| Objective: In the study of the ischemic model, people pay more attention to the global and local ischemic animal models, especially cerebral middle artery occlusion (MCAO) rat model. But MCAO rat model is a artificial mechanical embolic stroke, which isn't similar to the people's stroke process completely. So we make our efforts to look for a model that is similar to the people's stroke process. Intra-arterial injection of sodium laurate can produce endothelial damage. Yoshinori Toshima et al used this theory to inject appropriate sodium laurate into the left internal carotid artery, which triggered endothelial damage, platelet adhesion and aggregation to form occlusive thrombi, then produced microinfarcts. The stroke process of this model is similar to the people's stroke process. It can be used to study the anti-platelet, anti-coagulation, anti-inflammatory injury and thrombolytic therapy, which is in an important role to guide our study. Furthermore, the patients with lacunar infarcts aren't few. But the study about the lacunar infarct is limited in the clinic because of lacking animal model of lacunar infarct. Now we want to replicate this model in orderto use it in our study. On the basic of this model, we investigate the cerebrovasoprotective effects of the estradiol.Method: On the basis of Yoshinori Toshima's method, we replicated the rat model of cerebral microthrombosis: Fourty male Wistar rats were used in this study, which were divided randomly into three groups: Control group (n=10), experimental group (n=20) and treated group with estradiol (n=10). 14 rats in experimental group were anesthetized with 10% chloral hydrate (0.4ml/100g) and 100ug sodium laurate was injected into the right internal carotid artery on day 1 and 3. The rats in control group only received equivalent volumes of normal saline. Furthermore, the following modification was made: We change the polyethylene catheter to the 1 ml injector and change some operative procedure. The consequent behavior change of the rats was evaluated on day 2 and 4 with neurological deficit scoring in a posture reflex test. Consequence of ischemic brain damage was examined by histopathological analyses and the relation between the focus and neurological deficits was analysed too. The others in the experiment group were perfusion fixated 2 hours after the first injection of the sodium laurate. The brain tissues or middle cerebral arteries of them were analysed with transmission election microscopy. In order to evaluate the cerebrovasoprotective effects of the estradiol , 6 rats in treated group were treated with 17β-estradiol(100ug/kg.d) for 3 days after the first injection of sodium laurate. Then thedamage of the perforating arteries was examined by histopathological analyses. The brain tissues of another 4 rats in treated group were taken out to undergo transmission electron microscopic analyses 2 hours after the first injection of the sodium laurate.Result: Two hours after the injection of sodium laurate, what we can see under the transmission electron microscope as following: Endothelial cells damage, cell membrane braking down, asynechia and hydrops of the matrixes could be found. Some perforating arteries appear crush deformation. The neutrophil attached to the vascular wall in some perforating arteries. In some areas, we could see the fropsical gliocyte. The chromatin in the nucleus agglutinated to the border. Moreover we can see the necrotic neuron: The cellular form blured; The chromatin in the nudeus agglutinated and nucleoli disappeared. The swelling mitochondria became empty; some mitochondrial crista became blured. No damage of the MCA could be found if the dose of the sodium laurate is 100ug per time. If the dose was increased, the damage of the MCA could appear. According to the posture reflex test, twenty-four hours after the first and second injection of sodium laurate, 6 and 12 of 14 rats showed mild to severe neurological deficits respectively. Multiple small cerebral infarcts were observed in the hippocampu... |
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