Changes in regional vascular resistance after myocardial infarction in the dog.

The possibility that failure of vascular resistance to increase during hypotension in cardiogenic shock is a generalized phenomenon affecting many vascular beds was investigated in anesthetized dogs subjected to coronary arterial embolization. Blood flow in the carotid, mesenteric and renal vascular beds was monitored. Efferent vagus nerve stimulation, which, through bradycardia, produces hypotension of cardiac origin without myocardial damage, was associated with reflex vasoconstrictor responses in the carotid and mesenteric vascular beds; no change in resistance occurred in the renal vascular bed. In marked contrast, vasoconstriction failed to occur in any of the vascular beds in response to the hypotension produced by coronay embolization. These responses to cardiogenic shock mimicked those seen after ganglionic blockade, in which hypotension of partly cardiac origin was produced and reflex vasoconstriction blocked. The data support the previous hypothesis that myocardial infarction is associated with reflex inhibition of the reflex vasoconstrictor response to hypotension.