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Uma Sundaram - One of the best experts on this subject based on the ideXlab platform.
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inhibition of Intestinal Villus cell na k atpase mediates altered glucose and nacl absorption in obesity associated diabetes and hypertension
The FASEB Journal, 2019Co-Authors: Balasubramanian Palaniappan, Subha Arthur, Vijaya Sundaram, Molly R Butts, Shanmuga Sundaram, Kathiresh Mani, Soudamani Singh, Niraj Nepal, Uma SundaramAbstract:During obesity, diabetes and hypertension inevitably coexist and cause innumerable health disparities. In the obesity, diabetes, and hypertension triad (ODHT), deregulation of glucose and NaCl homeostasis, respectively, causes diabetes and hypertension. In the mammalian intestine, glucose is primarily absorbed by Na-glucose cotransport 1 (SGLT1) and coupled NaCl by the dual operation of Na-H exchange 3 (NHE3) and Cl-HCO3 [down-regulated in adenoma (DRA) or putative anion transporter 1 (PAT1)] exchange in the brush border membrane (BBM) of Villus cells. The basolateral membrane (BLM) Na/K-ATPase provides the favorable transcellular Na gradient for BBM SGLT1 and NHE3. How these multiple, distinct transport processes may be affected in ODHT is unclear. Here, we show the novel and broad regulation by Na/K-ATPase of glucose and NaCl absorption in ODHT in multiple species (mice, rats, and humans). In vivo, during obesity inhibition of Villus-cell BLM, Na/K-ATPase led to compensatory stimulation of BBM SGLT1 and DRA or PAT1, whereas NHE3 was unaffected. Supporting this new cellular adaptive mechanism, direct silencing of BLM Na/K-ATPase in Intestinal epithelial cells resulted in selective stimulation of BBM SGLT1 and DRA or PAT1 but not NHE3. These changes will lead to an increase in glucose absorption, maintenance of traditional coupled NaCl absorption, and a de novo increase in NaCl absorption from the novel coupling of stimulated SGLT1 with DRA or PAT1. Thus, these novel observations provide the pathophysiologic basis for the deregulation of glucose and NaCl homeostasis of diabetes and hypertension, respectively, during obesity. These observations may lead to more efficacious treatment for obesity-associated diabetes and hypertension.-Palaniappan, B., Arthur, S., Sundaram, V. L., Butts, M., Sundaram, S., Mani, K., Singh, S., Nepal, N., Sundaram, U. Inhibition of Intestinal Villus cell Na/K-ATPase mediates altered glucose and NaCl absorption in obesity-associated diabetes and hypertension.
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identification and characterization of rabbit small Intestinal Villus cell brush border membrane na glutamine cotransporter
American Journal of Physiology-gastrointestinal and Liver Physiology, 2008Co-Authors: Jamilur R Talukder, Ramesh Kekuda, Prosenjit Saha, Subha Arthur, Uma SundaramAbstract:Glutamine, the primary metabolic fuel for the mammalian small Intestinal enterocytes, is primarily assimilated by Na-amino acid cotransporters. Although Na-solute cotransport has been shown to exist in the brush border membrane (BBM) of the absorptive Villus cells, the identity of Na-glutamine cotransport in rabbit small Intestinal Villus cells was unknown. Na-dependent glutamine uptake is present in Villus BBM vesicles. An intravesicular proton gradient did not stimulate this Na-dependent glutamine uptake, whereas Li+ did not significantly suppress this uptake. These observations in concert with amino acid substitution studies suggested that Na-glutamine cotransporter in the Villus cell BBM was the newly identified cotransporter B0AT1 (SLC6A19). Quantitative real-time PCR identified the message for this cotransporter in Villus cells. Thus a full-length cDNA of B0AT1 was cloned and expressed in MDA-MB-231 cells. This expressed cotransporter exhibited characteristics similar to those observed in Villus cells from the rabbit small intestine. Antibody was generated for B0AT1 that demonstrated the presence of this cotransporter protein in the Villus cell BBM. Kinetic studies defined the kinetic parameters of this cotransporter. Thus this study describes the identification, cloning, and characterization of the Na-amino acid cotransporter responsible for the assimilation of a critical amino acid by the absorptive Villus cells in the mammalian small intestine.
