treated snakes strongly suggests that pH rather than P CO 2 normally affects chemoreceptor activity and ventilatory drive.
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effects of inhibition gastric acid secretion on arterial acid base status during digestion in the toad bufo marinus
Comparative Biochemistry and Physiology A-molecular & Integrative Physiology, 2003Co-Authors: Johnnie B Andersen, Denis V Andrade, Tobias WangAbstract:Digestion affects acid–base status, because the net transfer of HCl from the blood to the stomach lumen leads to an increase in levels in both extra- and intracellular compartments. The increase in plasma wx , the Alkaline y y HCO HCO 3 3 Tide, is particularly pronounced in amphibians and reptiles, but is not associated with an increased arterial pH, because of a concomitant rise in arterial PCO caused by a relative hypoventilation. In this study, we investigate whether the 2 postprandial increase in PaCO of the toad Bufo marinus represents a compensatory response to the increased plasma 2 wx or a state-dependent change in the control of pulmonary ventilation. To this end, we successfully prevented the y HCO3 Alkaline Tide, by inhibiting gastric acid secretion with omeprazole, and compared the response to that of untreated toads determined in our laboratory during the same period. In addition, we used vascular infusions of bicarbonate to mimic the Alkaline Tide in fasting animals. Omeprazole did not affect blood gases, acid–base and haematological parameters in fasting toads, but abolished the postprandial increase in plasma wx and the rise in arterial PCO that normally y HCO 32 peaks 48 h into the digestive period. Vascular infusion of , that mimicked the postprandial rise in plasma y HCO3 wx , led to a progressive respiratory compensation of arterial pH through increased arterial PCO . Thus, irrespective y HCO3 2
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effects of feeding on arterial blood gases in the american alligator alligator mississippiensis
The Journal of Experimental Biology, 2000Co-Authors: Morten Busk, James W. Hicks, Albert F Bennett, Johannes Overgaard, Tobias WangAbstract:Reptiles habitually ingest large meals at infrequent intervals, leading to changes in acid-base status as the net secretion of acid to the stomach causes a metabolic alkalosis (the Alkaline Tide). In chronically cannulated and undisturbed amphibians and reptiles, the pH changes in arterial blood are, nevertheless, reduced by a concomitant respiratory acidosis (increased P(CO2) caused by a relative hypoventilation). Alligators (Alligator mississippiensis) have been reported to exhibit exceptionally large increases in plasma [HCO3(−)] following feeding, but these studies were based on blood samples obtained by cardiac puncture, so stress and disturbance may have affected the blood gas levels. Furthermore, crocodilian haemoglobin is characterised by a unique binding of HCO3(−) that act to reduce blood oxygen-affinity, and it has been proposed that this feature safeguards oxygen offloading by counteracting pH effects on blood oxygen-affinity. Therefore, to study acid-base regulation and the interaction between the Alkaline Tide and oxygen transport in more detail, we describe the arterial blood gas composition of chronically cannulated and undisturbed alligators before and after voluntary feeding (meal size 7.5+/−1% of body mass). Digestion was associated with an approximately fourfold increase in metabolic rate (from 0.63+/−0.04 to 2.32+/−0.24 ml O(2) min(−1)kg(−1)) and was accompanied by a small increase in the respiratory gas exchange ratio. The arterial P(O2) of fasting alligators was 60.3+/−6.8 mmHg (1 mmHg = 0.133 kPa) and reached a maximum of 81.3+/−2.7 mmHg at 96 h following feeding; there was only a small increase in lactate levels, so the increased metabolic rate seems to be entirely aerobic. Plasma [HCO3(−)] increased from 24.4+/−1.1 to 36.9+/−1.7 mmol l(−1) (at 24 h), but since arterial P(CO2) increased from 29.0+/−1.1 to 36.8+/−1.3 mmHg, arterial pH remained virtually unaffected (changing from 7.51+/−0.01 to 7.58+/−0.01 at 24 h). The changes in plasma [HCO3(−)] were mirrored by equimolar reductions in plasma [Cl(−)]. The in vitro blood oxygen-affinity was reduced during the post-prandial period, whereas the estimated in vivo blood oxygen-affinity remained virtually constant. This supports the view that the specific HCO3(−) effect prevents an increased blood oxygen-affinity during digestion in alligators.
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metabolic ventilatory and acid base responses associated with specific dynamic action in the toad bufo marinus
Physiological and Biochemical Zoology, 1995Co-Authors: Tobias Wang, Warren W Burggren, Edward NobregaAbstract:Specific dynamic action (SDA), the postprandial increase in metabolic rate that has been well documented in numerous vertebrates, intensifies demand for O₂ delivery by the ventilatory and cardiovascular systems. Yet the well-documented increase in plasma pH following feeding (the "Alkaline Tide") should, paradoxically, result in a decrease rather than an increase in ventilation. The intent of this study was to investigate in the marine toad Bufo marinus whether there is a change in the relationship between metabolism, lung ventilation, and blood pH associated specifically with SDA. We measured $\dot{V}O_{2}$, $\dot{V}CO_{2}$; respiratory quotient ($R_{E}$); lung ventilation volume and frequency; arterial pH, PO₂, and hematocrit; and heart rate before and after the induction of SDA bypeptone injection directly into the stomach. Levels of $\dot{V}O_{2}$ and $\dot{V}CO_{2}$; approximately 40-60 mL · g⁻¹ h⁻¹, doubled 5-6 h afterpeptone injection and then declined within 24 h. Accompanying this profound pepton...