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Mathieu Dehaes - One of the best experts on this subject based on the ideXlab platform.
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perioperative cerebral hemodynamics and Oxygen Metabolism in neonates with single ventricle physiology
2015Co-Authors: Mathieu Dehaes, Erin M Buckley, Henry H Cheng, Peiyi Lin, Silvina L Ferradal, Kathryn A Williams, Rutvi Vyas, Katherine Hagan, Daniel Wigmore, Erica McdavittAbstract:Congenital heart disease (CHD) patients are at risk for neurodevelopmental delay. The etiology of these delays is unclear, but abnormal prenatal cerebral maturation and postoperative hemodynamic instability likely play a role. A better understanding of these factors is needed to improve neurodevelopmental outcome. In this study, we used bedside frequency-domain near infrared spectroscopy (FDNIRS) and diffuse correlation spectroscopy (DCS) to assess cerebral hemodynamics and Oxygen Metabolism in neonates with single-ventricle (SV) CHD undergoing surgery and compared them to controls. Our goals were 1) to compare cerebral hemodynamics between unanesthetized SV and healthy neonates, and 2) to determine if FDNIRS-DCS could detect alterations in cerebral hemodynamics beyond cerebral hemoglobin Oxygen saturation (SO2). Eleven SV neonates were recruited and compared to 13 controls. Preoperatively, SV patients showed decreased cerebral blood flow (CBFi), cerebral Oxygen Metabolism (CMRO2i) and SO2; and increased Oxygen extraction fraction (OEF) compared to controls. Compared to preoperative values, unstable postoperative SV patients had decreased CMRO2i and CBFi, which returned to baseline when stable. However, SO2 showed no difference between unstable and stable states. Preoperative SV neonates are flow-limited and show signs of impaired cerebral development compared to controls. FDNIRS-DCS shows potential to improve assessment of cerebral development and postoperative hemodynamics compared to SO2 alone.
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lower cerebral Oxygen Metabolism in neonates with congenital heart disease as compared to healthy neonates
2014Co-Authors: Rutvi Vyas, Henry H Cheng, Katherine Hagan, P E Grant, Jane W Newburger, M A Franceschini, Mathieu DehaesAbstract:Frequency domain near infrared spectroscopy (FD-NIRS) and diffuse correlation spectroscopy (DCS) can provide noninvasive means to study cerebral hemodynamics in neonates with congenital heart disease (CHD). Using these advanced optical technologies, our preliminary data shows that neonates with CHD have lower cerebral Oxygen Metabolism than healthy neonates.
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cerebral Oxygen Metabolism in neonatal hypoxic ischemic encephalopathy during and after therapeutic hypothermia
2014Co-Authors: Mathieu Dehaes, Peiyi Lin, Alpna Aggarwal, Rosa C Fortuno, Angela Fenoglio, Nadege Rochelabarbe, Janet S SoulAbstract:Pathophysiologic mechanisms involved in neonatal hypoxic ischemic encephalopathy (HIE) are associated with complex changes of blood flow and Metabolism. Therapeutic hypothermia (TH) is effective in reducing the extent of brain injury, but it remains uncertain how TH affects cerebral blood flow (CBF) and Metabolism. Ten neonates undergoing TH for HIE and seventeen healthy controls were recruited from the NICU and the well baby nursery, respectively. A combination of frequency domain near infrared spectroscopy (FDNIRS) and diffuse correlation spectroscopy (DCS) systems was used to non-invasively measure cerebral hemodynamic and metabolic variables at the bedside. Results showed that cerebral Oxygen Metabolism (CMRO2i) and CBF indices (CBFi) in neonates with HIE during TH were significantly lower than post-TH and age-matched control values. Also, cerebral blood volume (CBV) and hemoglobin Oxygen saturation (SO2) were significantly higher in neonates with HIE during TH compared with age-matched control neonates. Post-TH CBV was significantly decreased compared with values during TH whereas SO2 remained unchanged after the therapy. Thus, FDNIRS–DCS can provide information complimentary to SO2 and can assess individual cerebral metabolic responses to TH. Combined FDNIRS–DCS parameters improve the understanding of the underlying physiology and have the potential to serve as bedside biomarkers of treatment response and optimization.
