Renal Oxygen Delivery Research Articles

A Comparison of 4% Succinylated Gelatin Solution versus Normal Saline in Stable Normovolaemic Sheep: Global Haemodynamic, Regional Blood Flow and Oxygen Delivery Effects

The objective of this study was to compare the effects on regional blood flow and regional oxygen delivery of 4% succinylated gelatin solution (Gelofusine, B. Braun) with those of normal saline. This was a randomised, controlled, cross-over large animal study, which took place at the animal laboratory of university physiology institute. The subjects were seven merino cross-ewes. We implanted flow probes around the aorta, coronary, renal and mesenteric arteries. We randomised animals to observation (control), normal saline (one litre over 15 minutes) or Gelofusine (one litre over 15 minutes). We measured central haemodynamics, organ blood flows, arterial blood gases and haemoglobin every 30 minutes for 210 minutes. Compared to control, both Gelofusine and normal saline significantly and similarly increased mean arterial pressure, stroke volume, cardiac output and central venous pressure in the first hour (P < 0.05). Such changes, however, were transient except for the increase in cardiac output seen with Gelofusine. Normal saline significantly increased mesenteric blood flow in the first hour (P < 0.05), while Gelofusine caused a specific, sustained and progressive increase in renal blood flow and conductance (P < 0.05). Both fluids increased urine output and creatinine clearance (P < 0.05), but, due to haemodilution, both decreased renal oxygen delivery in the first hour (P < 0.05). Normal saline and Gelofusine have transient, volume expansion-related systemic haemodynamic effects, which are greater for Gelofusine. Saline had a more pronounced early effect on mesenteric blood flow, while Gelofusine had a sustained and progressive greater effect on renal blood flow. The transient increase in urine output and creatinine clearance seen with both fluids occurred while renal oxygen delivery decreased.

N-ACETYLCYSTEINE IMPROVES THE HEMODYNAMICS AND OXIDATIVE STRESS IN HYPOXIC NEWBORN PIGS REOXYGENATED WITH 100% OXYGEN

Neonatal asphyxia may lead to cardiac and renal complications perhaps mediated by oxygen free radicals. Using a model of neonatal hypoxia-reoxygenation, we tested the hypothesis that N-acetylcysteine (NAC) would improve cardiac function and renal blood flow. Eighteen piglets (aged 1-4 days old, weighing 1.4-2.2 kg) were anesthetized and acutely instrumented for continuous monitoring of pulmonary and renal artery flow (cardiac index [CI] and renal artery flow index [RAFI], respectively) and mean blood pressure. Alveolar hypoxia was induced for 2 h, followed by resuscitation with 100% oxygen for 1 h and 21% oxygen for 3 h. Animals were randomized to sham-operated, hypoxic control, and NAC treatment (i.v. bolus of 150 mg/kg given at 10 min of reoxygenation followed by 100 mg/kg per h infusion) groups. Myocardial and renal tissue glutathione content and lipid hydroperoxide levels were assayed, and histology was examined. After 2 h of hypoxia, all animals were acidotic (pH 6.96 +/- 0.04) and in cardiogenic shock with depressed renal blood flow. Upon reoxygenation, CI and RAFI increased but gradually deteriorated later. The NAC treatment prevented the decreased CI, stroke volume, mean blood pressure, systemic oxygen delivery, RAFI, and renal oxygen delivery at 2 to 4 h of reoxygenation observed in hypoxic controls (versus shams, all P < 0.05). The myocardial and renal tissue glutathione content was significantly higher in the NAC treatment group (versus controls). The CI and RAFI at 4 h of reoxygenation correlated with the tissue glutathione redox ratio (r = 0.5 and 0.6, respectively, P < 0.05). There were no significant differences in heart rate, pulmonary artery pressure, systemic oxygen uptake, and tissue lipid hydroperoxide levels between groups. No histologic injury was found in the heart or kidney. In this porcine model of neonatal hypoxia and 100% reoxygenation, NAC improved cardiac function and renal perfusion, with improved tissue glutathione content.

