Vascular responsiveness of the in situ perfused dog pancreas

Abstract

The in situ perfused dog pancreas was utilized to investigate: (a) the contribution of humoral vasoactive agents which are released in shock to maintain the development of pancreatic hypoperfusion, (b) the effectiveness of glucocorticoids as splanchnic vasodilator agents as a possible mechanism of thier beneficial effect in shock, and (c) the pancreatic vascular response to the cardiac glycoside, ouabain. Close intra-arterial injection of norepinephrine, epinephrine, vasopressin and angiotensin in concentrations present in shock animals significantly increased pancreatic vascular resistance, whereas bradykinin, prostaglandins E 1 and E 2 exerted a vasodilator effect. The glucocorticoids, methylprednisolone and dexamethasone, were without net vascular effect in the perfused pancreas at concentrations comparable to those known to be protective in hemorrhagic shock. Ouabain produced a well maintained increase in pancreatic vascular resistance. It is concluded that the release of vasoactive agents may significantly influence the pancreatic vascular response to prolonged hemorrhage. Use of ouabain in the treatment of circulatory shock states could result in severe deleterious effects to the organism because of its prolonged vasoconstriction of the pancreatic vasculature. No evidence of a vasodilator action of glucocorticoids in the pancreatic vasculature was found, suggesting other mechanisms for the protective action of these agents in shock.