ABSTRACT
BACKGROUND: Under normal conditions, cerebral blood flow is regulated as cerebral perfusion pressure changes (autoregulation). Inflammatory conditions like bacterial meiningitis result in a loss of cerebral autoregulation several hours after exposure to bacterial endotoxin. Endotoxin appears to produce effects via the production of reactive oxygen species, such as the superoxide anion. METHODS: Cerebral blood flow (CBF) was measured by hydrogen clearance in anesthetized rats 30 minutes after intravenous endotoxin 5 mg/kg or normal saline (control). Mean arterial pressure was reduced from 100 mmHg to 80 mmHg and 60 mmHg by hemorragic hypotension, and cerebral blood flow was measured at each pressure. RESULTS: In the control group, CBF did not change when arterial pressure was reduced to 80 mmHg (113.9 ml vs 111.9 ml), but declined significantly at 60 mmHg (113.9 ml vs 88.4 ml). In the group treated with endotoxin, both a reduction of mean arterial pressure to 80 mmHg (129.8 ml vs 101.8 ml) and 60 mmHg (129.8 ml vs 78.4 ml) caused a significant reduction in CBF, indicating that autoregualtion had been abolished. CONCLUSIONS: The results of this study indicate that within minutes of endotoxin exposure, CBF markedly increased, and that the autoregualtion of CBF was inhibited.