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mechanism of regulation of rabbit Intestinal Villus cell brush border membrane na h exchange by nitric oxide
American Journal of Physiology-gastrointestinal and Liver Physiology, 2007Co-Authors: Steven Coon, Guohong Shao, Sheik Wisel, Raju Vulaupalli, Uma SundaramAbstract:In the mammalian small intestine, coupled NaCl absorption occurs via the dual operation of Na/H and Cl/HCO3 exchange on the Villus cell brush border membrane (BBM). Although constitutive nitric oxi...
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na glucose and na neutral amino acid cotransport are uniquely regulated by constitutive nitric oxide in rabbit small Intestinal Villus cells
American Journal of Physiology-gastrointestinal and Liver Physiology, 2005Co-Authors: Steven Coon, Guohong Shao, James K Kim, Uma SundaramAbstract:Na-nutrient cotransport processes are not only important for the assimilation of essential nutrients but also for the absorption of Na in the mammalian small intestine. The effect of constitutive n...
E Martin - One of the best experts on this subject based on the ideXlab platform.
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dobutamine maintains Intestinal Villus blood flow during normotensive endotoxemia an intravital microscopic study in the rat
Journal of Critical Care, 1997Co-Authors: Andreas Secchi, Ruth Wellmann, E Martin, Heinfried SchmidtAbstract:Abstract Purpose: The gut plays a pivotal role in sepsis. Intestinal hypoperfusion with subsequent ischemia leads to translocation of endotoxin. Dobutamine has been demonstrated to increase mesenteric blood flow during endotoxic shock; however, its effects on mucosal blood flow especially in Intestinal villi is not known. Therefore, we investigated its influence on the blood flow and the arteriolar diameters in Intestinal villi in a model of normotensive endotoxemia. Materials and Methods: Twenty-one male Wistar rats were divided into three groups: (1) control, saline; (2) endotoxin, endotoxin 1.5 mg/kg during 60 minutes; and (3) dobutamine, endotoxin 1.5 mg/kg (60 minutes) and dobutamine 2.5 μg/kg/min during 120 minutes. Villus blood flow and arteriolar diameters were determined at 0 minutes, 60 minutes, and 120 minutes in each group using intravital microscopy. Results: Villus blood flow was constant in the control group, significantly reduced at 120 minutes in the endotoxin group (120 minutes, 55.1 ± 7.4%), and remained at baseline values in the dobutamine group. The arteriolar diameters remained constant in the control and the dobutamine groups, but they were significantly reduced in the endotoxin group at 120 minutes (7.8 ± 0.2 to 6.5 ± 0.7 Lm). Conclusion: Our results indicate that in rats with normotensive endotoxemia, arteriolar diameters and blood flow in Intestinal villi were reduced. Dobutamine prevented arteriolar constriction and maintained Villus blood flow at preendotoxemic values.
