Experimental cerebral ischemic lesions and autonomic and cardiac effects in cats and rats

Clinically, a pattern of autonomic and cardiac changes after hemispheric stroke has been observed that includes increased plasma catecholamines, electrocardiographic abnormalities, serum levels of cardiac enzymes, and myocytolysis on autopsy. Experimental models in both the cat and rat have been developed to examine some of the mechanisms responsible for these changes. Middle cerebral artery occlusion (MCAO) in the rat mimicked the increase in plasma catecholamines, electrocardiographic changes, sympathetic nerve discharge, and myocytolysis seen in the patient population. This model was also used to determine that stroke attenuates sympathoexcitatory reflexes and that right-sided strokes and increasing age exaggerate the autonomic and cardiac disturbances. Hypertension does not appear to exacerbate the stroke-induced sympathoadrenal increases. Lesion of the insular cortex mimics the autonomic changes in MCAO animals. Finally, changes in the content of neurochemicals in the insular cortex and amygdala have been measured that may be involved in mediating the autonomic changes elicited by MCAO.