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Anesthetized dogs were studied to characterize the renal hemodynamic response to acute, transient hypoxemia and to determine the role of renal prostaglandins (PGE and PGF) in that response. Acute hypoxemia of 10 minutes duration (mean arterial Po2 32 ± 9 torr) induced a reversible increase in renal blood flow (RBF) (measured by electromagnetic flow probe) and mean arterial pressure (MAP) with a decreased urinary flow rate (V) and no change in glomerular filtration rate (GFR) or renal vascular resistance (RVR). Urinary excretion of PGE (UPGE) and PGF (UPGF) (measured by radioimmunoassay) was not significantly changed by hypoxemia under these conditions. After inhibition of the prostaglandin system by administration of indomethacin (5 mg/kg) or meclofenamate (5 mg/kg) intravenously, a significant decrease in RBF and GFR with an increase in RVR occurred in response to hypoxemia. Furthermore, there was a significantly greater decline in URGE and UPGF with hypoxemia after prostaglandin inhibition than before treatment. Control (non-drug treated) animals demonstrated no difference in response to a second episode of hypoxemia relative to the first hypoxemic response. The significant changes in URGE (ΔUPGE), UPGF (ΔUPGF), and GFR with hypoxemia after treatment were not secondary exclusively to a decline in RBF, as shown by the similar response of ΔUPGE and GFR to hypoxemia in dogs in which RBF was enhanced with hypoxemia after treatment by means of an adjustable aortic clamp. Inhibition of prostaglandin synthesis, therefore, unfavorably altered the ability to maintain normal renal perfusion and function during acute hypoxemia in these animals. This renal response to hypoxemia may be mediated by decreased renal prostaglandin production under these conditions.

Altered renal hemodynamic and urinary prostaglandin response to acute hypoxemia after inhibition of prostaglandin synthesis in the anesthetized dog.