The effects of cyclopropane, halothane and ether on central baroreceptor pathways

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Abstract
The reductions in arterial pressure and preganglionic sympathetic activity evoked by aortic nerve stimulation in the rabbit were studied before and during administration of constant inspired concentrations of the inhalation anaesthetics cyclopropane, halothane, and ether. The background anaesthetic was pentobarbital, gallamine triethiodide was given, and pulmonary ventilation was with 100% 02- During light pentobarbital anesthesia, aortic nerve stimulation usually induced similar reductions in arterial pressure and preganglionic discharge, expressed as the maximum percentage reduction from prestimulation levels. There were 2 components in the sympathetic responses, attributable to A and C fiber excitation in the aortic nerve, which also contained a third fiber group with properties similar to those of B fibers. The arterial pressure, heart rate, and preganglionic sympathetic responses to aortic nerve stimulation were rapidly and profoundly inhibited by 50% cyclopropane, which also produced arterial hypertension. Halothane (3%) significantly inhibited the depressor responses, but even in the presence of severe hypotension the arterial pressure could usually be further reduced by aortic nerve stimulation. The inhibitory effects of 2% halothane were slow in onset and not pronounced. In the concentrations used, these actions of halothane were significantly less than those of cyclopropane. The inhibitory effects of ether on the depressor responses were roughly intermediate between those of cyclopropane and halothane; complete suppression of the responses occurred with high ether con-contrations, which were also liable to cause circulatory collapse. The three anesthetics significantly inhibit impulse transmission through central baroreceptor pathways; the implications of the findings are discussed in relation to the different circulatory actions of these anesthetics.