Abstract
Psychosocial stress is known to be a risk factor for sudden cardiac death. In animals, we have shown that operationally defined stressor-events must be present for coronary artery occlusion to result in ventricular fibrillation. Each type of stressor-event has been found to evoke the same pattern of electrochemical responses in the frontal granular cortex. These event-related responses include, negative-polarity slow potentials, extracellular potassium-reduction, and norepinephrine-release. The magnitudes of each of the cerebral responses is related to the animal’s level of acquisition and/or adaptation to the stressor-stimuli. The effect of stress on cardiac vulnerability is prevented by either the blockade of frontocortical projections to the brainstem cardiovascular nuclei or the intracerebral injection of 1-propranolol (0.01 mg/kg). We conclude that psychosocial stressors increase cardiac vulnerability through a learning-dependent noradrenergic process in frontocortical neurons.
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Skinner, J.E. (1985). Psychosocial Stress and Sudden Cardiac Death: Brain Mechanisms. In: Beamish, R.E., Singal, P.K., Dhalla, N.S. (eds) Stress and Heart Disease. Developments in Cardiovascular Medicine, vol 45. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2587-1_3
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