Our previous studies in the anesthetized pig have shown that two particular cerebral states can regulate the vulnerability of the ischemic heart to arrhythmias. Psychologically stressed pigs all show ventricular fibrillation following coronary artery occlusion, whereas unstressed animals, with heart rate held constant, do not manifest this lethal arrhythmia. In the infarcted myocardium of the sleeping animal, the number of ectopic arrhythmias increases during slow wave sleep, but decreases below the awake control level during rapid eye movement sleep; these effects also are independent of heart rate. The responses of the cerebral cortex to stressful stimuli (event-related slow potentials) and to slow wave sleep (8-12 Hz, EEG synchrony) both depend upon the integrity of the frontal granular cortex. Blockade of the frontocortical output pathway to the brainstem in stressed pigs will prevent the occurrence of ventricular fibrillation following coronary artery occlusion. Our present aims are to observe in the myocardium the electrophysiological and biochemical consequences of the shift from the deleterious to the salutary state of the brain. That is, we will compare myocardial measures during 1) stress vs. nonstress, 2) slow wave vs. rapid eye movement sleep and 3) nonblockade vs. blockade of the frontocortical-brainstem pathway. We have developed a thoracic window device for investigating the myocardium of the conscious pig. Through this window, electrodes can be introduced painlessly into the left ventricle and tissue biopsies extracted from it. Measurements of regional myocardial refractory period, intracellular action potentials, phosphorylase a/a+b and cyclic AMP will be made in association with the cerebral states. This data will enable us to understand how the brain conditions that regulate cardiac vulnerability actually control the heart. Such an understanding could eventually explain cerebral involvement in the mechanism of sudden cardiac death by ventricular fibrillation.