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

Abstract

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 Po 2 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.