Effects Of Propofol On Common Carotid Arterial Thrombosis In Rats

Objective:To investigate the effect and its mechanisms of propofol on common carotid arterial thrombosis in rats.Methods:Fifty healthy SD rats((?)=25,(?)=25, weight 250-300g) were randomly divided into control group(C group), model group(M group), propofol low dose group(PL group), medium dose group(PM group) and high dose group(PH group). In addition to the control group, the common carotid arterial thrombosis model was induced by ferric trichloride in the other groups. The different dosages of propofol(4mg/kg/h,8mg/kg/h and 16mg/kg/h) were continuous infused lh via caudal vein in the PL, PM and PH groups, the control and model groups were continuous infused normal saline(1m/h). The weight of common carotid arterial thrombus were measured,and pathologic changes were observe by HE staining. The CD62P of blood was determined by flow cytometry, and the TXA2, PGI2, P-selectin, t-PA and PAI-1 of plasma was examined by Elisa assay. The protein levels of Caspase-8 and Caspase-3 in abdominal aorta was detected by Western blot method.Results:(1)The changes of the weight of thrombus:compared with the model group, the weight of common carotid arterial thrombus were significantly decreased in the different dose of propofol groups (P<0.05 or P<0.01). (2)HE staining results indicated that there was no obvious pathological changes in the control group, the arterial lumen was completely blocked by thrombus and vascular endothelial cells was seriously stripped in the model group, the arterial lumen was incompletely blocked and endothelial cells was sightly stripped in the different dose of propofol groups. (3)The changes of the CD62P level:compared with the control group, the CD62P average fluorescent intensity was significantly increased in the model group. Compared with the model group, the CD62P average fluorescent intensity was significantly decreased in the different dose of propofol groups(All P<0.01). (4)The detection results of the plasma:compared with the control group, the levels of TXA2 and P-selectin were significantly increased, while the levels of PGI2 were decreased(All P<0.01) in the model group. Compared with the model group, the levels of TXA2 were significantly decreased in the medium and high dose groups (P<0.01), and the levels of P-selectin were different decreased in the different dose of propofol groups(P<0.05 or P<0.01), while the levels of PGI2 were increased in the medium and high dose groups(P<0.05, P<0.01). Compared with the control group, the levels of t-PA were significantly decreased (P<0.01), and t-PA/PAI-1 ratio was decreased in the model group. Compared with the model group, the levels of t-PA were significantly increased in the different dose of propofol groups(P<0.01), and the levels of PAI-1 were significantly decreased in the medium and high dose groups (P<0.05, P<0.01), and t-PA/PAI-1 ratio was increased in low, medium and high dose groups. (5)The changes of the expression of Caspase-8 and Caspase-3 protein compared with the control group, the expression of Caspase-8 and Caspase-3 protein were significantly increased in the model group. Compared with the model group, the expression of Caspase-8 and Caspase-3 protein were significantly decreased in the different dose of propofol groups(All P<0.01).Conclusion:Propofol can inhibit formation of arterial thrombosis. The mechanism may be that propofol has the effects of protecting vascular endothelial cells, inhibiting platelet activation, activating fibrinolytic system and inhibiting apoptosis.