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regional and hemispheric asymmetries of cerebral hemodynamic and Oxygen Metabolism in newborns
2013Co-Authors: Mathieu Dehaes, Peiyi Lin, Angela Fenoglio, Nadege Rochelabarbe, Ellen P Grant, Maria Angela FranceschiniAbstract:Understanding the evolution of regional and hemispheric asymmetries in the early stages of life is essential to the advancement of developmental neuroscience. By using 2 noninvasive optical methods, frequency-domain near-infrared spectroscopy and diffuse correlation spectroscopy, we measured cerebral hemoglobin Oxygenation (SO2), blood volume (CBV), an index of cerebral blood flow (CBFi), and the metabolic rate of Oxygen (CMRO2i) in the frontal, temporal, and parietal regions of 70 premature and term newborns. In concordance with results obtained using more invasive imaging modalities, we verified both hemodynamic (CBV, CBFi, and SO2) and metabolic (CMRO2i) parameters were greater in the temporal and parietal regions than in the frontal region and that these differences increased with age. In addition, we found that most parameters were significantly greater in the right hemisphere than in the left. Finally, in comparing age-matched males and females, we found that males had higher CBFi in most cortical regions, higher CMRO2i in the frontal region, and more prominent right–left CBFi asymmetry. These results reveal, for the first time, that we can detect regional and hemispheric asymmetries in newborns using noninvasive optical techniques. Such a bedside screening tool may facilitate early detection of abnormalities and delays in maturation of specific cortical areas.
Fredrik Palm - One of the best experts on this subject based on the ideXlab platform.
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determinants of renal Oxygen Metabolism during low na diet effect of angiotensin ii at1 and aldosterone receptor blockade
2020Co-Authors: Daniela Patinha, Carla Carvalho, Patrik Persson, Liselotte Pihl, Angelica Fasching, Malou Friederichpersson, Julie Oneill, Fredrik PalmAbstract:KEY POINTS Reducing Na+ intake reduces the partial pressure of Oxygen in the renal cortex and activates the renin-angiotensin-aldosterone system. In the absence of high blood pressure, these consequences of dietary Na+ reduction may be detrimental for the kidney. In a normotensive animal experimental model, reducing Na+ intake for 2 weeks increased renal Oxygen consumption, which was normalized by mineralocorticoid receptor blockade. Furthermore, blockade of the angiotensin II AT1 receptor restored cortical partial pressure of Oxygen by improving Oxygen delivery. This shows that increased activity of the renin-angiotensin-aldosterone system contributes to increased Oxygen Metabolism in the kidney after 2 weeks of a low Na+ diet. The results provide insights into dietary Na+ restriction in the absence of high blood pressure, and its consequences for the kidney. ABSTRACT Reduced Na+ intake reduces the PO2 (partial pressure of Oxygen) in the renal cortex. Upon reduced Na+ intake, reabsorption along the nephron is adjusted with activation of the renin-angiotensin-aldosterone system (RAAS). Thus, we studied the effect of reduced Na+ intake on renal Oxygen homeostasis and function in rats, and the impact of intrarenal angiotensin II AT1 receptor blockade using candesartan and mineralocorticoid receptor blockade using canrenoic acid potassium salt (CAP). Male Sprague-Dawley rats were fed standard rat chow containing normal (0.25%) and low (0.025%) Na+ for 2 weeks. The animals were anaesthetized (thiobutabarbital 120 mg kg-1 ) and surgically prepared for kidney Oxygen Metabolism and function studies before and after acute intrarenal arterial infusion of candesartan (4.2 μg kg-1 ) or intravenous infusion of CAP (20 mg kg-1 ). Baseline mean arterial pressure and renal blood flow were similar in both dietary groups. Fractional Na+ excretion and cortical Oxygen tension were lower and renal Oxygen consumption was higher in low Na+ groups. Neither candesartan nor CAP affected arterial pressure. Renal blood flow and cortical Oxygen tension increased in both groups after candesartan in the low Na+ group. Fractional Na+ excretion was increased and Oxygen consumption reduced in the low Na+ group after CAP. These results suggest that blockade of angiotensin II AT1 receptors has a major impact upon Oxygen delivery during normal and low Na+ conditions, while aldosterone receptors mainly affect Oxygen Metabolism following 2 weeks of a low Na+ diet.
