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作 者:珠勒皮亚.司马义 娜几娜.吾格提 布海力且木.买买提
机构地区:[1]新疆医科大学第一附属医院高血压科,乌鲁木齐市830054 [2]新疆医科大学第一附属医院心律失常科,乌鲁木齐市830054 [3]新疆库尔勒市第一人民医院心内科,库尔勒市841000
出 处:《中国动脉硬化杂志》2013年第5期404-408,共5页Chinese Journal of Arteriosclerosis
基 金:国家自然科学基金项目(30960105)
摘 要:目的应用超声心动图、免疫组织化学技术和电生理技术记录心肌梗死大鼠梗死周边区的有效不应期(ERP)及缝隙连接蛋白43(Cx43)改变,交感神经神经(TH)及神经生长因子(GAP43)改变,探讨心肌梗死大鼠心室重构、电重构及交感神经重构之间的关系。方法将成年SD大鼠30只,随机分为假手术组和心肌梗死组。假手术组仅开胸,不结扎冠状动脉。结果与假手术组相比,心肌梗死组LVIDd、LVIDs均显著增大(P<0.01),EF和FS缩短率显著降低(P<0.01)。与假手术组相比,心肌梗死组梗死周边区ERP显著缩短,差异有统计学意义(P<0.01)。心肌梗死组Cx43阳性蛋白表达低于假手术组,差异有统计学意义(P<0.01)。与假手术组相比,心肌梗死组GAP43阳性神经密度明显增加,差异有统计学意义(P<0.01)。心肌梗死组TH阳性神经密度不均一明显增加,差异有统计学意义(P<0.01)。结论大鼠心肌梗死后心室不但发生结构重构,同时也会发生神经重构和电重构,以及三者之间相互影响和共同作用导致恶性心律失常和猝死的发生。Aim To study on changes of infarcted border zone of effective refractory period (ERP), and ex- pression of connexin43 (Cx43), Tyrosine hydroxylase (TH) and nerve growth factor (GAPg3) in MI SD rat by echocardiograph,electrophysiological techniques and immunohistochemical technique. To explore relation of left ventricular remodeling, electrical remodeling and sympathetic nerve remodeling of myocardial infarction rat. Methods 30 SD rats of either sex weighting 220 - 250 g were euthanized under chlorine hydrate 0.3 mL/100 mg anesthesia and were randomly divid- ed into two groups : sham operation group (n = 15), MI group (n =15). Results Compared with the sham operation group, LVIDd,LVIDs were significantly increased and-EF, FS were shortened in MI group (P〈0.01). Compared with the sham operation group, ERP of infarcted border zone was significantly shortened in MI group(P〈0.01). Left ventricular CX43 could be seen under the fluorescence microscope in two groups of rats. the fluorescence became weak in MI group. Immunohistochemistry of left ventricular 43 and TH could be seen under the light microscope in two groups of rats. Compared with the sham operation group, GAP43 and TH had significantly higher expression in MI group (P〈0.01), respectively. Conclusions Ventricular remodeling, sympathetic remodeling and electrical remodeling occured in left ventricle after myocardial infarction in SD rat. The mutual influence and interaction lead to malignant arrhythmias and sudden death.
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