Effects of middle cerebral artery occlusion on baroreceptor reflex control of heart rate in the rat

Abstract

Neurons in the insular cortex have recently been shown to innervate medullary autonomic nuclei such as the nucleus tractus solitarii (NTS). The present study examines the effect of lesioning the insular cortex on baroreceptor-heart rate reflex in conscious rats. We did this by occluding the stem of the left proximal middle cerebral artery which causes a lesion of the insular and adjacent lateral frontoparietal cortices. Nine and 10 days after lesioning or sham operation, reflex heart rate responses were recorded following i.v. doses of the pressor agent phenylephrine and the depressor agent sodium nitroprusside. Baroreceptor reflex parameters were determined by computerized sigmoidal curve-fitting. The overall contribution of the sympathetic and the cardiac vagus were assessed by using peripherally acting muscarinic and β-adrenoceptor antagonists, respectively. Lesioned rats were compared to sham-operated rats. Lesioning the insular cortex did not affect mean blood pressure and heart rate. However, the lesion selectively enhanced reflex vagal bradycardia that occurred when mean blood pressure was artificially elevated. A greater vagal bradycardia with no change in the upper plateau indicated that ischemia was acting entirely on the baroreflex-dependent vagal cardiac motoneurons. There was no effect on the sympathetic heart rate range but the normalized gain of the sympathetic component was increased in those lesioned rats. These observations suggest that the unilateral cortical lesion chronically affected the baroreceptor control of heart rate through mechanisms differentially affecting the vagus and the cardiac sympathetic nerves.