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uremia induces abnormal Oxygen consumption in tubules and aggravates chronic hypoxia of the kidney via oxidative stress
2010Co-Authors: Fredrik Palm, Angelica Fasching, Masaomi Nangaku, Tetsuhiro Tanaka, Lina Nordquist, Peter Hansell, Takahisa Kawakami, Fuyuhiko Nishijima, Toshiro FujitaAbstract:In addition to causing uremic symptoms, uremic toxins accelerate the progression of renal failure. To elucidate the pathophysiology of uremic states, we investigated the effect of indoxyl sulfate (IS), a representative uremic toxin, on Oxygen Metabolism in tubular cells. We demonstrated an increase in Oxygen consumption by IS in freshly isolated rat and human proximal tubules. Studies utilizing ouabain, the Na-K-ATPase inhibitor, and apocynin, the NADPH oxidase inhibitor, as well as the in vivo gene-silencing approach to knock down p22(phox) showed that the increase in tubular Oxygen consumption by IS is dependent on Na-K-ATPase and oxidative stress. We investigated whether the enhanced Oxygen consumption led to subsequent hypoxia of the kidney. An increase in serum IS concentrations in rats administered indole was associated with a decrease in renal Oxygenation (8 h). The remnant kidney in rats developed hypoxia at 16 wk. Treatment of the rats with AST-120, an oral adsorbent that removes uremic toxins, reduced serum IS levels and improved Oxygenation of the kidney. Amelioration of hypoxia in the remnant kidney was associated with better renal functions and less histological injury. Reduction of serum IS levels also led to a decrease in oxidative stress in the kidney. Our ex vivo and in vivo studies implicated that uremic states may deteriorate renal dysfunction via dysregulating Oxygen Metabolism in tubular cells. The abnormal Oxygen Metabolism in tubular cells by uremic toxins was, at least in part, mediated by oxidative stress.
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intrarenal Oxygen in diabetes and a possible link to diabetic nephropathy
2006Co-Authors: Fredrik PalmAbstract:Diabetic nephropathy is a major cause of morbidity and mortality. The exact mechanism mediating the negative influence of hyperglycaemia on renal function remains unclear, although several hypotheses have been postulated. The cellular mechanisms include glucose-induced excessive formation of reactive Oxygen species, increased glucose flux through the polyol pathway and formation of advanced glycation end-products. The renal effects in vivo of each and every one of these mechanisms are even less clear. However, there is growing evidence that hyperglycaemia results in altered renal Oxygen Metabolism and decreased renal Oxygen tension and that these changes are linked to altered kidney function. Clinical data regarding renal Oxygen Metabolism and Oxygen tension are currently rudimentary and our present understanding regarding renal Oxygenation during diabetes is predominantly derived from data obtained from animal models of experimental diabetic nephropathy. This review will present recent findings regarding the link between hyperglycaemia and diabetes-induced alterations in renal Oxygen Metabolism and renal Oxygen availability. A possible link between reduced renal Oxygen tension and the development of diabetic nephropathy includes increased polyol pathway activity and oxidative stress, which result in decreased renal Oxygenation and subsequent activation of hypoxia-inducible factors. This initiates increased gene expression of numerous genes known to be involved in development of diabetic nephropathy.
Richard B Buxton - One of the best experts on this subject based on the ideXlab platform.
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the potential for gas free measurements of absolute Oxygen Metabolism during both baseline and activation states in the human brain
2020Co-Authors: Eulanca Y Liu, Jia Guo, Aaron B Simon, Frank Haist, David J Dubowitz, Richard B BuxtonAbstract:Abstract Quantitative functional magnetic resonance imaging methods make it possible to measure cerebral Oxygen Metabolism (CMRO2) in the human brain. Current methods require the subject to breathe special gas mixtures (hypercapnia and hyperoxia). We tested a noninvasive suite of methods to measure absolute CMRO2 in both baseline and dynamic activation states without the use of special gases: arterial spin labeling (ASL) to measure baseline and activation cerebral blood flow (CBF), with concurrent measurement of the blood Oxygenation level dependent (BOLD) signal as a dynamic change in tissue R2*; VSEAN to estimate baseline O2 extraction fraction (OEF) from a measurement of venous blood R2, which in combination with the baseline CBF measurement yields an estimate of baseline CMRO2; and FLAIR-GESSE to measure tissue R2′ to estimate the scaling parameter needed for calculating the change in CMRO2 in response to a stimulus with the calibrated BOLD method. Here we describe results for a study sample of 17 subjects (8 female, mean age = 25.3 years, range 21–31 years). The primary findings were that OEF values measured with the VSEAN method were in good agreement with previous PET findings, while estimates of the dynamic change in CMRO2 in response to a visual stimulus were in good agreement between the traditional hypercapnia calibration and calibration based on R2′. These results support the potential of gas-free methods for quantitative physiological measurements.
