Variable responses of regional renal oxygenation and perfusion to vasoactive agents in awake sheep.
Vasoactive agents are used in critical care to optimize circulatory function, but their effects on renal tissue oxygenation in the absence of anesthesia remain largely unknown. Therefore, we assessed the effects of multiple vasoactive agents on regional kidney oxygenation in awake sheep. Sheep were surgically instrumented with pulmonary and renal artery flow probes, and combination fiber-optic probes, in the renal cortex and medulla, comprising a fluorescence optode to measure tissue Po2 and a laser-Doppler probe to assess tissue perfusion. Carotid arterial and renal venous cannulas enabled measurement of arterial pressure and total renal oxygen delivery and consumption. Norepinephrine (0.1 or 0.8 μg·kg(-1)·min(-1)) dose-dependently reduced cortical and medullary laser Doppler flux (LDF) and Po2 without significantly altering renal blood flow (RBF), or renal oxygen delivery or consumption. Angiotensin II (9.8 ± 2.1 μg/h) reduced RBF by 21%, renal oxygen delivery by 28%, oxygen consumption by 18%, and medullary Po2 by 38%, but did not significantly alter cortical Po2 or cortical or medullary LDF. Arginine vasopressin (3.3 ± 0.5 μg/h) caused similar decreases in RBF and renal oxygen delivery, but did not significantly alter renal oxygen consumption or cortical or medullary LDF or Po2. Captopril had no observable effects on cortical or medullary LDF or Po2, at a dose that increased renal oxygen delivery by 24%, but did not significantly alter renal oxygen consumption. We conclude that vasoactive agents have diverse effects on regional kidney oxygenation in awake sheep that are not predictable from their effects on LDF, RBF, or total renal oxygen delivery and consumption.
Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, Victoria, Australia; Department of Anaesthesia and Intensive Care, AO Melegnano, PO Uboldo, Cernusco sul Naviglio, Italy;
Paolo
P
Calzavacca
Cardiovascular Disease Program, Biomedicine Discovery Institute and Department of Physiology, Monash University, Melbourne, Victoria, Australia;
Roger G
RG
Evans
Australian and New Zealand Intensive Care Research Center, Monash University, Melbourne, Victoria, Australia; and.
Michael
M
Bailey
Department of Intensive Care and Department of Medicine, Austin Health, Heidelberg, Victoria, Australia.
Rinaldo
R
Bellomo
Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, Victoria, Australia; clive.may@florey.edu.au.
Clive N
CN
May
D000804:Angiotensin II / Q000008:administration & dosage / Q000494:pharmacology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000008:administration & dosage / Q000494:pharmacology*; D000818:Animals; D001127:Arginine Vasopressin / Q000008:administration & dosage / Q000494:pharmacology; D002216:Captopril / Q000008:administration & dosage / Q000494:pharmacology; D005260:Female; D007668:Kidney / Q000187:drug effects* / Q000502:physiology*; D009638:Norepinephrine / Q000008:administration & dosage / Q000494:pharmacology; D010101:Oxygen Consumption; D012756:Sheep / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000008:administration & dosage / Q000494:pharmacology*
D000806:Angiotensin-Converting Enzyme Inhibitors; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D001127:Arginine Vasopressin; D002216:Captopril; D009638:Norepinephrine
captopril; hypoxia angiotensin II; intrarenal oxygenation; intrarenal perfusion; norepinephrine; renal blood flow; vasopressin