Failure of methylprednisolone to prevent nonuniform cardiac accelerator nerve discharge associated with coronary occlusion-induced arrhythmia: evidence against prostaglandin modulation of autonomic cardioaccelerator neural discharge in the anesthetized cat.

Postganglionic cardiac sympathetic neural discharge in the minute prior to arrhythmia produced by acute occlusion of the left anterior descending coronary artery was nonuniform, i.e., both increases or decreases occurred. It is hypothesized that the nonuniform neural discharge is transmitted to the heart, causing nonuniform changes in excitability and conduction which produce ventricular arrhythmias. Prostaglandins have been shown to exhibit both arrhythmogenic as well as antiarrhythmic actions. Methylprednisolone (30 or 50 mg/kg, i.v., a known inhibitor of prostaglandin synthesis) was given 30 minutes prior to coronary occlusion of the left anterior descending artery. Both doses of methylprednisolone failed to: exert any effect on the mean postganglionic cardiac sympathetic nerve discharge prior to coronary occlusion; eliminate the nonuniform neural discharge associated with occlusion-induced arrhythmia; increase the time to arrhythmia or death; and decrease the number of cats dying after acute coronary occlusion. Thus, it is hypothesized that methylprednisolone failed to prevent the arrhythmogenic actions of prostaglandins. The failure of methylprednisolone to decrease the time to arrhythmia suggests that, in this study, an antiarrhythmic mechanism for prostaglandins does not exist. The failure of methylprednisolone to prevent the occlusion-induced nonuniform cardiac sympathetic discharge suggests that prostaglandin modulation of the autonomic balance on the heart is not due to a direct action on the postganglionic cardiac sympathetic nerve.