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机构地区:[1]衡阳医学院生理教研室,湖南421001 [2]衡阳医学院药理教研室,湖南421001
出 处:《中国药理学通报》1993年第4期287-290,共4页Chinese Pharmacological Bulletin
摘 要:用黄嘌呤—黄嘌呤氧化酶(X—XOD)诱发豚鼠心乳头肌氧自由基损伤,观察绞股蓝总皂甙(CPS)抗心肌氧化损伤的作用.结果示在X—XOD作用下,乳头肌收缩力先升高后降低,功能不应期缩短,兴奋性提高,肾上腺素诱发的自律性增加,心肌中超氧化物歧化酶活性降低,而脂质过氧化物丙二醛(MDA)含量升高.先给GPS 50mg·L^(-1),再给X—XOD,乳头肌收缩高峰推迟,并抑制其负性肌力作用,同时,逆转X—XOD所致的乳头肌不应期、兴奋性与自律性的改变.心肌组织中MDA含量均得以回复.提示,GPS对豚鼠心肌的氧化损伤具有保护作用.This paper studied the protective effect of gypenosides (GPS) on oxidative damage of myocardium of guinea pig, Using xan-thine-xanthine oxidase (X-XOD) producing free radicals. In the isolated guinea pig papillary muscles, X- XOD produced the quick positive inotropism at first and then the continuous negative one, shortened the functional refractory period (FRP) and elevated the excitability and increased the automaticity induced by adrenaline, inhibited the activity of superoxide dismutase (SOD) and increased the content of malondi- aldehyde (MDA). GPS inhibited the negative inotropism of papillary muscles produced by X-XOD,resisted the changes of FRP, automaticity and excitability induced by X- XOD. Meanwhile, GPS antagonized the effect of X-XOD which decreased activity of SOD and increased the content of MDA. These studies indicate that GPS can protect the myocardium from oxidative damage.
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