CARDIOVASCULAR CONSEQUENCES OF EXPERIMENTAL STROKE

Clinically, it has been observed that stroke causes a number of cardio vascular disturbances that are detrimental to prognosis and may cause death. We have developed an experimental model of stroke, a middle cer ebral artery occlusion in the rat, that can mimic the acute cardiovasc ular responses observed clinically. This model has clearly demonstrate d that the insular cortex is necessary to produced the autonomic chang es and that these changes are exacerbated by right-sided infarcts and increasing age. In addition, we have demonstrated that there are neuro chemical changes associated with our stroke model that may mediate the cardiovascular complications. In particular, an increase in dynorphin in the central nucleus of the amygdala occurs with a peak at 3 to 5 d ays after the stroke and is directly due to damage in the insular cort ex. Finally, we have shown that there is a similar time course in the exaggerated cardiovascular responses to stress following middle cerebr al artery occlusion. Direct injection of dynorphin into the central nu cleus of the amygdala can enhance the cardiovascular response obtained by stimulation of the acoustic stress pathway, These observations hav e direct relevance to clinical stroke.