The hepatic hemodynamic response to cardiogenic shock was investigated in a porcine model produced by pericardial tamponade to better understand the pathophysiology of postshock hepatic insufficiency. Reductions of cardiac output to 50 percent of baseline levels produced marked hepatic ischemia by causing disproportionate reductions in blood flow through the celiac and hepatic arteries and portal vein. These were due to selective vasoconstriction of the splanchnic resistance vessels that was mimicked without tamponade by the infusion of angiotensin II, ablated by angiotensin-converting enzyme blockade, unaffected by alpha-adrenergic ablation, and correlated closely with levels of plasma renin activity. The ischemic liver injury of cardiogenic shock appears to be largely due to an exquisite responsiveness of the splanchnic vascular smooth muscle to endogenously released angiotensin II.