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目的研究苦碟子注射液治疗急性脑缺血后心肌组织内皮素(ET)、一氧化氮(NO)及一氧化氮合酶(NOS)的变化及“脑心同治”的生物学基础。方法电凝致大脑中动脉闭塞方法建立急性脑缺血诱发心肌损伤大鼠模型,随机分为假手术组、缺血6 h模型组、苦碟子注射液组各13只。记录心电图分析心率变异性,放射免疫法检测血清肾上腺素(E)、去甲肾上腺素(NE)和血浆ET含量,生化法检测NO含量和NOS活力,HE和HBFP染色法分别观察脑组织、心肌组织病理形态学变化。结果与假手术组比较,缺血6 h模型组中频段(MF)、高频段(HF)功率明显降低;血清NE、E含量和血浆ET含量升高;心肌组织i NOS活性升高,e NOS活性降低;出现神经细胞肿胀、结构不清,部分胞核缩小并深染等脑组织缺血改变,心肌纤维出现广泛、弥漫的亲复红染色。与缺血6 h模型组比较,苦碟子注射液组MF、HF功率升高;NE含量降低,E含量无明显变化;血浆ET含量降低;心肌组织i NOS活性降低;脑、心肌组织缺血改变明显改善。结论苦碟子注射液可有效减轻急性脑缺血引发的心肌损伤,其保护作用可能与降低交感神经紧张性、调节血管活性物质失衡等有关。
Objective To study the changes of endothelin (ET), nitric oxide (NO) and nitric oxide synthase (NOS) and the biological basis of “Tongxin Tongzhi” in the treatment of acute cerebral ischemia with Kudiezi injection. Methods A rat model of myocardial injury induced by acute cerebral ischemia was established by middle cerebral artery occlusion (CLP). Rats were randomly divided into sham operation group, ischemia 6 h model group and Kudiezi injection group. The heart rate variability was recorded by electrocardiogram (ECG) analysis. The levels of serum epinephrine (E), norepinephrine (NE) and plasma ET were measured by radioimmunoassay. The content of NO and NOS activity were detected by biochemical method. Histopathological changes. Results Compared with the sham-operation group, the MF and HF power of the model group at 6 h after ischemia decreased significantly, while the levels of NE, E and ET in the model group increased. The activity of i NOS in myocardium increased and eNOS Activity decreased; there is swelling of nerve cells, the structure is unclear, part of the nucleus shrinks and deep brain ischemia and other changes in myocardial fibrosis, widespread, diffuse pro-Fu red staining. Compared with 6 h ischemia group, Kupffer injection group MF and HF power increased; NE content decreased, E content had no significant change; plasma ET content decreased; myocardial tissue i NOS activity decreased; brain, myocardial ischemia Significant improvement. Conclusion Kudiezi injection can effectively reduce myocardial injury induced by acute cerebral ischemia, and its protective effect may be related to reducing sympathetic tone and regulating the imbalance of vasoactive substances.