Abstract
The mechanism of action and possible physiologic implications of glucagon-induced choleresis were investigated in two groups of dogs. Group I demonstrated, in chronic animal models, that glucagoninduced choleresis was not associated with increased bile acid output and was not blocked by somatostatin or Piptal, suggesting a direct stimulatory effect on bile acid-independent canalicular flow. In acute animal models (group II), glucagon infusion at rates which produced postprandial levels in the portal vein induced significant choleresis, implying that glucagon may have a physiologic role in the regulation of bile secretion. No consistent relation between bile secretion and portal venous blood flow could be demonstrated.
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