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dopexamine maintains Intestinal Villus blood flow during endotoxemia in rats
Critical Care Medicine, 1996Co-Authors: Heinfried Schmidt, Andreas Secchi, Ruth Wellmann, A Bach, H Bhrer, E MartinAbstract:Objective To determine the influence of dopexamine, a synthetic catecholamine ligand for dopaminergic and beta2-adrenergic receptors, on alterations of the Intestinal Villus microcirculation in a model of normotensive endotoxemia.Design Randomized, controlled trial.Setting Experimental laboratory.Su
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effect of low dose dopamine on Intestinal Villus microcirculation during normotensive endotoxaemia in rats
BJA: British Journal of Anaesthesia, 1996Co-Authors: Heinfried Schmidt, Andreas Secchi, Ruth Wellmann, A Bach, H Bohrer, E MartinAbstract:Hypoperfusion of the gut mucosa is thought to be a factor in the development of gut barrier failure during sepsis and septic shock. Dopamine stimulates DA-1 receptors which mediate regional vasodilatation in the gut. Therefore, we have investigated the effect of low-dose dopamine (3 micrograms kg-1 min-1) on the Intestinal Villus microcirculation during endotoxaemia in a rat model of normotensive endotoxaemia, using in vivo videomicroscopy. Blood flow in and the diameters of central Villus arterioles were measured before, immediately after and 60 min after a 1-h continuous infusion of endotoxin 1.5 mg/kg body weight. After baseline measurements were obtained, rats received either an infusion of 0.9% saline (group A; n = 7) or a volume-equivalent infusion of dopamine 3 micrograms kg-1 min-1 (group B; n = 7) throughout the study. Control animals (group C; n = 7) received no endotoxin or dopamine. In group A, Villus blood flow (mean baseline 8.4 (SEM 0.9) nl min-1) decreased by 29.7 (8.9)% to 5.9 (0.9) nl min-1 immediately after endotoxin challenge and by a total of 43.1 (7.3)% to 4.7 (0.7) nl min-1 after another 60 min. Simultaneously, Villus arteriolar diameters decreased from 7.8 (0.2) to 6.9 (0.3) microns and to 6.5 (0.3) microns, respectively. In group B, Villus blood flow (baseline 8.7 (0.4) nl min-1) was unchanged immediately after the 1-h infusion of endotoxin (8.3 (0.4) nl min-1). However, another 60 min later blood flow decreased by 28.8 (8.0)% to 6.1 (0.7) nl min-1. In contrast with group A, the diameters of the central Villus arterioles were unchanged despite administration of endotoxin (7.9 (0.2) microns; 8.1 (0.4) microns; 8.2 (0.5) microns). In group C, there were no changes in Villus blood flow or arteriolar diameters throughout the study. Our results indicated that low-dose dopamine did not prevent, but delayed and attenuated, the decrease in Intestinal Villus blood during normotensive endotoxaemia.
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effect of endotoxemia on Intestinal Villus microcirculation in rats
Journal of Surgical Research, 1996Co-Authors: Heinfried Schmidt, Andreas Secchi, Ruth Wellmann, A Bach, H Bohrer, Martha Maria Gebhard, E MartinAbstract:Intestinal mucosal hypoperfusion with subsequent ischemia during endotoxemia might cause a breakdown of the gut barrier with translocation of bacteria and their toxins into the systemic circulation, thus maintaining a "gut-derived" septic state. The aim of this study was to investigate the influence of endotoxin on the microcirculation of Intestinal villi, which represent the most vulnerable part of the mucosa. The changes in blood flow and in the diameters of the central Villus arterioles located in the distal ileum were monitored in control rats without lipopolysaccharide (LPS) exposure (n=7), and in rats receiving 1.5 mg/kg b.w. LPS (n=7) or 15 mg/kg b.w. LPS (n=7) over 60 min. The blood flow and the arteriolar diameters were determined using in vivo videomicroscopy at baseline, and 60 min and 120 min later. In control animals, no change in blood flow and arteriolar diameters were observed during the entire experiment. Administration of 1.5 mg/kg b.w. LPS reduced the blood flow to 69.5 +/- 9.0% of the baseline value at the end of the study period. This decrease in blood flow was associated with a decrease in the Villus arteriolar diameters by 17.4 +/- 2.5% from the baseline values. In animals exposed to 15 mg/kg b.w. LPS, the decrease in Villus blood flow at 60 min was 64.8 +/- 10.9% of baseline, and at 120 min 66.9 +/- 12.6% of baseline. The diameters of the Villus arterioles were reduced by 11.5 +/- 2.4% and 15.1 +/- 1.7%, respectively. In the control group and in the 1.5-mg/kg LPS group, the mean arterial blood pressure did not change during the entire study period. In the 15-mg/kg LPS group, the mean arterial pressure tended to decrease after 60 min. These data suggest a reduction of Villus blood flow due to vasoconstriction in the central Villus arterioles during normotensive endotoxmia, which might represent the mechanism for the mucosal ischemia observed in critically ill patients.
Heinfried Schmidt - One of the best experts on this subject based on the ideXlab platform.
