This preclinical study demonstrated that sympathetic cholinergic vasodilation occurs in skeletal muscle but not in the coronary circulation of dogs.
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Absence of coronary sympathetic cholinergic vasodilation in dogs cautions against uniform vascular mechanisms; leaves open relevance to human defense reactions.
The sympathetic control of left circumflex coronary blood flow was studied by stellate ganglion and hypothalamic stimulation. Flow was measured acutely in dogs under chloralose or pentobarbital anesthesia by an electromagnetic flowmeter. Coronary vasoconstriction was observed when the left stellate ganglion was stimulated after blocking beta receptors with propranolol or INPEA. The possibility of coronary sympathetic cholinergic vasodilation of the type found in skeletal muscle was examined in three types of experiments in which vasodilation occurred in skeletal muscle: (1) peripheral sympathetic nerve stimulation after chronic catecholamine depletion with reserpine, (2) peripheral sympathetic nerve stimulation after acute block of alpha and beta receptors, (3) hypothalamic stimulation to give a defense reaction after acute block of alpha and beta receptors. Within the limits of these experiments, skeletal muscle cholinergic vasodilation was demonstrated but coronary sympathetic cholinergic vasodilation was not, even as part of the defense reaction elicited by hypothalamic stimulation.
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Eric O. Feigl (1967) studied this question.
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