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背景:目前脑血管病尤其是缺血性脑血管病的治疗仍较棘手,溶栓可尽早地恢复脑血流,改善半暗带区的血液供应,缩小梗死面积,挽救未死的脑组织及其功能,但血管再通不可避免地造成损伤。超短波对机体有热效应及非热效应,有关非热效应的机制,目前尚不十分清楚。目的:通过制备脑缺血动物模型,来观察超高频电场-超短波对大鼠局灶性脑缺血再灌注损伤的保护作用并探讨其作用机制。设计:完全随机设计,对照实验研究。单位:中国医科大学附属第一医院理疗科实验室。材料:选用本校动物部提供的健康wister大鼠94只,雌雄不拘,体质量(250～350)g(清洁级,合格证号为[2000]015号),鼠龄18～20周。方法:用线栓法制备一侧大脑中动脉栓塞-再灌注大鼠模型,造成大鼠右脑缺血2h再灌注24h,采用5级评分法[1]评定神经功能缺损来筛选病例。脑含水量用干湿重法,梗死灶体积用TTC染色法测定,并分析缺血侧脑组织的超氧化物歧化酶(superoxidedismutase,SOD)和丙二醛含量及形态学变化。主要观察指标:测定神经行为学评分,脑梗死体积,脑含水量,SOD,丙二醛。结果:再灌注6h时给予超短波治疗能减轻大鼠缺血侧脑含水量,提高抗氧化酶SOD含量,降低自由基产物丙二醛的含量,病理损伤减轻,而对大鼠梗死灶体积影响不明显。结论:超短波对大鼠局灶性脑缺血再
Background: At present, the treatment of cerebrovascular diseases, especially ischemic cerebrovascular diseases, is still rather difficult. Thrombolysis can resume cerebral blood flow early, improve blood supply in the penumbra, reduce the infarct size, save the undeveloped brain tissue and Its function, but revascularization inevitably causes damage. Ultrashort wave on the body with thermal effects and non-thermal effects, the mechanism of non-thermal effects, is not yet very clear. OBJECTIVE: To observe the protective effect of ultra-high frequency electric field-ultrashort wave on focal cerebral ischemia-reperfusion injury in rats and to explore its mechanism by preparing animal models of cerebral ischemia. Design: Completely randomized design, controlled experimental study. Unit: First Affiliated Hospital of China Medical University Physiotherapy Laboratory. MATERIALS: A total of 94 healthy wister rats were selected from our department of animal husbandry. They were male and female with a weight of 250-350 g (clean grade, certificate no. [2000] 015), and were aged 18-20 weeks. Methods: One side of middle cerebral artery occlusion - reperfusion rat model was prepared by thread occlusion. Rats were subjected to right cerebral ischemia for 2 hours and reperfusion for 24 hours. The neurological deficits were screened by 5 grade scoring method [1]. The brain water content was determined by TTC staining with dry-wet method and infarct volume. The contents of superoxide dismutase (SOD) and malondialdehyde (MDA) and morphological changes in ischemic brain tissue were analyzed. MAIN OUTCOME MEASURES: Neurobehavioral score, cerebral infarction volume, brain water content, SOD, malondialdehyde were measured. Results: The treatment of ultrashort wave at 6h after reperfusion could reduce the content of water in the ischemic brain, increase the content of antioxidant enzyme SOD, decrease the content of malondialdehyde in free radical product, and alleviate the pathological damage, but have no effect on the infarct volume in rats obvious. Conclusion: FHF can cause focal cerebral ischemia in rats