摘要
目的：探讨一氧化氮（ＮＯ）在脑缺血再灌注损害中的重要作用，并研究脑持续性缺血和缺血再灌注过程中ＮＯ的变化规律。方法：采用大鼠颈内动脉线栓法制成大鼠大脑中动脉梗死（ＭＣＡＯ）模型，依氧合血红蛋白（ＨｂＯ２）ＮＯ法测定持续性脑缺血和缺血再灌注脑组织内ＮＯ含量的变化。结果：脑缺血３小时受损脑组织ＮＯ水平即增高〔（２．４９±０．９０）ｎｍｏｌ／Ｌ〕，再灌注后ＮＯ逐步升高；而持续性缺血组ＮＯ则表现降低后再升高的变化，脑缺血５１小时为（８．８２±０．７０）ｎｍｏｌ／Ｌ，脑缺血１７１小时为（３．０８±０．９５）ｎｍｏｌ／Ｌ，与脑缺血前比较，Ｐ均＜０．０１。ＮＯ在缺血３小时再灌注１６８小时和缺血１７１小时时均有明显降低，但仍高于脑缺血前水平（Ｐ均＜０．０１）。结论：两种不同脑缺血过程中脑缺血组织内ＮＯ的变化有不同的规律。
Objective:To investigate the changes in nitric oxide (NO) concentrations in focal ischemic cerebral tissue of rats and its role in permanent ischemia and cerebral ischemiareperfusion injury.Methods:The animal model of middle cerebral artery occlusion (MCAO) was established by ligature embolism method.The changes in NO concentrations were measured by oxyhemoglobin (HbO2)NO during permanent ischemia and ischemiareperfusion.Results:There was an increase in NO level in the injured brain tissue after 3 hours of ischemia 〔(249±090)nmol/L〕.After reperfusion,the NO level increased progressively,but it initially decreased and then increased during the permanent ischemia.NO levels were (882±070)nmol/L and (308±095)nmol/L at 51 and 171 hours after permanent ischemia,which were significantly higher compared to the baseline values (both P<001).Although there was a decrease in NO level at 168 hours after ischemia 3 hours and reperfusion as well as 171 hours after permanent ischemia,the NO level was higher than that of preischemia level(both P<001).Conclusions:Different kinetics of NO formation in focal ischemic cerebral tissue are evident during permanent ischemia or ischemiareperfusion,which may be associated with the various isoforms of NO synthetase during the cerebral ischemia.
出处
《中国危重病急救医学》
CAS
CSCD
1998年第4期197-200,共4页
Chinese Critical Care Medicine
关键词
脑缺血
一氧化氮
脑组织
病理
cerebral ischemia\ \ nitric oxide\ \ brain tissue
