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The effect of decerebration on the reflex response to left atrial distension Albrook, Sally Milton

Abstract

An increase in heart rate brought about by stimulation of the re centers at the junction of the pulmonary veins and the left atrium in dogs has been reported by Ledsome and Linden, (1964). Although extensive experimentation has shown the afferent pathway for such tachycardia is in the vagus nerve, and efferent impulses appear to travel via the cardiac sympathetics, the location of central synapses, and the degree of central control necessary for its existence are not known. Also unknown is the significance of this cardiovascular control mechanism in the unanaesthetized animal. The series of experiments described in this paper were designed to answer both these questions. A method for decerebrating mongrel dogs (8-18 Kg) by electrocoagulation was devised which avoided traumatic loss of blood, leaving a stable decerebrate preparation. The tachycardia initiated by the inflation of small balloons at the junction of the pulmonary veins with the left atrium was found to be unchanged by such a midcollicular decerebration. Both magnitude and neural characteristics of the increase in heart rate were unaltered. However, careful studies of these characteristics with both drugs and lesions of the spinal cord, revealed a discrepancy with previous reports. The tachycardia produced by balloon inflation could not be totally abolished by the infusion of the sympathetic blocking agent propranolol, either before or after decerebration. In addition small, but significant, increases in heart rate remained upon section of the spinal cord at the level of the first cervical vertebra. These results indicated that the efferent pathway for this reflex, though predominantly relayed by the cardiac sympathetics, may possess a vagal component. Using the same decerebrate preparation, two volatile anaesthetics were used to study the effects of anaesthetics on the response to balloon inflation. Halothane, or a nitrous oxide-sodium pentothal combination were administered prior to decerebration, then discontinued at completion of the section. Throughout the duration of both anaesthetics, cardiovascular reflexes such as the carotid sinus reflex, were depressed. The left atrial reflex was similarly small or absent as compared to dogs under chloralose anaesthesia. Removal of the anaesthetic circuit after successful decerebration coincided with the appearance of small but significant increases in heart rate at balloon inflation, and typical carotid sinus activity at occlusion of the carotid arteries. Neither reflex attained the magnitudes observed in dogs under chloralose anaesthesia, despite prolonged waiting, up to six hours after decerebration.

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