| Objective: A new rat model of cerebral infarction with blood stasis syndrome was developed to elucidate the contribution of vascular endothelial cell during focal cerebral cerebral infarction.Methods: fifty-eight SD rats were randomly divided into model group with 28 rats in which sodium laurate was injected into the left internal carotid artery of the anesthetized rats, simulation group with 21 rats in which sodium laurate was substituted with 0.9% sodium chloride solution, and control group with 9 rats(no treament). 6, 12, 24 hours after operation, 7 rats were respectively executed for index observation in model and simulation group, as well as 6 rats in control group, such as triplienyltetrazoliurn chloride(TTC) dyeing, neurological dificit, plasma tissue-type plasminogen activator(tPA) activity, plasminogen activator inhibitor(PAI) activity, thromboxaneB2 (TXB2) content, 6-keto.-PGF1 n content, histopathological analyses. In addition, 7 rats of model group at 6 hour after operation and 3 rats of control group were used for hemorheology inspection.Results: (1)In a postural reflex test, rats were tested for degree of abnormal posture. Neurological score was the highest at 6 hour after operation, descending significantly in the later period. (2)6hours after operation, infarct brain regions were not stained, showing white determined by TTC in the lateral cortex, subcortical caudatum, internal capsule and lateral hypothalarnus, and the infarct size did not expand with experiment course. On the other hand, no-ischemic regions were stained red. (3) Infarct region wasobserved pale and soft compared with contralater hemisphere by naked eye. The results were gained under optical microscope, including cortex neuron and hippocampus swelling, cells distance extending, cells neurosis, et al. (4)The activity of tPA at 6 hour after operation was significantly lower than that in simulation and control groups(P<0.05), while PAI activity significantly higher than others'(P<0.05). 6 hour after operation plasma TXB2 content was the highest compared with other groups(P<0.05), but no distinction concerning plasma 6-Keto-PGF1 content was detected in all groups. (5) There was obvious difference between control and model groups on blood viscosity, reduction viscosity and plasmaviscosity.Conclusion: Focal cerebral infarction blood stasis syndrome in rats could be induced by some sodium laurate, showing ischemic cerebrum necrosis., function disorder of vascular endothelium-platelet, fibrinolysis and hemorheology abnormity. This model could be an important method for researching the contribution of vascular endothelial cell during cerebral infarct development, prevention and cure by tradition Chinese medicine. |
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