Wang Shuguang, Xu Xiaohu, Gu Li
Forensic Pathology Department of Medical School of Shantou University, Shantou, Guangdong Province, PR China.
Indian J Med Res. 2006 Feb;123(2):131-8.
BACKGROUND & OBJECTIVE: 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.
INTERPRETATION & CONCLUSION: 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.
心肌功能减退可导致脑功能紊乱。c-fos和热休克蛋白（hsp）基因的表达被视为神经细胞损伤的标志物。我们进行本研究以探讨心肌缺血再灌注（I/R）对大鼠脑组织中这些分子事件的影响以及平均动脉血压（MAP）和脑血流速度（CBFV）的变化，以了解心脏缺血再灌注后脑病理学的基础。
将42只健康大鼠随机分为7组：假手术组（A）；心肌缺血15分钟，随后分别再灌注0.5、1、2、4和6小时（B2 - B6）以及中度血容量不足组（C）。通过结扎左冠状动脉前支建立I/R大鼠模型。采用免疫组织化学和原位杂交技术研究大脑、小脑、延髓和海马中c-fos、hsp70、hsp27和hsp90基因的表达。同时测量大鼠的MAP和CBFV。
心肌缺血/再灌注后，脑组织中c-fos和HSP70的表达增加，海马和大脑皮质中信号最强，而在任何实验组中均未检测到HSP27和HSP90α的标记。c-fos mRNA和hsp70 mRNA的表达与其编码蛋白具有相似的特征。心脏缺血再灌注后，反映心脏功能的MAP和脑血流下降。
我们的研究结果表明，脑损伤发生在心肌I/R的早期阶段。心肌I/R诱导脑组织损伤的确切机制尚不清楚。需要进一步研究以阐明这些方面。
