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Renal Oxygenation (renal + oxygenation)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Dopamine increases renal oxygenation: a clinical study in post-cardiac surgery patients

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 2 2010
BENGT REDFORS
Background: Imbalance of the renal medullary oxygen supply/demand relationship can cause ischaemic acute renal failure (ARF). The use of dopamine for prevention/treatment of ischaemic ARF has been questioned. It has been suggested that dopamine may increase renal oxygen consumption (RVO2) due to increased solute delivery to tubular cells, which may jeopardise renal oxygenation. Information on the effects of dopamine on renal perfusion, filtration and oxygenation in man is, however, lacking. We evaluated the effects of dopamine on renal blood flow (RBF), glomerular filtration rate (GFR), RVO2 and renal O2 demand/supply relationship, i.e. renal oxygen extraction (RO2Ex). Methods: Twelve uncomplicated, mechanically ventilated and sedated post-cardiac surgery patients with pre-operatively normal renal function were studied. Dopamine was sequentially infused at 2 and 4 ug/kg/min. Systemic haemodynamics were evaluated by a pulmonary artery catheter. Absolute RBF was measured using two independent techniques: by the renal vein thermodilution technique and by infusion clearance of paraaminohippuric acid (PAH), with a correction for renal extraction of PAH. The filtration fraction (FF) was measured by the renal extraction of 51Cr-EDTA. Results: Neither GFR, tubular sodium reabsorption nor RVO2 was affected by dopamine, which increased RBF (45,55%) with both methods, decreased renal vascular resistance (30,35%), FF (21,26%) and RO2Ex (28,34%). The RBF/CI ratio increased with dopamine. Dopamine decreased renal PAH extraction, suggestive of a flow distribution to the medulla. Conclusions: In post-cardiac surgery patients, dopamine increases the renal oxygenation by a pronounced renal pre-and post-glomerular vasodilation with no increases in GFR, tubular sodium reabsorption or renal oxygen consumption. [source]

Low-dose vasopressin increases glomerular filtration rate, but impairs renal oxygenation in post-cardiac surgery patients

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 8 2009
G. BRAGADOTTIR
Background: The beneficial effects of vasopressin on diuresis and creatinine clearance have been demonstrated when used as an additional/alternative therapy in catecholamine-dependent vasodilatory shock. A detailed analysis of the effects of vasopressin on renal perfusion, glomerular filtration, excretory function and oxygenation in man is, however, lacking. The objective of this pharmacodynamic study was to evaluate the effects of low to moderate doses of vasopressin on renal blood flow (RBF), glomerular filtration rate (GFR), renal oxygen consumption (RVO2) and renal oxygen extraction (RO2Ex) in post-cardiac surgery patients. Methods: Twelve patients were studied during sedation and mechanical ventilation after cardiac surgery. Vasopressin was sequentially infused at 1.2, 2.4 and 4.8 U/h. At each infusion rate, systemic haemodynamics were evaluated by a pulmonary artery catheter, and RBF and GFR were measured by the renal vein thermodilution technique and by renal extraction of 51chromium,ethylenediaminetetraacetic acid, respectively. RVO2 and RO2Ex were calculated by arterial and renal vein blood samples. Results: The mean arterial pressure was not affected by vasopressin while cardiac output and heart rate decreased. RBF decreased and GFR, filtration fraction, sodium reabsorption, RVO2, RO2Ex and renal vascular resistance increased dose-dependently with vasopressin. Vasopressin exerted direct antidiuretic and antinatriuretic effects. Conclusions: Short-term infusion of low to moderate, non-hypertensive doses of vasopressin induced a post-glomerular renal vasoconstriction with a decrease in RBF and an increase in GFR in post-cardiac surgery patients. This was accompanied by an increase in RVO2, as a consequence of the increases in the filtered tubular load of sodium. Finally, vasopressin impaired the renal oxygen demand/supply relationship. [source]

RENAL OXYGEN DELIVERY: MATCHING DELIVERY TO METABOLIC DEMAND

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 10 2006
Paul M O'Connor
SUMMARY 1The kidneys are second only to the heart in terms of O2 consumption; however, relative to other organs, the kidneys receive a very high blood flow and oxygen extraction in the healthy kidney is low. Despite low arterial,venous O2 extraction, the kidneys are particularly susceptible to hypoxic injury and much interest surrounds the role of renal hypoxia in the development and progression of both acute and chronic renal disease. 2Numerous regulatory mechanisms have been identified that act to maintain renal parenchymal oxygenation within homeostatic limits in the in vivo kidney. However, the processes by which many of these mechanisms act to modulate renal oxygenation and the factors that influence these processes remain poorly understood. 3A number of such mechanisms specific to the kidney are reviewed herein, including the relationship between renal blood flow and O2 consumption, pre- and post-glomerular arterial,venous O2 shunting, tubulovascular cross-talk, the differential control of regional kidney blood flow and the tubuloglomerular feedback mechanism. 4The roles of these mechanisms in the control of renal oxygenation, as well as how dysfunction of these mechanisms may lead to renal hypoxia, are discussed. [source]