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the potential for gas free measurements of absolute Oxygen Metabolism during both baseline and activation states in the human brain
2019Co-Authors: Eulanca Y Liu, Jia Guo, Aaron B Simon, Frank Haist, David J Dubowitz, Richard B BuxtonAbstract:Abstract Quantitative functional magnetic resonance imaging methods make it possible to measure cerebral Oxygen Metabolism (CMRO2) in the human brain. Current methods require the subject to breathe special gas mixtures (hypercapnia and hyperoxia). We tested a noninvasive suite of methods to measure absolute CMRO2 in both baseline and dynamic activation states without the use of special gases: arterial spin labeling (ASL) to measure baseline and activation cerebral blood flow (CBF), with concurrent measurement of the blood Oxygenation level dependent (BOLD) signal as a dynamic change in tissue R2*; VSEAN to estimate baseline O2 extraction fraction (OEF) from a measurement of venous blood R2, which in combination with the baseline CBF measurement yields an estimate of baseline CMRO2; and FLAIR-GESSE to measure tissue R2′ to estimate the scaling parameter needed for calculating the change in CMRO2 in response to a stimulus with the calibrated BOLD method. Here we describe results for a study sample of 17 subjects (8 female, mean age=25.3 years, range 21-31 years). The primary findings were that OEF values measured with the VSEAN method were in good agreement with previous PET findings, while estimates of the dynamic change in CMRO2 in response to a visual stimulus were in good agreement between the traditional hypercapnia calibration and calibration based on R2′. These results support the potential of gas-free methods for quantitative physiological measurements. Synopsis We tested noninvasive methods to measure absolute Oxygen Metabolism (CMRO2) in both baseline and activation states without the use of special gases: VSEAN to measure baseline O2 extraction fraction (OEF), and FLAIR-GESSE to measure R2′ to estimate the scaling parameter M. Primary findings were: CMRO2 changes to visual stimulation derived from R2′ were similar to estimates based on hypercapnia-derived M; OEF values were in good agreement with previous PET findings; and, variation of baseline CBF/CMRO2 coupling across subjects does not follow activation coupling, suggesting different mechanisms may be involved. These results support the potential of gas-free methods for quantitative physiological measurements. Purpose To demonstrate the potential for two non-invasive techniques, VSEAN and FLAIR-GESSE, for absolute measurements of CMRO2 during both baseline and activation states.
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variability of the coupling of blood flow and Oxygen Metabolism responses in the brain a problem for interpreting bold studies but potentially a new window on the underlying neural activity
2014Co-Authors: Richard B Buxton, Aaron B Simon, Valerie E M Griffeth, Farshad Moradi, Amir ShmuelAbstract:Recent studies from our group and others using quantitative fMRI methods have found that variations of the coupling ratio of blood flow (CBF) and Oxygen Metabolism (CMRO2) responses to a stimulus have a strong effect on the BOLD response. Across a number of studies an empirical pattern is emerging in the way CBF and CMRO2 changes are coupled to neural activation: if the stimulus is modulated to create a stronger response (e.g., increasing stimulus contrast), CBF is modulated more than CMRO2; on the other hand, if the brain state is altered such that the response to the same stimulus is increased (e.g., modulating attention, adaptation or excitability), CMRO2 is modulated more than CBF. Because CBF and CMRO2 changes conflict in producing BOLD signal changes, this finding has an important implication for conventional BOLD-fMRI studies: the BOLD response exaggerates the effects of stimulus variation but is only weakly sensitive to modulations of the brain state that alter the response to a standard stimulus. A speculative hypothesis is that variability of the coupling ratio of the CBF and CMRO2 responses reflects different proportions of inhibitory and excitatory evoked activity, potentially providing a new window on neural activity.
