The effects of cardiac sympathetic nerve stimulation on perfusion of stenotic coronary arteries in the dog.

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Abstract
The interaction of sympathetic vasoconstriction with the coronary reserve distal to stenoses and the role of .alpha.-adrenergic mechanisms in the genesis of myocardial ischemia were studied in 42 anesthetized open-chest dogs. Left cardiac sympathetic nerve stimulation was performed after bilateral cervical vagotomy: with intact coronary arteries, with an intermediate stenosis and with a severe stenosis on the circumflex coronary artery. Stenoses were produced by a wire snare and defined as an intermediate by the reduction of the reactive hyperemia repayment following a 15-s occlusion from 460 .+-. 100 to 140 .+-. 30%; a severe stenosis was defined by only 25 .+-. 8% reactive hyperemia repayment. Cardiac sympathetic nerve stimulation decreased the end-diastolic coronary resistance of intact coronary arteries from 0.79 .+-. 0.05 to 0.53 .+-. 0.06 mm Hg .times. min .times. 100 g/ml (P < 0.01), and the end-diastolic poststenotic resistance of the moderately stenosed arteries from 0.65 .+-. 0.08 to 0.50 .+-. 0.07 mm Hg .times. min .times. 100 g/ml (P < 0.01). Cardiac sympathetic nerve stimulation increased the end-diastolic resistance distal to severe stenoses from 0.57 .+-. 0.04 to 0.97 .+-. 0.18 mm Hg .times. min .times. 100 g/ml (P < 0.01). This stimulation resulted in net lactate production of the circumflex-perfused myocardium; 4 dogs died by ventricular fibrillation. There was a hyperbolic correlation of the cardiac sympathetic nerve stimulation-induced change in resistance to the degree of coronary hyperemic reserve (r = 0.81). Phentolamine (2 mg/kg, i.v.) and rauwolscine (0.2 mg/kg, i.v.) prevented the increase in resistance distal to severe stenoses during cardiac sympathetic nerve stimulation, whereas prazosin (1.2 mg/kg, i.v.) was ineffective. After .beta.-blockade with propranolol (2 mg/kg, i.v.), rauwolscine still prevented the increase in poststenotic resistance during cardiac sympathetic nerve stimulation. Apparently, there is a continuous unmasking of sympathetic vasoconstriction with increasing severity of a stenosis and, thus, decreasing coronary reserve. This vasoconstriction is mediated by postjunctional .alpha.2-receptors and can induce myocardial ischemia distal to severe coronary stenoses.