Carbon monoxide regulates cerebral blood flow in epileptic seizures but not in hypercapnia

被引：35

作者：

Montécot, C ^{[1
]}

Seylaz, J ^{[1
]}

Pinard, E ^{[1
]}

机构：

[1] Univ Paris 07, CNRS, UPR 646,IFR 6, Lab Rech Cerebrovasc, F-75010 Paris, France

来源：

NEUROREPORT | 1998年 / 9卷 / 10期

关键词：

cerebral blood flow; carbon monoxide; epilepsy; hypercapnia; kainate;

D O I：

10.1097/00001756-199807130-00035

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

CARBON monoxide (CO) is an endogenously produced gas sharing many properties with nitric oxide (NO), notably activating soluble guanylate cyclase and relaxing blood vessels. The brain can generate high quantities of CO from a constitutive enzyme, haem oxygenase (HO-2). To determine whether CO is involved in the regulatory mechanisms of cerebral blood flow (CBF), two conditions associated with a reproducible CBF increase were studied in rats: epileptic seizures induced by kainate, and hypercapnia. The HO inhibitor tin protoporphyrin (Sn-PP) did not modify the basal level of CBF, significantly reduced the increase in CBF during status epilepticus, and did not affect the cerebrovascular response to hypercapnia. It is concluded that CO participates in the regulation of CBF in specific conditions, notably those associated with glutamate release. NeuroReport 9: 2341-2346 (C) 1998 Rapid Science Ltd.

引用

页码：2341 / 2346

页数：6

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