The Effects of Normal and Hypertonic Saline on Regional Blood Flow and Oxygen Delivery

Boluses of crystalloids are frequently given to patients to optimize vital organ perfusion. However, their effect on regional blood flow and oxygen delivery in the normal mammalian circulation has not been studied. We compared the effects of normal or hypertonic (3%) saline or control on regional blood flow and oxygen delivery in normal animals. We conducted a randomized, controlled animal study in seven merino cross-ewes. We implanted chronic flow probes around aorta, coronary, renal, and mesenteric arteries. We randomized animals to three different interventions: observation (control), normal saline (1 L over 15 min), or 3% saline (300 mL over 15 min). We continuously measured central hemodynamics and organ blood flow for 210 min. Both fluids increased heart rate, cardiac output, central venous pressure, peripheral conductance, coronary and mesenteric blood flow, and conductance in the first hour (P < 0.05). In the second and third hour, both maintained a greater cardiac output, total peripheral conductance, and mesenteric blood flow (P < 0.05) than control, but the difference decreased. In contrast, renal blood flow was unaffected and, because of hemodilution, renal oxygen delivery was decreased in the first hour (P < 0.05). Simultaneously, urine output and creatinine clearance increased (P < 0.05) in both groups. Finally, 3% saline significantly, but transiently, increased serum sodium and osmolarity. Normal and hypertonic saline have similar systemic and regional hemodynamic effects. They also have no effect on renal blood flow and initially decrease renal oxygen delivery while increasing urine output.

Influence of fluid resuscitation on renal microvascular PO2 in a normotensive rat model of endotoxemia

IntroductionSeptic renal failure is often seen in the intensive care unit but its pathogenesis is only partly understood. This study, performed in a normotensive rat model of endotoxemia, tests the hypotheses that endotoxemia impairs renal microvascular PO2 (μPO2) and oxygen consumption (VO2,ren), that endotoxemia is associated with a diminished kidney function, that fluid resuscitation can restore μPO2, VO2,ren and kidney function, and that colloids are more effective than crystalloids.MethodsMale Wistar rats received a one-hour intravenous infusion of lipopolysaccharide, followed by resuscitation with HES130/0.4 (Voluven®), HES200/0.5 (HES-STERIL® ® 6%) or Ringer's lactate. The renal μPO2 in the cortex and medulla and the renal venous PO2 were measured by a recently published phosphorescence lifetime technique.ResultsEndotoxemia induced a reduction in renal blood flow and anuria, while the renal μPO2 and VO2,ren remained relatively unchanged. Resuscitation restored renal blood flow, renal oxygen delivery and kidney function to baseline values, and was associated with oxygen redistribution showing different patterns for the different compounds used. HES200/0.5 and Ringer's lactate increased the VO2,ren, in contrast to HES130/0.4.ConclusionThe loss of kidney function during endotoxemia could not be explained by an oxygen deficiency. Renal oxygen redistribution could for the first time be demonstrated during fluid resuscitation. HES130/0.4 had no influence on the VO2,ren and restored renal function with the least increase in the amount of renal work.

Vasopressin in the ICU

Vasopressin is one of the most important endogenously released stress hormones during shock. In this review, studies published in the past year that add to our understanding of the use of vasopressin in the ICU are discussed. Endogenous vasopressin levels are inappropriately low in adults with severe sepsis but not in children with meningococcal septic shock. Vasopressin but not norepinephrine improved renal blood flow and oxygen delivery and prolonged survival in animal models of septic shock. In human vasodilatory shock, the combination of low-dose vasopressin and norepinephrine was found to be safe and effective. In humans, vasopressin can cause gastrointestinal hypoperfusion and ischemic skin lesions. In hypodynamic animal models of sepsis vasopressin compromised oxygen delivery and decreased systemic and gut blood flow.High-dose bolus vasopressin appeared promising in animal studies of hemorrhagic shock and cardiopulmonary arrest and in a large, randomized clinical trial of vasopressin versus epinephrine in human cardiopulmonary arrest with asystole. However, poor neurologic outcomes raised controversy in introducing vasopressin into CPR guidelines. There is growing evidence that vasopressin infusion in septic shock is safe and effective. Several studies published this year support the hypothesis that vasopressin should be used as a continuous low-dose infusion (between 0.01 and 0.04 U/min in adults) and not titrated as a single vasopressor agent. However, multiple studies highlight the clinical equipoise that exists regarding the use of vasopressin in vasodilatory shock. Guidelines on management of septic shock recommend "cautious use of vasopressin pending further studies."

