CORTICAL BLOOD-FLOW AND CEREBRAL PERFUSION-PRESSURE IN A NEW NONCRANIOTOMY MODEL OF SUBARACHNOID HEMORRHAGE IN THE RAT

Background and Purpose Acute cerebral ischemia after subarachnoid hemorrhage (SAH) is a major cause of morbidity whose precise etiology is unclear. The purpose of this study was to examine the relationships between cerebral perfusion pressure (CPP) and cortical blood flow during SAH using a new experimental model in the rat. Methods CPP (mean arterial pressure minus intracranial pressure), cortical laser-Doppler flowmetry (LDF), and electroencephalogram were continuously recorded during and after SAH in 16 ventilated rats. SAH was produced by advancing an intraluminal suture from the external carotid artery through the internal carotid artery to perforate the vessel near its intracranial bifurcation. Results Eight rats (50%) died within 24 hours of SAH. In all rats, blood was widely distributed throughout the basal, convexity, and interhemispheric subarachnoid spaces and throughout the ventricular system. CPP decreased after SAH at an initial rate of 1.1+/-0.2 mm Hg/s, reaching its nadir 59+/-9 seconds after the onset of SAH. During the same period, LDF fell at a rate of 1.4+/-0.3%/s (P=NS vs CPP). After reaching its nadir, CPP rose at a rate of 0.4+/-0.01 mm Hg/s, but LDF continued to fall at 0.2+/-0.03%/s (P<.05 vs CPP) reaching a nadir of 21.7+/-2.5% significantly later than CPP (189.5+/-39 s after SAH, P<.05). No correlation was found between peak changes in CPP and LDF. Electroencephalogram activity followed the changes in LDF, reaching nadir values 289+/-55 seconds after SAH. Conclusions These findings demonstrate that although reduced CPP causes the initial decrease in cortical blood flow after SAH, secondary reductions occurring after CPP has reached its nadir are caused by other factors such as acute vasoconstriction. This noncraniotomy model of SAH in the rat has several advantages over existing models.