Acute myocardial and plasma catecholamine changes in experimental stroke.

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Abstract
Focal cerebral ischemia in humans increases the incidence of cardiac arrhythmias, and serum cardiac enzyme and plasma norepinephrine levels. In addition, systemic administration of catecholamines causes myocardial damage. This suggests that cerebral ischemia may cause myocardial damage as a consequence of elevated plasma norepinephrine levels. Therefore, experiments were done in 23 chloralosed, paralyzed and artificially ventilated cats to investigate the effects of occluding (n = 17) or sham-occluding (n = 6) the left middle cerebral artery on the myocardium and on circulating levels of plasma catecholamines. After occlusion of the middle cerebral artery for 12-22 hr, 41% (7/17) of the hearts had either acute myocardial necrosis (3/7), focal hemorrhage (3/7), or both (1/7). In animals with acute myocardial damage the levels of plasma norepinephrine and epinephrine were significantly increased compared to pre- middle cerebral artery occlusion values (+46 +/- 18% and +142 +/- 45%, respectively). As well, in cats with acute myocardial damage, changes from initial levels of plasma norepinephrine and epinephrine were significantly increased over those of experimental cats without acute myocardial damage. In animals which did not have acute myocardial damage (10/17) the circulating plasma levels of catecholamines were not significantly different from pre-occlusion values. Similarly, sham occlusion did not alter plasma catecholamine levels. These data demonstrate that a percentage of animals subjected to middle cerebral artery occlusion have myocardial damage and an increase in plasma concentration of norepinephrine and epinephrine. This suggests that a rise in plasma catecholamine levels, due to increased sympathetic activity after middle cerebral artery occlusion, may cause myocardial damage.