Increased erythropoietin synthesis in patients with COLD or left heart failure is related to alterations in renal haemodynamics.

The mechanisms controlling erythropoietin (EPO) synthesis by the kidney in patients with chronic obstructive lung disease (COLD) or congestive left heart failure (CLHF) remain incompletely understood. Renal dysfunction occurs as a consequence of decreased renal blood flow (RBF) in these diseases. Because alterations in renal haemodynamics may affect EPO synthesis and red blood cell production, we investigated the potential relationships between renal function and plasma EPO synthesis in patients with COLD or CLHF. Thirty-two patients with COLD and 13 with CLHF underwent determination of renal physiology parameters, plasma EPO levels and haemoglobin levels. Plasma EPO concentrations were increased in patients with COLD or CLHF as compared to normal subjects, and were inversely correlated to haemoglobin concentrations. In patients with COLD or CLHF, plasma EPO was negatively correlated with both RBF and renal oxygen delivery (ROD) and positively correlated with filtration fraction. Plasma EPO was not correlated with glomerular filtration rate, fractional excretion of sodium, PO2 or PCO2. Among the patients with COLD, those with polycythemia (haemoglobin > 150 g L-1) had lower plasma EPO and higher RBF and ROD values than those with normocythemia (haemoglobin < or = 150 g L-1). Taken together, our data suggest that in patients with COLD or CLHF the critical determinant for EPO production is impairment of renal haemodynamics.

Pentoxifylline prevents the transition from the hyperdynamic to hypodynamic response during sepsis.

The cardiovascular response to sepsis includes an early, hyperdynamic phase followed by a late, hypodynamic phase. Although administration of pentoxifylline (PTX) produces beneficial effects in sepsis, it remains unknown whether this agent prevents the transition from the hyperdynamic to the hypodynamic response during the progression of sepsis. To study this, male adult rats were subjected to polymicrobial sepsis by cecal ligation and puncture (CLP). At 1 h after CLP, PTX (50 mg/kg body wt) or vehicle was infused intravenously over 30 min. At 20 h after CLP (i.e., the late stage of sepsis), cardiac output and organ blood flow were measured by radioactive microspheres. Systemic and regional (i.e., hepatic, intestinal, and renal) oxygen delivery (DO2) and oxygen consumption (VO2) were determined. Moreover, plasma levels of lactate and alanine aminotransferase (ALT) were measured, and histological examinations were performed. In additional animals, the necrotic cecum was excised at 20 h after CLP, and mortality was monitored for 10 days thereafter. The results indicate that cardiac output, organ blood flow, and systemic and regional DO2 decreased by 36-65% (P < 0.05) at 20 h after CLP. Administration of PTX early after the onset of sepsis, however, prevented reduction in measured hemodynamic parameters and increased systemic and regional DO2 and VO(2) by 50-264% (P < 0.05). The elevated levels of lactate (by 173%, P < 0.05) and ALT (by 718%, P < 0.05), as well as the morphological alterations in the liver, small intestine, and kidneys during sepsis were attenuated by PTX treatment. In addition, PTX treatment decreased the mortality rate from 50 to 0% (P < 0.05) after CLP and cecal excision. Because PTX prevents the occurrence of hypodynamic sepsis, this agent appears to be a useful adjunct for maintaining hemodynamic stability and preventing lethality from sepsis.

