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% O-2). rCBF was measured in 10 dissected brain regions using [C-14]iodoantipyrine; rCGU was measured by 2-deoxy-D-[C-14]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. Bilateral lesions in the spinal trigeminal nucleus (PaO2 = 35 +/- 1; n = 6), or transection of the IXth and Xth cranial nerves did not affect the rCBF response to hypoxia (PaO, = 41 +/- 2; n = 6) (P > 0.05) indicating that the effect of RVL lesions was not attributable to interference with arterial baro- or chemoreceptor reflexes. We conclude that neurons within RVL are not responsible for maintaining tonic levels of rCBF. However they contribute to the cerebrovascular vasodilation elicited by hypoxia but not hypercapnia. The cerebrovascular response to hypoxia appears reflexive and, in part, due to stimulation of oxygen-sensing neurons in RVL. In contrast, the vasodilation elicited by hypercapnia reflects local chemical signals in the cerebral microcirculation.