HEMODYNAMICS OF PANCREATIC ISCHEMIA IN CARDIOGENIC-SHOCK IN PIGS

Background & Aims: Previous studies have shown that the renin-angioten sin axis plays a pivotal role in vasoconstriction of the gastric, inte stinal, and hepatic circulations during cardiogenic shock. The aim of this study was to evaluate the fundamental hemodynamic mechanism of pa ncreatic ischemia during cardiogenic shock induced by pericardial tamp onade. Methods: Cardiogenic shock was induced by pericardial tamponade . Cardiac output (and total peripheral vascular resistance) was determ ined by thermodilution. Pancreatic blood flow (and vascular resistance ) was determined with radiolabeled microspheres. Results: Graded incre ases in pericardial pressure produced corresponding decreases in cardi ac output to 42% +/- 1% and arterial pressure to 67% +/- 3% of baselin e and increases in total peripheral vascular resistance to 146% +/- 5% of baseline. Pancreatic blood flow decreased disproportionately to 30 % +/- 3% of baseline, because of a disproportionate increase in pancre atic vascular resistance to 220% +/- 19% of baseline. Previously confi rmed blockade of the renin-angiotensin axis ablated this response, whe reas confirmed blockade of the alpha-adrenergic system or vasopressin system had no significant effect. Without shock, central intravenous i nfusions of angiotensin II closely mimicked this selective vasoconstri ction. Conclusions: Angiotensin-mediated selective pancreatic vasocons triction results in significant pancreatic ischemia during cardiogenic shock.