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dynamic models of bold contrast
2012Co-Authors: Richard B BuxtonAbstract:This personal recollection looks at the evolution of ideas about the dynamics of the blood Oxygenation level dependent (BOLD) signal, with an emphasis on the balloon model. From the first detection of the BOLD response it has been clear that the signal exhibits interesting dynamics, such as a pronounced and long-lasting post-stimulus undershoot. The BOLD response, reflecting a change in local deoxyhemoglobin, is a combination of a hemodynamic response, related to changes in blood flow and venous blood volume, and a metabolic response related to Oxygen Metabolism. Modeling is potentially a way to understand the complex path from changes in neural activity to the BOLD signal. In the early days of fMRI it was hoped that the hemodynamic/metabolic response could be modeled in a unitary way, with blood flow, Oxygen Metabolism, and venous blood volume–the physiological factors that affect local deoxyhemoglobin–all tightly linked. The balloon model was an attempt to do this, based on the physiological ideas of limited Oxygen delivery at baseline and a slow recovery of venous blood volume after the stimulus (the balloon effect), and this simple model of the physiology worked well to simulate the BOLD response. However, subsequent experiments suggest a more complicated picture of the underlying physiology, with blood flow and Oxygen Metabolism driven in parallel, possibly by different aspects of neural activity. In addition, it is still not clear whether the post-stimulus undershoot is a hemodynamic or a metabolic phenomenon, although the original venous balloon effect is unlikely to be the full explanation, and a flow undershoot is likely to be important. Although our understanding of the physics of the BOLD response is now reasonably solid, our understanding of the underlying physiological relationships is still relatively poor, and this is the primary hurdle for future models of BOLD dynamics.
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interpreting Oxygenation based neuroimaging signals the importance and the challenge of understanding brain Oxygen Metabolism
2010Co-Authors: Richard B BuxtonAbstract:Functional magnetic resonance imaging (fMRI) is widely used to map patterns of brain activation based on blood Oxygenation level dependent (BOLD) signal changes associated with changes in neural activity. However, because Oxygenation changes depend on the relative changes in cerebral blood flow (CBF) and cerebral metabolic rate of Oxygen (CMRO2), a quantitative interpretation of BOLD signals, and also other functional neuroimaging signals related to blood or tissue Oxygenation, is fundamentally limited until we better understand brain Oxygen Metabolism and how it is related to blood flow. However, the positive side of the complexity of Oxygenation signals is that when combined with dynamic CBF measurements they potentially provide the best tool currently available for investigating the dynamics of CMRO2. This review focuses on the problem of interpreting Oxygenation-based signals, the challenges involved in measuring CMRO2 in general, and what is needed to put Oxygenation-based estimates of CMRO2 on a firm foundation. The importance of developing a solid theoretical framework is emphasized, both as an essential tool for analyzing Oxygenation-based multimodal measurements, and also potentially as a way to better understand the physiological phenomena themselves. The existing data, integrated within a simple theoretical framework of O2 transport, suggests the hypothesis that an important functional role of the mismatch of CBF and CMRO2 changes with neural activation is to prevent a fall of tissue pO2. Future directions for better understanding brain Oxygen Metabolism are discussed.
William J. Powers - One of the best experts on this subject based on the ideXlab platform.
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brief inhalation method to measure cerebral Oxygen extraction fraction with pet accuracy determination under pathologic conditions
1991Co-Authors: Denis I Altman, Lennis L Lich, William J. PowersAbstract:The initial validation of the brief inhalation method to measure cerebral Oxygen extraction fraction (OEF) with positron emission tomography (PET) was performed in non-human primates with predominantly normal cerebral Oxygen Metabolism (CMRO2). Sensitivity analysis by computer simulation, however, indicated that this method may be subject to increasing error as CMRO2 decreases. Accuracy of the method under pathologic conditions of reduced CMRO2 has not been determined. Since reduced CMRO2 values are observed frequently in newborn infants and in regions of ischemia and infarction in adults, we determined the accuracy of the brief inhalation method in non-human primates by comparing OEF measured with PET to OEF measured by arteriovenous Oxygen difference (A-VO2) under pathologic conditions of reduced CMRO2 (0.27-2.68 ml 100g-1 min-1). A regression equation of OEF (PET) = 1.07 {times} OEF (A-VO2) + 0.017 (r = 0.99, n = 12) was obtained. The absolute error in Oxygen extraction measured with PET was small (mean 0.03 {plus minus} 0.04, range -0.03 to 0.12) and was independent of cerebral blood flow, cerebral blood volume, CMRO2, or OEF. The percent error was higher (19 {plus minus} 37), particularly when OEF is below 0.15. These data indicate that the brief inhalation method can be usedmore » for measurement of cerebral Oxygen extraction and cerebral Oxygen Metabolism under pathologic conditions of reduced cerebral Oxygen Metabolism, with these limitations borne in mind.« less
