Abstract
Thirty anesthetized cats were randomly assigned to one of three groups of 10 cats each: nimodipine treatment, nimodipine treatment combined with induced hypertension, or a control group. The behavior of the cerebral pial arteries was measured by means of microscopic observation through a cranial window. The middle cerebral artery of each cat was clipped for 1 hour via the transorbital approach. Five hours after circulation was reestablished in the middle cerebral artery. Evans blue dye was injected intravenously: 30 minutes later, the animal was killed. Administration of nimodipine or saline in the treated or control group was started 5 minutes before the middle cerebral artery was clipped and maintained until the end of the experiment. Induced hypertension was produced by administration of dopamine during the occlusion. Damage to the blood-brain barrier (BBB) was judged by extravasation of Evans blue dye. Cerebral edema and infarction were evaluated from histological findings. They were most prominent in the control group; the extent of the hemisphere affected was as follows (mean ± standard error): extravasation. 40.5 ± 8.8%: edema, 43.2 ± 5.7%: infarction, 35.5 ± 9.6%. On the other hand, the extravasation of Evans blue dye and cerebral edema were significantly more extensive in the group treated with nimodipine and induced hypertension (extravasation, 28.2 ± 9.6% of the hemisphere; edema, 30.3 ± 7.1%) than in the group treated with nimodipine alone (extravasation. 18.5 ± 8.7% of the hemisphere; edema, 19.4 ± 6.3%). but the infarction size was similar in both groups (16.6 ± 4.9% of the hemisphere in the former; 17.0 ± 6.2 in the latter). Based on these results, we arc cautious in combining calcium entry blocking agents such as nimodipine with induced hypertension in patients with acute cerebral ischemia.
Correction to: Activation of TGR5 protects blood brain barrier via the BRCA1/Sirt1 pathway after middle cerebral artery occlusion in rats
