Chemical stimulation of the ventrolateral medullary depressor area decreases ipsilateral cerebral blood flow in anesthetized rats

Abstract

In anesthetized (chloralose and urethane), paralyzed and artificially ventilated rats, the neurons in the ventrolateral medullary depressor area (VLDA) were chemically stimulated by microinjections of l-glutamate (2.5–5 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). Unilateral chemical stimulation of the VLDA (n = 11) produced a significant (P < 0.05) decrease in CBF of the cerebral cortex ipsilateral to the stimulated VLDA; the CBF was41 ± 5 (mean±S.E.M.)and29 ± 4ml·min −1 · (100g) −1 before and during the chemical stimulation of VLDA. The decrease in CBF was not due to the decrease in arterial blood pressure (ABP) caused by the chemical stimulation of the VLDA because the CBF during the chemical stimulation of the VLDA was significantly smaller (P<0.01) than the CBF during controlled hemorrhagic hypotension (n=10). In another group of rats (n=6), moderate hypertension was induced by blood transfusion. Unilateral chemical stimulation of the VLDA in these rats decreased ABP but it remained within normotensive range. A significant (P<0.05) decrease in CBF (from46 ± 12to29 ± 7ml·min −1 · (100g) −1) and a significant (P<0.01) increase in cerebrovascular resistance (from2.7 ± 0.4to4.3 ± 0.6mmHg per[ml·min −1·(100g) −1]) was observed in the ipsilateral cerebral cortex of these rats. Chemical stimulation of the VLDA did not affect the reactivity of the cerebral vessels to hypercapnea (n=5). Microinjection of 0.9% sodium chloride solution (100 nl) into the VLDA had no effects on cerebral circulation (n = 6). These results suggest that the neurons within the VLDA may play a role in the control of cerebral circulation.