OBJECTIVE: The aim of this study was to correlate changes in regional cerebral blood flow (rCBF) to the degree of cerebral vasospasm in the canine two-hemorrhage model of subarachnoid hemorrhage (SAH). METHODS: SAH was induced in 13 adult beagle dogs using the two-hemorrhage model. Eleven beagle dogs served as controls. Angiography of the basilar artery and measurements of rCBF with colored microspheres were performed on days 1 and 8. Diameter of the basilar artery was calculated at equidistant points from the angiogram. RESULTS: In controls, basilar artery diameter (mm) and rCBF (mL/min/g) were equal on days 1 and 8. In the SAH group, basilar artery diameter decreased significantly (1.27 +/- 0.17 [mean +/- SD]-0.84 +/- 0.15 mm). rCBF decreased significantly (P < .05) in the cerebrum (1.69 +/- 0.54 [mean +/- SD]-1.06 +/- 0.45 mL/min/g), cerebellum (1.18 +/- 0.40-0.80 +/- 0.32 mL/min/g), and brain stem (0.81 +/- 0.33-0.51 +/- 0.21 mL/min/g). However, decrements in CBF were not correlated to the reduction in vessel caliber in the corresponding vascular territory. CONCLUSION: Induced SAH in the canine model produces a significant impairment in rCBF irrespective of the degree of vasospasm of large cerebral vessels. The findings support the presumptive role of the microvasculature in regard to delayed cerebral ischemia after SAH.
OBJECTIVE: The aim of this study was to correlate changes in regional cerebral blood flow (rCBF) to the degree of cerebral vasospasm in the canine two-hemorrhage model of subarachnoid hemorrhage (SAH). METHODS:SAH was induced in 13 adult beagle dogs using the two-hemorrhage model. Eleven beagle dogs served as controls. Angiography of the basilar artery and measurements of rCBF with colored microspheres were performed on days 1 and 8. Diameter of the basilar artery was calculated at equidistant points from the angiogram. RESULTS: In controls, basilar artery diameter (mm) and rCBF (mL/min/g) were equal on days 1 and 8. In the SAH group, basilar artery diameter decreased significantly (1.27 +/- 0.17 [mean +/- SD]-0.84 +/- 0.15 mm). rCBF decreased significantly (P < .05) in the cerebrum (1.69 +/- 0.54 [mean +/- SD]-1.06 +/- 0.45 mL/min/g), cerebellum (1.18 +/- 0.40-0.80 +/- 0.32 mL/min/g), and brain stem (0.81 +/- 0.33-0.51 +/- 0.21 mL/min/g). However, decrements in CBF were not correlated to the reduction in vessel caliber in the corresponding vascular territory. CONCLUSION: Induced SAH in the canine model produces a significant impairment in rCBF irrespective of the degree of vasospasm of large cerebral vessels. The findings support the presumptive role of the microvasculature in regard to delayed cerebral ischemia after SAH.