Cerebral autoregulation in the hyperacute phase after experimental subarachnoid hemorrhage using an endovascular perforation model

Abstract Impaired cerebral blood flow contributes to delayed neurological deficits after subarachnoid hemorrhage, but cerebral autoregulation which regulates cerebral blood flow to the brain in the hyperacute phase is poorly defined. We characterized early pressure- and flow-based reactivity in a rat subarachnoid hemorrhage perforation model. This is a retrospective analysis of older data acquired to investigate a different hypothesis. Male Sprague–Dawley rats underwent endovascular perforation subarachnoid hemorrhage. Arterial blood pressure, intracranial pressure, and bilateral laser Doppler flow were continuously recorded. Pressure reactivity (PRx*) and flow reactivity (LDx*) were calculated as 5-min moving Pearson correlations between arterial and intracranial pressure and arterial pressure and laser Doppler flowmetry, respectively. Exposure above impairment thresholds (PRx*>0.3; LDx*>0.5) was compared pre-subarachnoid hemorrahge (−30–0 min) versus post-subarachnoid hemorrhage (15–60 min) and related to hemorrhage severity. Group-mean PRx* and LDx* remained below impairment thresholds. Nevertheless, time with PRx*>0.3 increased after subarachnoid hemorrhage (median 0.0% vs 1.9%, p<0.001) and correlated with intracranial pressure elevation (r=0.527, p<0.001). LDx* showed no significant pre–post change in either hemisphere. PRx* and LDx* correlated weakly (r=0.089, p<0.001) with frequent discordance. Cerebral autoregulation is largely preserved within 60 min after subarachnoid hemorrhage, with transient pressure-reactivity impairment in a subset linked to intracranial pressure peaks. Pressure- and flow-based indices provide non-interchangeable information.