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研究多巴胺（ＤＡ）与卡托普利（Ｃａｐ）合用对外源性羟自由基（·ＯＨ）灌注所致家兔心肌损伤的治疗效果．结果表明，ｉｖ·ＯＨ生成液后立即静滴ＤＡ１０μｇ·ｋｇ－１·ｍｉｎ－１，３０ｍｉｎ，输注期间心肌收缩能力明显升高，但停药后逐渐恶化．血清脂质过氧化产物丙二醛（ＭＤＡ）含量明显升高，心肌超微结构损伤．Ｃａｐ（给·ＯＨ前２ｍｉｎｉｖ２．５ｍｇ·ｋｇ－１）及Ｃａｐ＋ＤＡ组则保持心功能指标和ＭＤＡ在正常范围，但单独Ｃａｐ组心肌收缩功能指标在开始１５ｍｉｎ有下降趋势．两组心肌细胞超微结构大致正常．结果提示，Ｃａｐ＋ＤＡ联合用药对·ＯＨ所致心功能降低的保护作用优于单独Ｃａｐ治疗，同时克服了单用ＤＡ加重心肌损伤的不足．
To study the therapeutic effect of dopamine (DA) and captopril on rabbit myocardial injury induced by exogenous hydroxyl radical (· OH) perfusion. The results showed that iv. OH immediately after intravenous infusion of DA10μg · kg-1 · min-1, 30min, myocardial contractility significantly increased during infusion, but gradually deteriorated after treatment. Serum lipid peroxidation products malondialdehyde (MDA) content was significantly increased myocardial ultrastructure damage. Caps (2.5 mg · kg-1 for 2 min before OH · OH) and Cap + DA maintained cardiac function and MDA in the normal range. However, the myocardial contractile function in Cap group alone decreased at the first 15 min. The ultrastructure of myocardial cells in both groups was roughly normal. The results suggest that Cap + DA combination is superior to Cap alone in treating heart failure caused by · OH and overcomes the deficiency of myocardial damage with DA.