Nifedipine Prevents Sympathetic Vasoconstriction Distal to Severe Coronary Stenoses


    loading  Checking for direct PDF access through Ovid

Abstract

Cardiac sympathetic nerve stimulation (CSNS) can induce vasoconstriction distal to severe coronary stenoses by activation of vascular α2-adrenoceptors. Whether nifedipine can antagonize this CSNS-induced vasoconstriction was tested in 11 anesthetized, vagotomized dogs. CSNS decreased the end-diastolic resistance of intact coronary arteries from 0.76 ± 0.07 to 0.56 ± 0.05 mm Hg · min · 100 g/ml (p < 0.05). In contrast, the resistance distal to severe stenoses, which were defined by a reduction of the postocclusive reactive hyperemia to almost zero, was increased during CSNS from 0.52 ± 0.06 to 0.87 ± 0.14 mm Hg · min · 100 g/ml (p < 0.05). This increase in resistance was associated with severe ischemia, as indicated by a net lactate production of the circumflex-perfused myocardium and a decrease in systolic segment shortening from 8.4 ± 0.7 to 7.0 ± 0.7% (p < 0.05). Both intracoronary (10 μg) and intravenous (10 μg/kg) administration of nifedipine did not change the poststenotic resistance at rest, but did prevent the CSNS-induced increase in resistance, the decrease in regional contraction, and the net lactate production. We conclude that nifedipine can prevent the deleterious role of α-adrenoceptor-mediated vasoconstriction in the genesis of myocardial ischemia.

    loading  Loading Related Articles