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RENAL VASCULAR PROTECTION BY PROSTAGLANDINS DURING HYPOXEMIA IN UNANESTHETIZED FETAL LAMB

Fetal hypoxemia is thought to induce marked vasoconstriction, particularly in the renal (K) circulation. To study regional vascular responses to hypoxemia, 10 fetal lambs (110-135 days gestation) were instrumented with Doppler flow (F) probes on K, mesenteric(M), and iliac (I) arteries and with aortio and vena caval catheters for injection of radio-nuclide microspheres. After recovery from operation administration of 10%. O2 to conscious ewes reduced fetal PaO2 from 22 to 11 mmHg, heart rate from 175 to 129 beats/min, and increased mean arterial pressure from 44 to 53 mmHg. Hypoxemia reduced KF(23%), significantly less, P<.05, than MF (42%) and IF (80%). Pretreatment with meclofenamate, 10 mg/kg, an inhibitor of prostaglandin synthetase, did not alter normoxic control values nor any responses to hypoxemia except in the K bed, where F fell by 55%. The hypoxemia induced decreases in KF and increases in K resistance were significantly greater, P<.01, than observed without meclofenamate, and were no longer significantly different from M and I responses. Thus, hypoxemia induces a differential pattern of response in the unanesthetized fetus with constriction less in K, than M and I beds. Prostaglandin control of the K bed is important even in the fetal circulation and appears to protect the K bed during hypoxemia. Where maintenance of KF is important, as during stress, the administration of prostaglandin synthetase inhibitors could be deleterious.