Renovascular adaptive changes in chronic hypoxic polycythemia

Chronic hypoxia in rats produces polycythemia, and the plasma fraction falls, reducing renal plasma flow (RPF) relative to renal blood flow (RBF). Polycythemia also causes increased blood viscosity, which tends to reduce RBF and renal oxygen delivery. We studied how renal regulation of electrolyte balance and renal tissue oxygenation (which is crucial for erythropoietin regulation) are maintained in rats during hypoxic exposure. Rats of two strains with differing polycythemic responses, with surgically implanted catheters in the urinary bladder, femoral artery, and left renal and right external jugular veins, were exposed to a simulated high altitude (0.5 atm) for 0, 1, 3, 14, and 30 days, after which RPF (para-aminohippurate clearance), glomerular filtration rate (GFR, polyfructosan clearance), hematocrit and blood gases were measured, and RBF, renal vascular resistance and hindrance (resistance/viscosity), renal oxygen delivery, and renal oxygen consumption were calculated. During chronic hypoxia RBF increased, but RPF decreased because of the polycythemia. GFR remained normal because the filtration fraction (FF) increased. Renal vascular resistance decreased, and renal vascular hindrance decreased more markedly. Renal oxygen delivery and consumption both increased. During chronic hypoxia GFR homeostasis apparently took precedence over RBF autoregulation. The large decrease in renal vascular hindrance suggested that renal vascular remodeling contributes to GFR regulation. The reduced hindrance also prevented a vicious cycle of increasing polycythemia and blood viscosity, decreasing RBF, and increasing renal hypoxia and erythropoietin release.

Influence of fluid resuscitation on renal function in bacteremic and endotoxemic rats

Purpose: Fluid resuscitation, which is the most important primary therapy in sepsis, is not always able to prevent acute renal failure. In this study, we investigated in two different rat models of distributive shock whether fluid resuscitation would increase renal plasma flow (RPF) and subsequently glomerular filtration rate (GFR). Materials and Methods: In pentobarbital anesthetized Wistar rats Haemaccel (Behring Pharma, Hoechst, the Netherlands) infusion (1.2 mL/100 g/h for 3 hours) was started immediately during either bacteremia (bolus of living Escherichia coli bacteria, 109 or endotoxemia (1 hour infusion of E. coli endotoxin, 8 mg/kg), as well as in time-matched healthy controls. Results: After 3 hours, this treatment had increased RPF (clearance of 1311-hippurate) above normal in control (+67%) and bacteremic rats (+75%), whereas in endotoxemic animals, the significantly decreased RPF was normalized. On the other hand, in bacteremic animals, the lowered GFR (clearance of creatinine; ×44%) was normalized, whereas in endotoxemic animals GFR remained depressed (×30%). The lack of improvement in GFR during endotoxemia was also indicated by a profound fall in urine flow, which by contrast steadily increased in control and bacteremic rats owing to volume loading. In both shocked groups, the decreased renal oxygen delivery was normalized, but the higher renal oxygen consumption than expected on the basis of the work needed for sodium reabsorption was not influenced by Haemaccel treatment, despite the fact that it caused this work load to rise in bacteremic but not in endotoxemic rats. In both shock models, renal cortical adenosine triphosphate content did not differ from healthy controls and was not influenced by volume loading. Conclusions: In conclusion, our study suggests that a decrease in GFR caused by live bacteria in the circulation may benefit from fluid resuscitation, while during endotoxemia this therapy could not prevent acute renal failure.

Renal function and oxygen consumption during bacteraemia and endotoxaemia in rats.

