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The possibility that failure of vascular resistance to increase contributes to hypotension after myocardial infarction was examined in the hindlimbs of dogs following embolization of the coronary arteries. Vascular resistance did not change significantly during sustained severe hypotension after embolization in either the intact hindlimb or in simultaneously autoperfused innervated and denervated hindlimbs using constant flow. In nonembolized animals, an immediate large increase in hindlimb vascular resistance occurred when equivalent hypotension was produced by stimulation of the distal end of the sectioned vagus nerve. Lack of such response during hypotension after embolization suggested that inhibition of reflex vasoconstriction had occcurred. Bilateral cervical vagotomy allowed normal reflex vasoconstriction to proceed during hypotension after infarction. These data indicate that (1) since vascular resistance is unchanged in both innervated and denervated hindlimbs, normal neurogenic vascular tone is sustained during hypotension after myocardial infarction and (2) the baroreceptor reflex, which normally promotes vasoconstriction during hypotension, is inhibited reflexly following myocardial infarction, probably by activation of cardiac vagal afferents.

Inhibition of Reflex Vasoconstriction after Experimental Coronary Embolization in the Dog