ACUTE VASOCONSTRICTION AFTER SUBARACHNOID HEMORRHAGE

OBJECTIVE: Decreased cerebral blood flow (CBF) and cerebral ischemia o ccurring immediately after subarachnoid hemorrhage (SAH) may be caused tay acute microvascular constriction, However, CEF: can also be influ enced by changes in intracranial pressure (ICP) and cerebral perfusion pressure (CPP). The goal of these experiments was to assess the signi ficance of acute vasoconstriction after SAH and its relationship to ch anges in CBF, ICP, CPP, and extracellular glutamate concentrations. ME THODS: Three experiments were performed using the endovascular filamen t technique to produce SAH. In the first experiment, CBF, ICP, and CPP were measured for 60 minutes after SAH (n = 21) and were correlated w ith the 24-hour mortality rate. in the second experiment, rats undergo ing SAH (n = 23) or a sham procedure (n = 7) were perfused 60 minutes after SAH for measurement of the circumference and wall thickness of t he internal carotid and anterior cerebral arteries and correlation wit h CBF, ICP, and CPP. In the third experiment (n = 11), extracellular g lutamate concentrations determined by hippocampal and cortical microdi alysis and high performance liquid chromatography were correlated with physiological changes. RESULTS: CBF reductions to less than 40% of ba seline for 60 minutes after SAH predicted 24-hour mortality with 100% accuracy and were used to define ''lethal'' SAH. In contrast, ICP and CPP 60 minutes after SAH were not correlated with the mortality rate, The vascular circumference was significantly smaller in lethal than in sublethal SAH or sham-operated rats (P < 0.001). Vessel measurements were correlated with both CBF and hemorrhage size (P < 0.01). Extracel lular glutamate concentration increased to 600% of baseline after leth al SAH in both hippocampus and cortex and was inversely correlated wit h CBF (r = 0.9, P < 0.001) but did not increase after sublethal SAH. C ONCLUSION: Acute vasoconstriction after SAH occurs independently of ch anges in ICP and CPP and is associated with decreased CBF, larger hemo rrhage size, persistent elevations of extracellular glutamate, and poo r outcome. Acute vasoconstriction seems to contribute directly to isch emic brain injury after SAH. Further evaluations of pharmacological ag ents with the potential to reverse acute vasoconstriction may increase CBF and improve outcome.