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dobutamine maintains Intestinal Villus blood flow during normotensive endotoxemia an intravital microscopic study in the rat
Journal of Critical Care, 1997Co-Authors: Andreas Secchi, Ruth Wellmann, E Martin, Heinfried SchmidtAbstract:Abstract Purpose: The gut plays a pivotal role in sepsis. Intestinal hypoperfusion with subsequent ischemia leads to translocation of endotoxin. Dobutamine has been demonstrated to increase mesenteric blood flow during endotoxic shock; however, its effects on mucosal blood flow especially in Intestinal villi is not known. Therefore, we investigated its influence on the blood flow and the arteriolar diameters in Intestinal villi in a model of normotensive endotoxemia. Materials and Methods: Twenty-one male Wistar rats were divided into three groups: (1) control, saline; (2) endotoxin, endotoxin 1.5 mg/kg during 60 minutes; and (3) dobutamine, endotoxin 1.5 mg/kg (60 minutes) and dobutamine 2.5 μg/kg/min during 120 minutes. Villus blood flow and arteriolar diameters were determined at 0 minutes, 60 minutes, and 120 minutes in each group using intravital microscopy. Results: Villus blood flow was constant in the control group, significantly reduced at 120 minutes in the endotoxin group (120 minutes, 55.1 ± 7.4%), and remained at baseline values in the dobutamine group. The arteriolar diameters remained constant in the control and the dobutamine groups, but they were significantly reduced in the endotoxin group at 120 minutes (7.8 ± 0.2 to 6.5 ± 0.7 Lm). Conclusion: Our results indicate that in rats with normotensive endotoxemia, arteriolar diameters and blood flow in Intestinal villi were reduced. Dobutamine prevented arteriolar constriction and maintained Villus blood flow at preendotoxemic values.
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dopexamine maintains Intestinal Villus blood flow during endotoxemia in rats
Critical Care Medicine, 1996Co-Authors: Heinfried Schmidt, Andreas Secchi, Ruth Wellmann, A Bach, H Bhrer, E MartinAbstract:Objective To determine the influence of dopexamine, a synthetic catecholamine ligand for dopaminergic and beta2-adrenergic receptors, on alterations of the Intestinal Villus microcirculation in a model of normotensive endotoxemia.Design Randomized, controlled trial.Setting Experimental laboratory.Su
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effect of low dose dopamine on Intestinal Villus microcirculation during normotensive endotoxaemia in rats
BJA: British Journal of Anaesthesia, 1996Co-Authors: Heinfried Schmidt, Andreas Secchi, Ruth Wellmann, A Bach, H Bohrer, E MartinAbstract:Hypoperfusion of the gut mucosa is thought to be a factor in the development of gut barrier failure during sepsis and septic shock. Dopamine stimulates DA-1 receptors which mediate regional vasodilatation in the gut. Therefore, we have investigated the effect of low-dose dopamine (3 micrograms kg-1 min-1) on the Intestinal Villus microcirculation during endotoxaemia in a rat model of normotensive endotoxaemia, using in vivo videomicroscopy. Blood flow in and the diameters of central Villus arterioles were measured before, immediately after and 60 min after a 1-h continuous infusion of endotoxin 1.5 mg/kg body weight. After baseline measurements were obtained, rats received either an infusion of 0.9% saline (group A; n = 7) or a volume-equivalent infusion of dopamine 3 micrograms kg-1 min-1 (group B; n = 7) throughout the study. Control animals (group C; n = 7) received no endotoxin or dopamine. In group A, Villus blood flow (mean baseline 8.4 (SEM 0.9) nl min-1) decreased by 29.7 (8.9)% to 5.9 (0.9) nl min-1 immediately after endotoxin challenge and by a total of 43.1 (7.3)% to 4.7 (0.7) nl min-1 after another 60 min. Simultaneously, Villus arteriolar diameters decreased from 7.8 (0.2) to 6.9 (0.3) microns and to 6.5 (0.3) microns, respectively. In group B, Villus blood flow (baseline 8.7 (0.4) nl min-1) was unchanged immediately after the 1-h infusion of endotoxin (8.3 (0.4) nl min-1). However, another 60 min later blood flow decreased by 28.8 (8.0)% to 6.1 (0.7) nl min-1. In contrast with group A, the diameters of the central Villus arterioles were unchanged despite administration of endotoxin (7.9 (0.2) microns; 8.1 (0.4) microns; 8.2 (0.5) microns). In group C, there were no changes in Villus blood flow or arteriolar diameters throughout the study. Our results indicated that low-dose dopamine did not prevent, but delayed and attenuated, the decrease in Intestinal Villus blood during normotensive endotoxaemia.
