Chemical stimulation of the rostral ventrolateral medullary pressor area decreases cerebral blood flow in anesthetized rats

Abstract

In urethane-anesthetized, paralyzed and artificiallyi ventilated rats, the neurons in the rostyral ventyrolaterla me4dullar pressor area (VLPA)_ were chemically stimulated by microinjections of L-glutamate (1.7–5.0 nmole in 100 nl of 0.9% sodium chloride solution) and the cerebral blood flow (CBF) was determined using a combination of labeled microspheres ( 57Co, 113Sn and 46Sc). In one group of rats ( n = 11), unilateral chemical stimulation of the VLPA produced a significant ( P < 0.01) increase in arterial blood pressure (ABP), a significant ( P < 0.05) decrease in CBF, and a significant ( P < 0.01) increase in cerebrovascular resistance (CVR) in the cerebral cortex ipsilateral to the stimulated VLPA. The CBF was 52 ± 3 (mean ± S.E.M.) and 48 ± 4 ml·min −1 · (100 g) −1 before and during the chemical stimulation of VLPA; the CVR was 1.9 ± 0.1 and 2.6 ± 0.3 mmHg per ml·min −1 · (100 g) −1 before and during the stimulation. In order to measure CBF at normotension, moderate hypotension was induced by controlled hemorrhage in another group of rats ( n = 8). Unilateral chemical stimulation of the VLPA in these rats increased ABP but it remained within normotensive range. The CBFs of ipsilateral and contralateral cerebral cortices decreased significantly ( P < 0.05) from 57 ± 14 to 41 ± 9 and from 50 ± 12 to 39 ± 9 ml·min −1 · (100 g) −1, respectively. The CVRs of ipsilateral and contralateral cortices increased significantly ( P < 0.05) from 2.6 ± 0.06 to 3.5 ± 0.8 and from 2.7 ± 0.5 to 3.5 ± 0.8 mmHg/[ml·min −1 · (100 g) −1], respectively. In another group of rats ( n = 10), cervical sympathetic trunks were sectioned bilaterally and the CBF was measured during the chemical stimulation of the VLPA while the ABP was at normotensive levels. The CBF and the CVR did not change significantly in these rats. During the chemical stimulation of the VLPA, CBF increased in response to the changes in arterial p aCO 2 indicating that the reactivity of cerebral vasculature was intact ( n = 5). Microinjection of l-glutamate into an area adjacent to the VLPA had no effects on cerebral circulation ( n = 6). These results suggest that the neurons within the VLPA may play a role in the control of cerebral circulation via the cervical sympathetic nerves.