Abstract
The effects of ganglionic blockade were studied on the changes in coronary blood flow and myocardial contraction produced by electrical stimulation of the left cardiac sympathetic nerves in anesthetized open-chest dogs. Stimulation of the left ventral ansa subclavia (AS) and the ventrolateral cervical cardiac nerve (VLCCN) produced 2 peaks of increase in coronary blood flow, in myocardial contractile force (MCF) and in left ventricular pressure (LVP). The first peak was, in some experiments, preceded by an initial transient decrease in coronary blood flow. Bilateral cervical vagotomy or intravenous injection of atropine did not affect the initial changes in coronary blood flow. In dogs pretreated with intravenous propranolol or practolol, the stimulation of either AS or VLCCN evoked a prolonged decrease in coronary blood flow without appreciable changes in systemic blood pressure and myocardial contractility. The decrease in coronary flow resulting from AS stimulation was blocked not only by intravenous injection of phentolamine but also by hexamethonium (C6) given into the pericardial cavity or in the coronary artery. On the other hand, the decrease elicited by stimulation of VLCCN was abolished by phentolamine but not influenced by intracoronary and intrapericardial C6, while hypotension and brady-cardia produced by cervical vagosympathetic stimulation were completely blocked by C6. From the present data, it may be concluded that in coronary vessels there exist adrenergic alpha receptors corresponding to the sympathetic vasoconstrictor nerve of which preganglionic fibers terminate in the stellate and inferior cervical ganglia, and that the intracardiac ganglion cells play little role in the coronary vasoconstrictor response after beta adrenergic receptor blockade.
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