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effect of endotoxemia on Intestinal Villus microcirculation in rats
Journal of Surgical Research, 1996Co-Authors: Heinfried Schmidt, Andreas Secchi, Ruth Wellmann, A Bach, H Bohrer, Martha Maria Gebhard, E MartinAbstract:Intestinal mucosal hypoperfusion with subsequent ischemia during endotoxemia might cause a breakdown of the gut barrier with translocation of bacteria and their toxins into the systemic circulation, thus maintaining a "gut-derived" septic state. The aim of this study was to investigate the influence of endotoxin on the microcirculation of Intestinal villi, which represent the most vulnerable part of the mucosa. The changes in blood flow and in the diameters of the central Villus arterioles located in the distal ileum were monitored in control rats without lipopolysaccharide (LPS) exposure (n=7), and in rats receiving 1.5 mg/kg b.w. LPS (n=7) or 15 mg/kg b.w. LPS (n=7) over 60 min. The blood flow and the arteriolar diameters were determined using in vivo videomicroscopy at baseline, and 60 min and 120 min later. In control animals, no change in blood flow and arteriolar diameters were observed during the entire experiment. Administration of 1.5 mg/kg b.w. LPS reduced the blood flow to 69.5 +/- 9.0% of the baseline value at the end of the study period. This decrease in blood flow was associated with a decrease in the Villus arteriolar diameters by 17.4 +/- 2.5% from the baseline values. In animals exposed to 15 mg/kg b.w. LPS, the decrease in Villus blood flow at 60 min was 64.8 +/- 10.9% of baseline, and at 120 min 66.9 +/- 12.6% of baseline. The diameters of the Villus arterioles were reduced by 11.5 +/- 2.4% and 15.1 +/- 1.7%, respectively. In the control group and in the 1.5-mg/kg LPS group, the mean arterial blood pressure did not change during the entire study period. In the 15-mg/kg LPS group, the mean arterial pressure tended to decrease after 60 min. These data suggest a reduction of Villus blood flow due to vasoconstriction in the central Villus arterioles during normotensive endotoxmia, which might represent the mechanism for the mucosal ischemia observed in critically ill patients.
Joohye Song - One of the best experts on this subject based on the ideXlab platform.
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gut microbiota regulates lacteal integrity by inducing vegf c in Intestinal Villus macrophages
EMBO Reports, 2019Co-Authors: Kibaek Choe, Seunghwan Jeong, Taija Makinen, Charles D. Surh, Seon Pyo Hong, Joohye SongAbstract:Abstract A lacteal is a blunt‐ended, long, tube‐like lymphatic vessel located in the center of each Intestinal Villus that provides a unique route for drainage of absorbed lipids from the small intestine. However, key regulators for maintaining lacteal integrity are poorly understood. Here, we explore whether and how the gut microbiota regulates lacteal integrity. Germ depletion by antibiotic treatment triggers lacteal regression during adulthood and delays lacteal maturation during the postnatal period. In accordance with compromised lipid absorption, the button‐like junction between lymphatic endothelial cells, which is ultrastructurally open to permit free entry of dietary lipids into lacteals, is significantly reduced in lacteals of germ‐depleted mice. Lacteal defects are also found in germ‐free mice, but conventionalization of germ‐free mice leads to normalization of lacteals. Mechanistically, VEGF‐C secreted from Villus macrophages upon MyD88‐dependent recognition of microbes and their products is a main factor in lacteal integrity. Collectively, we conclude that the gut microbiota is a crucial regulator for lacteal integrity by endowing its unique microenvironment and regulating Villus macrophages in small intestine.
