Abstract

In a series of experiments in anesthetized dogs, the origin and mechanism of reduced renal blood flow (RBF) during acute portal hypertension was investigated. With acute superior mesenteric vein (SMV) occlusion and normalization of cardiac hemodynamics RBF remained reduced at 66 ± 14 ml/min compared to baseline of 160 ± 25 ml/min ( P < 0.01). Neither acute superior mesenteric artery occlusion, nor acute hepatic portal hypoperfusion with normal SMV pressures maintained by SMV-caval shunt, resulted in reduction of RBF. Cross-perfusion studies failed to produce alterations of RBF in recipient dogs from donor dogs with SMV occlusion, reduced RBF, and normal cardiac outputs. Finally, splanchnic ganglionectomy prevented RBF reduction during SMV occlusion after volume restoration. We conclude that reduced RBF during acute portal hypertension is a result of an intestinal-renal neurogenic reflex initiated by intestinal venous congestion.

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