| Cerebral infarction is one of important diseases of human death and disability. Cigarette smoking is one of important risk factors that can be interfered in atherosclerosis and cerebral thrombosis. Cigarette smoking may significantly increase stroke risk. However, the underlying mechanisms are unclear.Recently, it is reported that cell adhesion molecules play an important role in process of atherosclerosis. It is an early event that monocytes adhere to vascular endothelial cells, then migrating into endothelium and taking in lipid, further to transform to foam cells. Intercellular adhesion molecule-1 plays an important role in mediating adhesion of monocyte-endothelial cell, which Bclongs to immu-noglobulin super family (IGSF). Dysfunction of vascular endothelial cells plays an important role in occurrence and development of cerebrovascular diseases. Cigarette smoking can insult in damage or dysfunction of endothelial cells. Nowadays it is generally Bclieved that endothelial cell dysfunction is the early event of atherogenesis.Two-layer antibody sandwich enzyme-linked immunosorbent assay ( ELISA) was used to determine serum level of sICAM-1 in TIA patients, and cerebral hemodynamic changes were assessed by transcranial Doppler( TCD) , to investigate pathogenesis of cerebral atherosclerosis and cerebral thrombosis.Subjects and methodsSubjects were assigned into four groups: (l)TIA smokers. (2)TIA nonsmok-ers; TIA patients who frequently had attacks within two weeks were selected. Diagnostic criterion was accorded with the fourth national cerebrovascular disea-ses meeting revised criterion. (3)healthy smokers. (4)healthy nonsmokers. According to smoking criterion regulated by world health organization ( WHO): smoke a cigarette per day, and continuously for one year. None of the subjects had a history of recent infectious diseases or had clinical evidence of any cardiovascular events or kidney or liver diseases or had hypertension or diabetes melli-tus and so on.Venous blood was drawn in the morning after an overnight fast. Blood sample was then centrifuged and serum was retained. Determination of serum sl-CAM-1 concentrations was performed in duplicate with an ELISA. Cerebral blood velocity was measured in bilateral large arteries with TCD before and after smoking a cigarette. Statistical analyses were performed with SPPS11. 0 software, and Student' s t test paired -samples t test one-way analysis of variance (ANOVA) and linear correlation analysis were employed.ResultsThe level of serum sICAM-1 in cases of smokers with HA was higher than that of non-smokers with TIA (P < 0. 05 ) and was much higher than that of healthy non-smokers (P <0. 01) ; The level in healthy smokers was higher than that of healthy non-smokers (P < 0- 05) ; The level of serum sICAM-1 in cases of smokers with TIA was higher than that of healthy smokers ( P < 0. 05 ) , the level in cases of non-smokers with TIA was higher than that of healthy non-smokers (P<0.05).The level in severe smokers was higher than that of mild smokers andhealthy non-smokers (respectively, P <0. 01) ; The level in moderate smokerswas higher than that of mild smokers and healthy non-smokers ( respectively, P< 0.05 ) ; The level of serum sICAM-1 was well correlated with smoking index ( r= 0.428, P<0.01).The blood flow velocity in bilateral MCA was increased compared with that of before smoking a cigarette (respectively, P <0.05).DiscussionICAM-1 is widely distributed in vivo, but the expression is the strongest on vascular endothelial cells. In normal conditions, the expression is little on VEC. But in pathologic conditions, the expression is significantly enhanced. It is an early event of increased expression of ICAM-1 on EC in cerebral thrombosis.Some adhesion molecules had be detected in human atherosclerotic plaques. Rohde LE et al reported, elevated serum sICAM-1 level was well correlated with increased carotid IMT, an index of early atherosclerosis. Fassbend-er K et al observed significantly increased serum con...
|
PDF Full Text Request