Relative Cerebral Ischemia in SHR Due to Hypotensive Hemorrhage: Cerebral Function, Blood Flow and Extracellular Levels of Lactate and Purine Catabolites

Summary: Cerebral blood flow (CBF, by laser Doppler flowmetry) and extracellular cortical concentrations (by microdialysis) of adenosine, inosine, xanthine, hypoxan-thine, and lactate were measured together with somato-sensory evoked potentials (SEP) in chloralose-anaes-thetized spontaneously hypertensive rats (SHR) during relative cerebral ischemia induced by hypotensive hem-orrhage. Reduction of mean arterial blood pressure (MABP) to 40-50 mm Hg, which decreased SEP to about 50% of prebleeding control level, decreased CBF only to about 75% of control due to cerebrovascular "auto-regulation." A secondary, marked rise in cerebrovascular resistance (CVR) occurred after about 15 min in parallel with a striking increase in heart rate (after initial brady-cardia). This late rise in heart rate is probably elicited by relative ischemia in medullary centers. The increase in CVR might indicate increased sympathetic nerveactivity to the circle of Willis and large cerebral arteries. Cortical lactate increased initially but started to decline after about 30 min, and after 2 h it was not significantly higher than control. Cortical adenosine, inosine, hypoxanthine, and xanthine increased slowly and were significantly el-evated after 50 min of hemorrhage. After 80 min, adeno-sine and inosine had returned to initial levels, while hypo-xanthine and xanthine were further elevated. Despite the apparent partial recovery of metabolic disturbances dur-ing late hemorrhage, and with a blood flow maintained at 75% of resting control, SEP did not improve. It is sug-gested that the depression of SEP is not primarily caused by circulatory-metabolic derangements, but instead by activation of specific inhibitory systems.