Cerebellar lesions alter autonomic responses to transient isovolaemic changes in arterial pressure in anaesthetized cats.

Abstract

In previous studies, bilateral lesions of the rostral fastigial nucleus (rFN) of the cerebellum impaired recovery of mean arterial pressure (MAP) after many forms of hypotension. This study examined effects of cerebellar lesions on baroreflex responses during transient, isovolaemic, non-orthostatic changes in MAP in anaesthetized cats. Bilateral rFN lesions did not alter the rate or extent of fall in MAP induced by nitroprusside, but reduced by 39% the reflex increase in heart rate per unit decrease in pressure (delta HR/delta MAP). Femoral artery resistance remained below control levels. Lesions prolonged the time for 50% MAP recovery after nitroprusside by 93%. During phenylephrine-induced MAP increases, bilateral rFN lesions augmented reflex delta HR/delta MAP by 68%. In intact cats, the reflex decrease in HR after phenylephrine was blocked by electrical stimulation of the rFN, but appeared immediately after stimulation was stopped. Stimulation alone increased both MAP and HR. Propranolol failed to block either the increased HR or the suppression of reflex cardiodeceleration induced by rFN stimulation. Decreases in resting HR after rFN lesions may reflect removal of tonic cerebellar inhibition of cardiac parasympathetic tone. Thus, the cerebellum can influence autonomic output and modify baroreflex sensitivity by augmenting cardiovascular responses mediated by the sympathetic nervous system and inhibiting those mediated by the parasympathetic nervous system.