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Gut microbiota regulates lacteal integrity by inducing VEGF-C in Intestinal Villus macrophages
'Royal College of Obstetricians & Gynaecologists (RCOG)', 2019Co-Authors: Suh S., Charles D. Surh, Seon Pyo Hong, Choe K., Jeong S.-h., Mäkinen T., Kwang Soon Kim, Alitalo K., Gou Young Koh, Joohye SongAbstract:A lacteal is a blunt-ended, long, tube-like lymphatic vessel located in the center of each Intestinal Villus that provides a unique route for drainage of absorbed lipids from the small intestine. However, key regulators for maintaining lacteal integrity are poorly understood. Here, we explore whether and how the gut microbiota regulates lacteal integrity. Germ depletion by antibiotic treatment triggers lacteal regression during adulthood and delays lacteal maturation during the postnatal period. In accordance with compromised lipid absorption, the button-like junction between lymphatic endothelial cells, which is ultrastructurally open to permit free entry of dietary lipids into lacteals, is significantly reduced in lacteals of germ-depleted mice. Lacteal defects are also found in germ-free mice, but conventionalization of germ-free mice leads to normalization of lacteals. Mechanistically, VEGF-C secreted from Villus macrophages upon MyD88-dependent recognition of microbes and their products is a main factor in lacteal integrity. Collectively, we conclude that the gut microbiota is a crucial regulator for lacteal integrity by endowing its unique microenvironment and regulating Villus macrophages in small intestine. © 2019 The Autho
Andreas Secchi - One of the best experts on this subject based on the ideXlab platform.
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dobutamine maintains Intestinal Villus blood flow during normotensive endotoxemia an intravital microscopic study in the rat
Journal of Critical Care, 1997Co-Authors: Andreas Secchi, Ruth Wellmann, E Martin, Heinfried SchmidtAbstract:Abstract Purpose: The gut plays a pivotal role in sepsis. Intestinal hypoperfusion with subsequent ischemia leads to translocation of endotoxin. Dobutamine has been demonstrated to increase mesenteric blood flow during endotoxic shock; however, its effects on mucosal blood flow especially in Intestinal villi is not known. Therefore, we investigated its influence on the blood flow and the arteriolar diameters in Intestinal villi in a model of normotensive endotoxemia. Materials and Methods: Twenty-one male Wistar rats were divided into three groups: (1) control, saline; (2) endotoxin, endotoxin 1.5 mg/kg during 60 minutes; and (3) dobutamine, endotoxin 1.5 mg/kg (60 minutes) and dobutamine 2.5 μg/kg/min during 120 minutes. Villus blood flow and arteriolar diameters were determined at 0 minutes, 60 minutes, and 120 minutes in each group using intravital microscopy. Results: Villus blood flow was constant in the control group, significantly reduced at 120 minutes in the endotoxin group (120 minutes, 55.1 ± 7.4%), and remained at baseline values in the dobutamine group. The arteriolar diameters remained constant in the control and the dobutamine groups, but they were significantly reduced in the endotoxin group at 120 minutes (7.8 ± 0.2 to 6.5 ± 0.7 Lm). Conclusion: Our results indicate that in rats with normotensive endotoxemia, arteriolar diameters and blood flow in Intestinal villi were reduced. Dobutamine prevented arteriolar constriction and maintained Villus blood flow at preendotoxemic values.
