Cardiac ischemic changes and arrhythmias induced by hypothalamic stimulation

Abstract

It has been shown that in cats, short periods of stimulation of discrete hypothalamic areas (anterior, posterior and lateral) can lead to temporary and repeatable pressor responses associated with consistent electrocardiographic ischemic-like changes (ST-T deviations) and arrhythmias (bradycardia, tachycardia and ectopic beats). Significant quantitative and qualitative differences in these responses are demonstrable, depending on whether succinylcholine or gallamine is used. The pressor responses from all areas are completely abolished by C2 spinal section and are therefore of sympathetic origin; but whether or not they are from specific hypothalamic areas or from some common sympathetic pathways traversing these areas has not been determined. Parasympathetic cardiac changes (bradycardia) appear to be specifically mediated only from the anterior hypothalamus, although with high intensity stimulation they can also arise from other areas. Sympathetic cardiac changes (tachycardia and ST-T deviations) ensue from all three areas, but appear to be specifically mediated only from the lateral hypothalamus. Intense, prolonged and repeated lateral stimulation enhances the development and persistence of ischemic-like electrocardiographic disturbances, and with bilateral stimulation can induce significant postmortem pathologic changes (distinct myocardial infarction in some animals), although acute fatal ventricular fibrillation was never observed. It is postulated that these sympathetic cardiac changes are mediated by norepinephrine rather than by epinephrine. The findings suggest that hypothalamic stimulations might be involved in some of the arrhythmias reported in patients with cerebrovascular accidents.