Contribution of oxygen-sensitive neurons of the rostral ventrolateral medulla to hypoxic cerebral vasodilatation in the rat

1. We sought to determine whether hypoxic stimulation of neurons of the rostral ventrolateral reticular nucleus (RVL) would elevate regional cerebral blood flow (rCBP) in anaesthetized paralysed rats. 2. Microinjection of sodium cyanide (NaCN; 150-450 pmol) into the RVL rapidly (within 1-2 s), transiently dose-dependently and site-specifically elevated rCBF, measured by laser Doppler flowmetry, by 61.3 ± 22.1% (P < 0.01), increased arterial pressure (AP; +30 ± 8 mmHg; P < 0.01), and triggered a synchronized 6 Hz rhythm of EEG activity. 3. Following cervical spinal cord transection, NaCN and also dinitrophenol (DNP) significantly (P < 0.05) elevated rCBP and synchronized the EEG; but did not elevate AP; the response to NaCN was attenuated by hyperoxia and deepening of anaesthesia. 4. Electrical stimulation of NaCN-sensitive sites in the RVL in spinalized rats increased rCBF measured autoradiographically with ¹⁴C-iodoantipyrine (Kety method) in the mid-line thalamus (by 182.3 ± 17.2%; P < 0.05) and cerebral cortex (by 172.6 ± 15.6%; P < 0.05) regions, respectively, directly or indirectly innervated by RVL neurons, and in the remainder of the brain. In contrast regional cerebral glucose utilization (rCGU), measured autoradiographically with ¹⁴C-2-deoxyglucose (Sokoloff method), was increased in proportion to rCBF in the mid-line thalamus (165.6 ± 17.8%, P < 0.05) but was unchanged in the cortex. 5. Bilateral electrolytic lesions of NaCN-sensitive sites of RVL, while not altering resting rCBF or the elevation elicited by hypercarbia (arterial CO₂ pressure, P(a,CO₂) ~ 69 mmHg), reduced the vasodilatation elicited by normocapnic hypoxaemia (arterial O₂ pressure, P(a,O₂), ~ 27 mmHg) by 67% (P < 0.01) and flattened the slope of the P(a,O₂)-rCBF response curve. 6. We conclude that the elevation of rCBF produced in the cerebral cortex by hypoxaemia is in large measure neurogenic, mediated trans-synaptically over intrinsic neuronal pathways, and initiated by excitation of oxygen-sensitive neurons in the RVL.