Acute and delayed vasoconstriction after subarachnoid hemorrhage: Local cerebral blood flow, histopathology, and morphology in the rat basilar artery

Abstract

The decreased local cerebral blood flow (LCBF) and cerebral ischemia that occur after subarachnoid hemorrhage (SAH) may be caused by acute and/or delayed vasospasm. In 36 Sprague-Dawley (350-450g) rats SAH was induced by transclival puncture of the basilar artery. Mean arterial blood pressure (MABP), LCBF, intracranial pressure (ICP), and cerebral perfusion pressure (CPP) were measured in all rats for 30 min before and 60 min after SAH was induced. One set of control (n : 7) and experimental animals (n : 7) was sacrificed after the 60 min of initial post-hemorrhage measurements were recorded. Four days after SAH induction, LCBF and MABP were measured again for 60 min in subgroups of surviving experimental rats (n : 7) and control rats (n : 7). Histopathologic and morphologic examinations of the basilar artery were performed in each subgroup. There was a sharp drop in LCBF just after SAH was induced (55.50 ±11.46 mlLD/min/100g and 16.1 ± 3.6 mlLD/min/100 g for baseline and post-SAH, respectively; p < 0.001). The flow then gradually increased but had not returned to pre-SAH values by 60 min (p < 0.05). At 4 days after SAH induction, although LCBF was lower than that observed in the control group and pre-SAH values, it was not significantly different from either of these flow rates (p > 0.05). ICP (baseline 7.05 ± 0.4 mmHg) increased acutely to 75.2 ± 7.1 mmHg, but returned to normal levels by 60 min after SAH. CPP (baseline 84.5 ± 6.3 mmHg) dropped accordingly (to 18.6 ± 3.1 mmHg), and then increased, reaching 72.2 ± 4.9 mmHg at 60 min after SAH (p > 0.05). Examinations of the arteries revealed decreased inner luminal diameter and distortion of the elastica layer in the early stage. LCBF in nonsurviver rats (n:8) was lower than that in the animals that survived (p < 0.01). At 4 days post-hemorrhage. the rats' basilar arteries showed marked vasculopathy. The findings showed that acute SAH alters LCBF, ICR and CPP, and that decreased LCBF affects mortality rate. Subsequent vasculopathy occurs in delayed fashion, and this was observed at 4 days after the hemorrhage event.