The hypothesis that renal failure during septic shock may occur as a result of hypoxia-related cell dysfunction was investigated in two rat models of distributive shock. Pentobarbitone-anaesthetized rats received either a bolus (1 ml) of living Escherichia coli bacteria (hospital-acquired strain, 1 x 10(9) CFU/ml; BA-group, n = 7), or a 1-h infusion of endotoxin (E. coli O127.B8: 8 mg/kg; ET-group, n = 7), or saline to serve as time matched controls (C-group, n = 7). Urine flow in the BA- and ET-group reached a nadir at 1 h, but thereafter increased and reached values higher than control at 3 h. At this time point, renal oxygen delivery had decreased, in the BA-group mainly due to a fall in arterial oxygen content and in the ET-group to a fall in renal plasma flow (clearance of 131I-hippurate). However, renal oxygen extraction had significantly increased, by 31% in the BA and by 59% in the ET group, while renal oxygen consumption remained the same. Net tubular sodium reabsorption had decreased by 55% in the BA and by 25% in the ET group, due to a fall in glomerular filtration rate (clearance of creatinine). Hence, an excess oxygen consumption was found which was caused neither by an increased renal glucose release nor by the presence of an increased number of leukocytes stuck in the glomeruli. Renal tubular cells showed normal morphology. An indication that proximal tubular function in the BA and ET group remained largely intact were normal ATP levels, absence of urinary glucose, and a normal fractional excretion of sodium. However, since urine flow had increased in shocked rats at 3 h, water appeared selectively lost. Our data indicate that in rat models of septic shock renal failure is not caused by cortical hypoxia or a shortage of cellular energy supply.

Short-term effects of intra-aortic balloon pumping on renal blood flow and renal oxygen consumption in cardiogenic shock

Intra-aortic balloon pumping is frequently used in patients with cardiogenic shock when oliguria persists despite maximal pharmacologic support. The objective of this study was to measure the effect of intra-aortic balloon pumping on renal blood flow, renal oxygen delivery, and renal oxygen consumption in such patients. Central hemodynamics, renal blood flow, and oxygen transport were measured in 10 patients in low cardiac output states. Measurements were made with and without intra-aortic balloon counterpulsation. Renal blood flow was measured by continuous renal vein thermodilution. Small improvements were observed in cardiac output (3.1 ± 0.8 vs 3.5 ± 0.8 L/min, P < .01) and pulmonary capillary wedge pressure (22 ± 5.6 vs 19 ± 5.3 mmHg, P < .05), but mean arterial blood pressure was unchanged (69 ± 11 vs 69 ± 5 mmHg, not significant). Baseline renal blood flow was reduced to approximately 37%, renal oxygen delivery to 31%, and renal oxygen consumption to 60% of normal values. No significant improvement was seen in single-kidney renal blood flow (184 ± 108 vs 193 ± 107 mL/min), renal oxygen delivery (28 ± 16 vs 30 ± 16 mL/min), or renal oxygen consumption (4.9 ± 2.0 vs 4.7 ± 2.5 mL/min) in response to 1:1 counterpulsation. In comparison with measurements made during short-term suspension of counterpulsation, 1:1 aortic balloon pumping failed to result in an increase in renal blood flow, oxygen delivery, or oxygen consumption from the low levels observed in these patients.

Renal function during chronic anemia in the ovine fetus

Our purpose was to determine how prolonged anemia alters fetal renal function and acid-base balance. In seven ovine fetuses made progressively anemic over 1 wk by serial isovolemic hemorrhage, hematocrit was reduced from 33.3 +/- 4.5 to 14.0 +/- 1.0%. Femoral arterial oxygen content was less and renal plasma flow was greater in anemic fetuses (1.5 +/- 0.1 ml/dl and 339 +/- 58 ml.min-1.100 g kidney-1) than in 6 control fetuses (7.0 +/- 1.3 ml/dl and 160 +/- 34 ml.min-1.100 g kidney-1). Urine flow and sodium excretion were also greater in anemic fetuses (1.2 +/- 0.6 ml/min and 79 +/- 49.5 mumol/min) than in controls (0.5 +/- 0.2 ml/min and 16 +/- 9.8 mumol/min). This higher sodium excretion was apparently due to a lower fractional sodium reabsorption in anemic fetuses compared with controls (84.1 +/- 5.8 vs. 96.5 +/- 1.7%), rather than to differences in either glomerular filtration rate or amount of filtered sodium. In addition, the higher sodium excretion in anemic fetuses was associated with greater urinary lactate and inorganic phosphate excretions and larger amniotic fluid volumes than in controls. From these data we conclude that when fetal renal oxygen delivery is limited by a prolonged reduction in hematocrit, excretions of sodium and water, as well as other osmotically active solutes, increase, and this results in an increase in amniotic fluid volume.

