Electrical or chemical stimulation of afferent cardiac sympathetic nerve fibers evoked reflex increases in myocardial contractility (dP/dt max) mediated entirely by the spinal cord.
We studied the reflex changes in myocardial contractility elicited by electrical stimulation of afferent cardiac sympathetic nerve fibers or chemical stimulation of their cardiac endings. Veratridine injected directly into the left coronary artery was the chemical stimulus. The maximum rate of rise of left ventricular pressure, dP/dt max, was used as an index of myocardial contractility. The stimuli evoked increases in dP/dt max in vagotomized cats with or without spinal transection (C1). Electrical stimulation provoked the same effect in vagotomized dogs. Increases in dP/dt max occurred which were independent of changes in heart rate, preload, or afterload. They were reflex in nature since they were abolished by section of the upper thoracic sympathetic rami or cardiac sympathetic nerves. These results are the first demonstration of a cardiocardiac reflex which can be mediated entirely by the spinal cord. Electrical stimulation in vagotomized cats and dogs also produced a reflex increase in arterial blood pressure partly due to sympathetic vasoconstriction.
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Circulation Research
University of Utah
American Heart Association
Istituto Nazionale per le Ricerche Cardiovascolari
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Malliani et al. (Tue,) reported a other. Electrical stimulation of afferent cardiac sympathetic nerve fibers or chemical stimulation (veratridine) was evaluated on Changes in myocardial contractility (dP/dt max). Electrical or chemical stimulation of afferent cardiac sympathetic nerve fibers evoked reflex increases in myocardial contractility (dP/dt max) mediated entirely by the spinal cord.