Epinephrine infusion produced a 25% increase in myocardial perfusion without beta-blockade, but a 20% decrease via nonuniform microvascular constriction in the presence of beta-blockade.
Does epinephrine have nonuniform effects on coronary microvascular diameters in the presence or absence of beta-adrenergic blockade in an open-chest cat model?
Epinephrine produces uniform coronary vasodilation and increased perfusion normally, but causes nonuniform microvascular constriction and decreased perfusion when beta-adrenergic receptors are blocked.
This study was designed to examine the hypothesis that epinephrine has nonuniform effects on coronary microvascular diameters.Measurements of coronary microvascular diameter were completed in anesthetized, open-chest cat preparations in which the epicardial microcirculation was viewed through an intravital microscope using stroboscopic epi-illumination.Images of coronary microvessels were digitized and analyzed on a video monitor.With arterial pressure controlled, measurements in the absence and presence of /3-adrenergic blockade (propranolol 1 mg/kg) were obtained during epinephrine infusion (1-2 /xg/kg/min).In the absence of/3-adrenergic blockade, epinephrine produced a 25% increase in myocardial per fusion.Under these conditions, coronary vasodilation was observed in all classes of coronary arterial and arteriolar vessels.In the presence of /3-adrenergic blockade, epinephrine produced a significant decrease in myocardial perfusion (-20%).Nonuniform effects on diameter were observed in arterial and venous segments of the coronary circulation.These data are consistent with the view that in the absence of /3-adrenergic blockade, the functional coronary hyperemia associated with epinephrine administration is produced by uniform coronary arterial and arteriolar dilation.In the presence of /3-adrenergic blockade, with metabolic effects controlled, epinephrine produced a decrease in myocardial perfusion, which is related to a nonuniform decrease in coronary microvascular diameters.Such heterogeneous effects on microvascular diameters result in a redistribution of coronary microvascular resistance.(Circulation Research 1987;61(suppl II):II-47-11-53) S timulation of cardiac sympathetic nerves or cate- cholamine infusion produces /3-adrenergic receptor-mediated increases in heart rate and myocardial contractility, which result in an increase in coronary blood flow.Concurrent with the metabolic coronary hyperemia, there is activation of a-adrenergic receptors, which produces coronary vasoconstriction. 1 -2 Although there is substantial information regarding pharmacologic and metabolic coronary hyperemia as well as a-adrenergic constriction at the macrovascular level in the coronary circulation, there is a paucity of information regarding the microvascular sites at which such dilation and constrictor mechanisms may occur. 13ttempts to examine segmental a-adrenergic constriction in the coronary circulation have been confined to studies that simultaneously measure large epicardial coronary artery resistance and total coronary vascular resistance.In the intact animal, Kelley and Feigl 4 examined segmental a-adrenergic coronary constrictor mechanisms in large coronary arteries.Large coronary arteries constricted during sympathetic nerve stimulation or norepinephrine infusion following /3-adrenergic
Chilian et al. (Sun,) reported a other. Epinephrine vs. Absence vs presence of β-adrenergic blockade (propranolol 1 mg/kg) was evaluated on Myocardial perfusion and coronary microvascular diameters. Epinephrine infusion produced a 25% increase in myocardial perfusion without beta-blockade, but a 20% decrease via nonuniform microvascular constriction in the presence of beta-blockade.
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