Lesions of the rostral ventrolateral medulla reduce the cerebrovascular response to hypoxia.

Sympathoexcitatory neurons of the rostral ventrolateral medulla are tonically active and required for maintenance of resting levels of arterial pressure. They are also selectively excited by hypoxia and responsible for the associated sympathoexcitation. Since electrical or chemical stimulation of RVL will increase regional cerebral blood flow (rCBF) independently of changes in regional cerebral glucose utilization (rCGU) we investigated whether the RVL was also required to maintain resting levels of rCBF and also participated in the cerebrovascular vasodilation elicited by hypoxia. Rats were anesthetized (chloralose; 40 mg/kg, s.c.), paralyzed (tubocurarine) and ventilated (100% O2). rCBF was measured in 10 dissected brain regions using [14C]iodoantipyrine; rCGU was measured by 2-deoxy-D-[14C]glucose. In controls (n = 6) rCBF ranged from 56 +/- 5 in corpus callosum to 101 +/- 6 ml/min x 100 g in inferior colliculus. Hypoxic-hypoxia (PaO2 = 36 +/- 1 mmHg, n = 6) increased rCBF in all structures maximally, at 204% of control, in occipital cortex. Hypercapnia (PaCO2 = 63.5 +/- 0.9, n = 5) also increased rCBF (P < 0.01) maximally to 299% of control in superior colliculus. Spinal cord transection with maintenance of arterial pressure did not affect resting rCBF and increased the vasodilation to hypoxia (PaO2 = 39 +/- 1 mmHg, n = 5) from 2- to 3-fold in all structures (P < 0.01). Bilateral lesions within the RVL had no effect on resting rCBF or rCGU. However, they significantly reduced, in all areas by 50-69% (P < 0.01, n = 5), the cerebrovascular dilation elicited by hypoxia but not hypercapnia.(ABSTRACT TRUNCATED AT 250 WORDS)