Nitric oxide and pancreatic islet blood flow after induced portal hypertension in rats.
Portal hypertension (PH) is associated with a hyperdynamic splanchnic circulation, partially mediated by nitric oxide-dependent mechanisms. The aim of the present study was to evaluate the influence of PH and nitric oxide on pancreatic islet blood flow. PH was induced by a calibrated stenosis of the portal vein in male Sprague-Dawley rats. Control were sham-operated. Ten days later pancreatic, duodenal, colonic, and arterial hepatic blood flows were measured with microspheres. All splanchnic blood flow values were markedly increased in the PH rats. The fraction of whole pancreatic blood flow diverted through the islets increased from approximately 5 to 15%. Intravenous administration of the nitric oxide synthase inhibitor NG-nitro-L-arginine (25 mg/kg body weight) in rats with PH 10 min before blood flow measurements decreased pancreatic, duodenal, colonic, and arterial hepatic blood flow to control values. Pancreatic islet blood flow was also decreased, but more markedly than that of the whole pancreas. Pancreatic islet morphology was normal, and the rate of islet cell replication was not influenced. PH induced a preferential increase in pancreatic islet blood flow, which is likely to be associated with an increased production of nitric oxide.