在自发性高血压大鼠、糖尿病和非糖尿病的Fischer 344大鼠中，烟酰胺（维生素B3）延迟治疗可减少局灶性脑缺血后的梗死体积。

Delayed treatment with nicotinamide (vitamin B3) reduces the infarct volume following focal cerebral ischemia in spontaneously hypertensive rats, diabetic and non-diabetic Fischer 344 rats.

作者信息

Sakakibara Yohtaro, Mitha Alim P, Ayoub Issam A, Ogilvy Christopher S, Maynard Kenneth I

机构信息

Neurophysiology Laboratory, Neurosurgical Service, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.

出版信息

Brain Res. 2002 Mar 22;931(1):68-73. doi: 10.1016/s0006-8993(02)02263-1.

DOI:10.1016/s0006-8993(02)02263-1

PMID:11897090

Abstract

Since hypertension and/or hyperglycemia are risk factors for stroke, we examined whether the putative neuroprotectant, nicotinamide (NAm), could protect spontaneously hypertensive rats (SHR) or diabetic Fischer 344 rats against focal cerebral ischemia using a model of permanent middle cerebral artery occlusion (MCAo). Intravenous NAm given 2 h after MCAo significantly reduced the infarct volume of SHR (750 mg/kg, 31%, P<0.01) and diabetic (500 mg/kg, 56%, P<0.01) as well as non-diabetic (500 mg/kg, 73%, P<0.01) Fischer 344 rats when compared with saline-injected controls. Thus delayed treatment with NAm protected hypertensive and hyperglycemic rats against a robust model of stroke.

摘要

由于高血压和/或高血糖是中风的危险因素，我们研究了假定的神经保护剂烟酰胺（NAm）是否能使用永久性大脑中动脉闭塞（MCAo）模型保护自发性高血压大鼠（SHR）或糖尿病Fischer 344大鼠免受局灶性脑缺血的影响。MCAo后2小时静脉注射NAm，与注射生理盐水的对照组相比，显著降低了SHR（750mg/kg，31%，P<0.01）、糖尿病Fischer 344大鼠（500mg/kg，56%，P<0.01）以及非糖尿病Fischer 344大鼠（500mg/kg，73%，P<0.01）的梗死体积。因此，NAm延迟治疗可保护高血压和高血糖大鼠免受严重中风模型的影响。