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观察实验性心肌梗塞后充血性心衰大鼠服用卡托普利前后的血流动力学变化。结果表明,与梗塞前无心衰时相比,大鼠收缩压及舒张压降低,LVEDP、±dp/dt_、尿量、体重及心肺重量无明显变化,同时尿6-酮-前列腺素F_(1a)明显降低。提示卡托普利能降低心肌梗塞后心衰大鼠的心肌耗氧量、保护其心功能,其机制可能与促进PGI_2合成有关。对合用吲哚美辛的大鼠,上述疗效明显减弱或消失,可能与其抑制PGI_2合成从而抵消了卡托普利的有益作用有关。
To observe the hemodynamic changes before and after captopril in rats with congestive heart failure after experimental myocardial infarction. The results showed that systolic blood pressure and diastolic blood pressure decreased, LVEDP, ± dp / dt_, urine volume, body weight and cardiopulmonary weight had no significant changes compared with those without heart failure before infarction. Urinary 6-keto-prostaglandin F_ 1a) significantly reduced. These results suggest that captopril can decrease myocardial oxygen consumption and protect cardiac function after heart failure in myocardial infarction rats. The mechanism may be related to the promotion of PGI_2 synthesis. For indomethacin-treated rats, the above effects were significantly weakened or disappeared, which may be related to its inhibition of PGI-2 synthesis and counteracting the beneficial effects of captopril.