Sequential changes in renal oxygen consumption and sodium transport during hyperdynamic sepsis in sheep.

The sequence of changes in systemic and renal oxygen delivery (QO2) and consumption (VO2) and renal function in an ovine model of progressive hyperdynamic sepsis was investigated. Nine chronically instrumented awake sheep were given a continuous intravenous Escherichia coli endotoxin infusion (20 ng.kg-1.min-1) for 3 days. After 8 h of the infusion, systemic arterial blood pressure and vascular resistance stayed decreased by 30% (P less than 0.001). Systemic QO2 progressively increased to a maximum of 157% of baseline values at 24 h and was associated with a decreased O2 extraction ratio from 33 +/- 2 (SE) to 23 +/- 2% (P less than 0.05), resulting in an unchanged systemic VO2. Renal blood flow and renal QO2 decreased by 40% during the first 12 h, returning to and staying at baseline values after 24 h. Renal VO2 decreased significantly by 35% at 12 h and then partially recovered to baseline values. Plasma creatinine clearance was maximally reduced to 25% of baseline values at 12 h and thereafter remained significantly (P less than 0.01) below 50% of baseline values. Both total and fractional sodium excretion fell at 12 h by 95 and 74%, respectively, and remained reduced over time, indicating conserved tubular function. The ratio of moles of sodium reabsorbed to moles of O2 consumed by the kidney was transiently reduced, from 33.4 +/- 4.1 to 12.4 +/- 3.6 at 12 h (P less than 0.05), indicating a relative increase in energy expenditure for tubular transport or renal synthetic activities, but recovered to baseline values after 24 h.(ABSTRACT TRUNCATED AT 250 WORDS)

METABOLIC EFFECTS OF SODIUM NITROPRUSSIDE ON THE PIG KIDNEY IN VIVO: STUDIES BY PHOSPHORUS-31 MAGNETIC RESONANCE SPECTROSCOPY

Phosphorus-31 magnetic resonance spectroscopy was applied to the pig kidney in vivo to determine the metabolic effects of infusion of sodium nitroprusside, and of more severe hypotension produced by venesection or halothane. Sodium nitroprusside 7-20 micrograms kg-1 min-1 reduced mean systemic arterial pressure (AP) of the pig from 89 to 46 mm Hg. Glomerular filtration rate and total sodium reabsorption were reduced proportionally. Renal metabolism, assessed by the ratio [ATP]: [Pi] (inorganic phosphate), did not change. Adding halothane or venesection to nitroprusside hypotension caused a further reduction in systemic AP to 42 and 39 mm Hg, respectively. Renal [ATP] decreased in direct proportion to mean AP. It is concluded that sodium nitroprusside, even in high doses, does not reduce renal oxygen delivery as assessed by the ability of the kidney to maintain normal ATP content. However, haemorrhage or an increase in halothane dosage results in irreversible damage to the energy producing processes of the kidney. This may be relevant to the clinical use of the drug.

Effects of packed cell volume reduction on renal haemodynamics and the renin-angiotensin-aldosterone system in patients with secondary polycythaemia and hypoxic cor pulmonale.

Polycythaemia was corrected by erythrapheresis in ten patients with hypoxic cor pulmonale who were stable on regular diuretic therapy. Renal haemodynamics, renal function and the renin-angiotensin-aldosterone system were assessed before and afterwards. Before erythrapheresis effective renal plasma flow (ERPF) was reduced (63% predicted) but glomerular filtration rate (GFR) was preserved (88% predicted) by a rise in filtration fraction (FF) (138% predicted). A negative correlation existed between ERPF and packed cell volume (r = -0.723; P less than 0.02) and also between ERPF and PaCO2 (r = -0.710; P less than 0.05). Polycythaemia was sufficient to maintain renal oxygen delivery (97% predicted). After erythrapheresis systemic blood pressure, blood volume and blood viscosity all decreased. ERPF increased by 18% (P less than 0.02). FF fell by 11% (P less than 0.05) and GFR was unchanged. Renal oxygen delivery diminished by 25% (P less than 0.001). Plasma renin activity was increased in five patients and plasma aldosterone increased in two patients before erythrapheresis. No sustained fall occurred in plasma renin activity or plasma aldosterone, possibly because the haemodynamic consequences of the procedure had opposing actions on renin secretion. Although the reduction in FF would per se tend to enhance renal sodium and water excretion, a diuresis or natriuresis did not occur consistently.

