| IntroductionCerebral infarction is one of the important diseases that can lead human to be disabled or even dead. The nerve cells couldn't regenerate if they were impaired ,so cerebral infarction would have a serious effect on brain that could hurt body and mind badly once it occurred . Now we still have no especially effec-tivetherapy for cerebral infarction. Studying the risk factor and pathogenesis of cerebral infarction can prevent its occurrence , and find a new method for the preventions and cures of this disease.Among lots of risk factors, smoking is associated with cerebral infarction closely. Framingham's study illustrates that smoking is an independent risk factor of ischemic stroke. The relative risk of stroke in heavy smokers is 2 - 4 times than no smokers. But the definite mechanisms of cerebral infarction resulted from cigarette smoking are still not clear. There are several hypotheses lying in their relation of causality, one of which is termed by endothelial impairment. If cerebrovascular endothelium is impaired, the expression of vascular cell adhesion molecule -1 ( VCAM - 1) will be increased. VCAM - 1 play an important role in thrombosis. VCAM - 1 mainly present in vascular endothelial cell , it can hardly express on the normal vascular endothelium, and its expression will increase significantly after the stimulation of cytokines. In 6 hours after cerebral ischemia VCAM -1 will appear, and in 12 hours the expression of it will reach to a peak . VCAM - 1 binds to lymphocyte function - associated antigen - 1 (LFA - 1) lying in the surface of leukocyte , which result in interaction between leukocyte and endothelial cell, and recruit the leukocyte in circulation, atthe same time the leukocyte can release some inflammatory factors and cyto-kines, which facilitate the expression of VCAM - 1 to progress , and then there will be more and more leukocytes adhere to the wall of vessels, all of these constitute to the base of thrombosis. Blann et al have found that cigarettes smoking can result in the expression of soluble VCAM -1 in circulation increased in patients with atheromatosis .At present , it has not been reported that cigarette smoking can induce the expression of VCAM - 1 in cerebrovascular endothelium . This study used rat smoking models and immunohischemical methods to observe the smoking - induced expression of VCAM - 1 in middle cerebral arteries and their branches in rats , analysed the dose - effect relationship between the expressions of VCAM - 1 and the quantity of cigarettes smoking . On the other hand we used fish line to block the middle cerebral arteries of rats in order to make models of cerebral infarction , by these models we could compare the sizes of cerebral infarction in smoking rats with those in no — smoking rats . By this way we can find the molecular mechanisms of cerebral infarction caused by smoking , which can help us to provide the theoretic foundation to smoking - induced brain damage and its therapy .Materials and methodsLaboratory animals were distributed randomly into large - dose smoking group , small - dose smoking group and control group . And then we made rat smoking models and rat cerebral infarction models , used TTC staining to measure the sizes of rat cerebral infarction , and use immunohistochemical methods to detect the expression of VCAM -1 in cerebrovascular endothelial cells in smoking rats . Then we used microgram analysis instrument to collect and analyze the average gray value of cellular plasma staining , used SPSS11. 5 software to process data with analysis of variance and S - N - K .
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