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brief inhalation method to measure cerebral Oxygen extraction fraction with pet accuracy determination under pathologic conditions
1991Co-Authors: Denis I Altman, Lennis L Lich, William J. PowersAbstract:The initial validation of the brief inhalation method to measure cerebral Oxygen extraction fraction (OEF) with positron emission tomography (PET) was performed in non-human primates with predominantly normal cerebral Oxygen Metabolism (CMRO2). Sensitivity analysis by computer simulation, however, indicated that this method may be subject to increasing error as CMRO2 decreases. Accuracy of the method under pathologic conditions of reduced CMRO2 has not been determined. Since reduced CMRO2 values are observed frequently in newborn infants and in regions of ischemia and infarction in adults, we determined the accuracy of the brief inhalation method in non-human primates by comparing OEF measured with PET to OEF measured by arteriovenous Oxygen difference (A-VO2) under pathologic conditions of reduced CMRO2 (0.27-2.68 ml 100g-1 min-1). A regression equation of OEF (PET) = 1.07 {times} OEF (A-VO2) + 0.017 (r = 0.99, n = 12) was obtained. The absolute error in Oxygen extraction measured with PET was small (mean 0.03 {plus minus} 0.04, range -0.03 to 0.12) and was independent of cerebral blood flow, cerebral blood volume, CMRO2, or OEF. The percent error was higher (19 {plus minus} 37), particularly when OEF is below 0.15. These data indicate that the brief inhalation method can be usedmore » for measurement of cerebral Oxygen extraction and cerebral Oxygen Metabolism under pathologic conditions of reduced cerebral Oxygen Metabolism, with these limitations borne in mind.« less
Daniela Patinha - One of the best experts on this subject based on the ideXlab platform.
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determinants of renal Oxygen Metabolism during low na diet effect of angiotensin ii at1 and aldosterone receptor blockade
2020Co-Authors: Daniela Patinha, Carla Carvalho, Patrik Persson, Liselotte Pihl, Angelica Fasching, Malou Friederichpersson, Julie Oneill, Fredrik PalmAbstract:KEY POINTS Reducing Na+ intake reduces the partial pressure of Oxygen in the renal cortex and activates the renin-angiotensin-aldosterone system. In the absence of high blood pressure, these consequences of dietary Na+ reduction may be detrimental for the kidney. In a normotensive animal experimental model, reducing Na+ intake for 2 weeks increased renal Oxygen consumption, which was normalized by mineralocorticoid receptor blockade. Furthermore, blockade of the angiotensin II AT1 receptor restored cortical partial pressure of Oxygen by improving Oxygen delivery. This shows that increased activity of the renin-angiotensin-aldosterone system contributes to increased Oxygen Metabolism in the kidney after 2 weeks of a low Na+ diet. The results provide insights into dietary Na+ restriction in the absence of high blood pressure, and its consequences for the kidney. ABSTRACT Reduced Na+ intake reduces the PO2 (partial pressure of Oxygen) in the renal cortex. Upon reduced Na+ intake, reabsorption along the nephron is adjusted with activation of the renin-angiotensin-aldosterone system (RAAS). Thus, we studied the effect of reduced Na+ intake on renal Oxygen homeostasis and function in rats, and the impact of intrarenal angiotensin II AT1 receptor blockade using candesartan and mineralocorticoid receptor blockade using canrenoic acid potassium salt (CAP). Male Sprague-Dawley rats were fed standard rat chow containing normal (0.25%) and low (0.025%) Na+ for 2 weeks. The animals were anaesthetized (thiobutabarbital 120 mg kg-1 ) and surgically prepared for kidney Oxygen Metabolism and function studies before and after acute intrarenal arterial infusion of candesartan (4.2 μg kg-1 ) or intravenous infusion of CAP (20 mg kg-1 ). Baseline mean arterial pressure and renal blood flow were similar in both dietary groups. Fractional Na+ excretion and cortical Oxygen tension were lower and renal Oxygen consumption was higher in low Na+ groups. Neither candesartan nor CAP affected arterial pressure. Renal blood flow and cortical Oxygen tension increased in both groups after candesartan in the low Na+ group. Fractional Na+ excretion was increased and Oxygen consumption reduced in the low Na+ group after CAP. These results suggest that blockade of angiotensin II AT1 receptors has a major impact upon Oxygen delivery during normal and low Na+ conditions, while aldosterone receptors mainly affect Oxygen Metabolism following 2 weeks of a low Na+ diet.
