Lesions of nucleus tractus solitarii globally impair cerebrovascular autoregulation.

We studied the effects of acute bilateral electrolytic lesions of the nucleus tractus solitarii (NTS) on regional cerebral blood flow (rCBF) and its autoregulation in rats anesthetized (alpha-chloralose, 40 mg/kg), paralyzed (tubocurarine), and artificially ventilated. rCBF or regional cerebral glucose utilization (rCGU) was measured 30 min after NTS lesions, by the 14C-iodoantipyrine technique or 2-deoxyglucose method, respectively. Cerebrovascular autoregulation was assessed in groups of 4-5 rats at three levels of arterial pressure (AP): 90, 125, and 140 mmHg. AP was lowered by hemorrhage or elevated by intravenous infusion of phenylephrine. NTS lesions did not alter rCBF at 125 mmHg (P greater than 0.05) but resulted in loss of autoregulation (P less than 0.05, analysis of variance). In contrast, lesions of the cuneate nucleus or transection of the baroreceptor afferents did not alter autoregulation. NTS lesions did not affect the reactivity of the cerebrovascular bed to hypercarbia (PaCO2 57.4 +/- 1; n = 5) or hypocarbia (PaCO2 24.4 +/- 1; n = 5) nor the rCGU in any brain regions (P greater than 0.05; n = 5). We conclude that lesions of the NTS impair cerebrovascular autoregulation. The effect is not due to changes in metabolism, nonspecific effects of the lesions, vasoparalysis, or interruption of the baroreceptor reflex arch. Neural pathways originating in or passing through the NTS can regulate the cerebrovascular autoregulation of the entire brain.