Renal oxygen delivery and consumption during progressive hypoxemia in the anesthetized dog.

The relationship between renal oxygen delivery (RDO2) and function was evaluated during progressive hypoxemia. Seven anesthetized, spontaneously breathing dogs were given progressively lower oxygen concentrations to breathe while monitoring renal O2 consumption (RVO2), renal hemodynamic and excretory function. In addition, basal RVO2 was determined in three models of kidneys without filtration. RDO2 averaged 3648 mumole O2/min/100 g during normoxia. Basal RVO2 averaged 100 mumole O2/min/100 g kidney while total RVO2 was 466 mumole O2/min/100 g kidney during normoxia, leaving 366 mumole O2/min/100 g consumed by those processes involved in tubular transport. During hypoxemia, all renal parameters were well maintained until the lowest PaO2 (24.2 Torr). At this level, total RVO2 and RDO2 were significantly reduced. However, RDO2 remained well above RVO2 throughout hypoxemia. The reduction in RVO2 was a direct result of decreased O2 demand, as glomerular filtration and tubular load were also reduced. This associated decrease in O2 demand and RVO2 was indicated by the fact that the renal (a - v)O2 difference remained low and unchanged (1.9 vol%), fractional sodium excretion was unchanged, and the ratio of tubular sodium reabsorption to RVO2 also remained unchanged (30.8 meq Na/mmole O2). It was concluded that hypoxemia, while reducing both RDO2 and RVO2 at the lowest PaO2 (24.2 Torr), did not functionally impair renal excretory function by limiting RDO2 to the tubular transport processes. A reduction in RBF is far more likely to compromise the RDO2 needed to sustain basal and active transport processes than hypoxemia itself.

Reinforcement of reflex epinephrine release by angiotensin II.

ARTICLESReinforcement of reflex epinephrine release by angiotensin IITS Harrison, A Birbari, and JF SeatonTS Harrison, A Birbari, and JF SeatonPublished Online:01 Jan 1973https://doi.org/10.1152/ajplegacy.1973.224.1.31MoreSectionsPDF (914 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByNeurohormonal interactions on the renal oxygen delivery and consumption in haemorrhagic shock-induced acute kidney injury12 August 2013 | Acta Physiologica, Vol. 209, No. 1The Early Endocrine Response to InjuryHypovolaemia can potentiate hypoglycaemic stressinduced adrenaline release in the anaesthetized ratNeuroscience Letters, Vol. 112, No. 2-3Renal modulation of electrically stimulated adrenal medullary secretionJournal of Surgical Research, Vol. 36, No. 2Reversal by naloxone of hemorrhagic shock in anephric catsEuropean Journal of Pharmacology, Vol. 65, No. 1Catecholamine responses to orthostatic stimulation in anephric manJournal of Surgical Research, Vol. 26, No. 4Renin-angiotensin mediation of adrenal catecholamine secretion induced by haemorrhageEuropean Journal of Pharmacology, Vol. 44, No. 2 More from this issue > Volume 224Issue 1January 1973Pages 31-34 Copyright & PermissionsCopyright © 1973 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1973.224.1.31PubMed4345738History Published online 1 January 1973 Published in print 1 January 1973 Metrics

Hydrostatic pressures in peritubular capillaries and tubules in the rat kidney

Hydrostatic pressures in peritubular capillaries and tubules in the rat kidney

Energy requirement for sodium reabsorption in the in vivo rabbit kidney.

Energy requirement for sodium reabsorption in the in vivo rabbit kidney.