Responsiveness to cardiac sympathetic nerve stimulation during maximal coronary dilation produced by adenosine.

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Abstract
Effects of adrenergic constrictor stimuli on total and transmural myocardial blood flow during maximal coronary dilation produced by adenosine were examined. The goal was to determine if coronary vessels maximally dilated with adenosine respond to constrictor stimuli and if the constrictor effect is uniform transmurally. In anesthetized dogs, the circumflex coronary artery was perfused at constant pressure. Total circumflex flow was measured with an electromagnetic flowmeter; transmural flow was measured with 9-.mu.m radiolabeled spheres injected into the perfusion tubing. Propranolol (2 mg/kg, i.v.) was administered to block myocardial and coronary .beta.-receptors. Coronary responses to cardiac sympathetic nerve stimulation (CSNS) at 10 Hz and intracoronary administration of angiotensin (0.125 and 0.50 .mu.g/min), phenylephrine (0.50 and 2.00 .mu.g/min), norepinephrine (0.25 and 1.0 .mu.g/min) and tyramine (200 .mu.g/min) were obtained during intracoronary infusion of adenosine (4.7 .mu.m/min). This dose of adenosine abolished reactive hyperemia; a higher dose of adenosine did not produce further increases in flow. Control flow during adenosine averaged 382 .+-. 50 (SE) for endocardium and 524 .+-. 44 ml/min per 100 g for epicardium. During adenosine, CSNS at 10 Hz decreased epicardial flow to 308 .+-. 44 ml/min per 100 g; (P < 0.05), but did not decrease endocardial flow (378 .+-. 58 ml/min per 100 g; NS [not significant]). In contrast, angiotensin, phenylephrine, norepinephrine and tyramine produced significant decreases (P < 0.05) in both endocardial and epicardial flows. Coronary arteries maximally dilated with adenosine are responsive to constrictor effects of adrenergic and nonadrenergic stimuli, and during adenosine treatment, the administration of angiotensin, phenylephrine, norepinephrine and tyramine decreases both endocardial and epicardial flow, but sympathetic nerve stimulation decreases epicardial flow without significant decreases in endocardial flow. This non-uniform influence of nerve stimulation on transmural myocardial flow does not appear to relate to mechanical or metabolic factors or to characteristics of coronary adrenergic receptors.

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