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dopexamine maintains Intestinal Villus blood flow during endotoxemia in rats
Critical Care Medicine, 1996Co-Authors: Heinfried Schmidt, Andreas Secchi, Ruth Wellmann, A Bach, H Bhrer, E MartinAbstract:Objective To determine the influence of dopexamine, a synthetic catecholamine ligand for dopaminergic and beta2-adrenergic receptors, on alterations of the Intestinal Villus microcirculation in a model of normotensive endotoxemia.Design Randomized, controlled trial.Setting Experimental laboratory.Su
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effect of low dose dopamine on Intestinal Villus microcirculation during normotensive endotoxaemia in rats
BJA: British Journal of Anaesthesia, 1996Co-Authors: Heinfried Schmidt, Andreas Secchi, Ruth Wellmann, A Bach, H Bohrer, E MartinAbstract:Hypoperfusion of the gut mucosa is thought to be a factor in the development of gut barrier failure during sepsis and septic shock. Dopamine stimulates DA-1 receptors which mediate regional vasodilatation in the gut. Therefore, we have investigated the effect of low-dose dopamine (3 micrograms kg-1 min-1) on the Intestinal Villus microcirculation during endotoxaemia in a rat model of normotensive endotoxaemia, using in vivo videomicroscopy. Blood flow in and the diameters of central Villus arterioles were measured before, immediately after and 60 min after a 1-h continuous infusion of endotoxin 1.5 mg/kg body weight. After baseline measurements were obtained, rats received either an infusion of 0.9% saline (group A; n = 7) or a volume-equivalent infusion of dopamine 3 micrograms kg-1 min-1 (group B; n = 7) throughout the study. Control animals (group C; n = 7) received no endotoxin or dopamine. In group A, Villus blood flow (mean baseline 8.4 (SEM 0.9) nl min-1) decreased by 29.7 (8.9)% to 5.9 (0.9) nl min-1 immediately after endotoxin challenge and by a total of 43.1 (7.3)% to 4.7 (0.7) nl min-1 after another 60 min. Simultaneously, Villus arteriolar diameters decreased from 7.8 (0.2) to 6.9 (0.3) microns and to 6.5 (0.3) microns, respectively. In group B, Villus blood flow (baseline 8.7 (0.4) nl min-1) was unchanged immediately after the 1-h infusion of endotoxin (8.3 (0.4) nl min-1). However, another 60 min later blood flow decreased by 28.8 (8.0)% to 6.1 (0.7) nl min-1. In contrast with group A, the diameters of the central Villus arterioles were unchanged despite administration of endotoxin (7.9 (0.2) microns; 8.1 (0.4) microns; 8.2 (0.5) microns). In group C, there were no changes in Villus blood flow or arteriolar diameters throughout the study. Our results indicated that low-dose dopamine did not prevent, but delayed and attenuated, the decrease in Intestinal Villus blood during normotensive endotoxaemia.
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effect of endotoxemia on Intestinal Villus microcirculation in rats
Journal of Surgical Research, 1996Co-Authors: Heinfried Schmidt, Andreas Secchi, Ruth Wellmann, A Bach, H Bohrer, Martha Maria Gebhard, E MartinAbstract:Intestinal mucosal hypoperfusion with subsequent ischemia during endotoxemia might cause a breakdown of the gut barrier with translocation of bacteria and their toxins into the systemic circulation, thus maintaining a "gut-derived" septic state. The aim of this study was to investigate the influence of endotoxin on the microcirculation of Intestinal villi, which represent the most vulnerable part of the mucosa. The changes in blood flow and in the diameters of the central Villus arterioles located in the distal ileum were monitored in control rats without lipopolysaccharide (LPS) exposure (n=7), and in rats receiving 1.5 mg/kg b.w. LPS (n=7) or 15 mg/kg b.w. LPS (n=7) over 60 min. The blood flow and the arteriolar diameters were determined using in vivo videomicroscopy at baseline, and 60 min and 120 min later. In control animals, no change in blood flow and arteriolar diameters were observed during the entire experiment. Administration of 1.5 mg/kg b.w. LPS reduced the blood flow to 69.5 +/- 9.0% of the baseline value at the end of the study period. This decrease in blood flow was associated with a decrease in the Villus arteriolar diameters by 17.4 +/- 2.5% from the baseline values. In animals exposed to 15 mg/kg b.w. LPS, the decrease in Villus blood flow at 60 min was 64.8 +/- 10.9% of baseline, and at 120 min 66.9 +/- 12.6% of baseline. The diameters of the Villus arterioles were reduced by 11.5 +/- 2.4% and 15.1 +/- 1.7%, respectively. In the control group and in the 1.5-mg/kg LPS group, the mean arterial blood pressure did not change during the entire study period. In the 15-mg/kg LPS group, the mean arterial pressure tended to decrease after 60 min. These data suggest a reduction of Villus blood flow due to vasoconstriction in the central Villus arterioles during normotensive endotoxmia, which might represent the mechanism for the mucosal ischemia observed in critically ill patients.
