脑血流
热休克蛋白
海马体
热休克蛋白70
缺血
内科学
医学
休克(循环)
再灌注损伤
麻醉
血流
心脏病学
病理
内分泌学
生物
基因
生物化学
作者
Shuguang Wang,Xiaoling Xu,Li Gu
出处
期刊:PubMed
日期:2006-02-01
卷期号:123 (2): 131-8
被引量:3
摘要
Myocardial hypofunction could lead to the derangement of brain functions. The expression of c-fos and heat shock protein (hsp) genes was recognized as markers of neural cell injury. We under took this study to investigate the influence of myocardial ischaemia and reperfusion (I/R) on these molecular events in the rat brain tissue and changes in mean arterial blood pressure (MAP) and the cerebral blood flow velocity (CBFV), to understand the basis of cerebral pathology following cardiac ischaemia and reperfusion.Healthy rats (n=42) were randomly allocated into seven groups: sham-operated (A); myocardial ischaemia for 15 min, followed by 0.5, 1, 2, 4 and 6 h of reperfusion respectively (B2-B6) and hypovolemia at medium level (C). I/R rat models were established by ligating the anterior branch of the left coronary artery. Expressions of the c-fos, hsp70, hsp27 and hsp90 genes in the cerebrum, cerebellum, medullaoblongata and hippocampus, were studied with immunohistochemistry and in situ hybridization. The MAP and CBFV of the rats were also measured.The expressions of c-fos and HSP70 in brain tissue increased after myocardial ischaemia/ reperfusion, with the strongest signal appearing in the hippocampus and cerebral cortex, while labeling for HSP27 and HSP90 alpha were not detectable in any of the experimental groups. The expressions of c-fos mRNA and hsp70 mRNA shared the similar characteristics with their encoding proteins. MAP, reflection of cardiac function and cerebral blood flow decreased following cardiac ischaemia and reperfusion.Our findings suggested that the brain damages occurred from the early phase of myocardial I/R. The exact mechanism of cerebral tissue injuries induced by myocardial I/R is not known. Further studies need to be done to throw light on these aspects.
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