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洋地黄对急性缺血期间心内膜下和心外膜下功能障碍的影响。

Effects of digitalis on subendocardial and subepicardial dysfunction during acute ischemia.

作者信息

Banka V S, Yamazaki H, Agarwal J B, Bodenheimer M M, Helfant R H

出版信息

Circulation. 1982 Jun;65(7):1315-20. doi: 10.1161/01.cir.65.7.1315.

Abstract

The effects of digitalis (ouabain infusion, priming dose of 10 micrograms/kg/min followed by 2.0 micrograms/kg/min) on subepicardial and subendocardial ischemic dysfunction during partial occlusion (59.4% reduction in coronary flow) and total coronary occlusion were evaluated in 14 dogs using pairs of ultrasonic crystals implanted in the epicardial and endocardial layers. After 30 minutes of partial coronary occlusion, systolic shortening in the ischemic zone decreased from 12.4 +/- 2.9% to -0.4 +/- 0.9% (p less than 0.001) in the epicardium and from 18.9 +/- 3.1% to -1.0 +/- 1.1% (p less than 0.001) in the endocardium. Ouabain infusion increased the systolic shortening from -0.4 +/- 0.9% to 10.6 +/- 3.1% (p less than 0.001) in the epicardium and from -1.0 +/- 1.1% to 17.2 +/- 3.4% (p less than 0.001) in the endocardium. The end-diastolic length did not change. In contrast, after 30 minutes of total coronary occlusion, systolic shortening in both epicardial and endocardial layers was replaced by systolic lengthening and remained unaffected by ouabain infusion in both layers. Systolic shortening in the nonischemic epicardial and endocardial layers increased consistently. We conclude that ouabain improves the contractile function of both ischemic epicardial and endocardial layers layers after partial coronary occlusion and does not worsen subendocardial ischemic dysfunction. After total coronary occlusion, however, the contraction of the ischemic zone is unaffected by ouabain.

摘要

在14只犬中,使用植入心外膜和心内膜层的成对超声晶体,评估了洋地黄(哇巴因输注,初始剂量为10微克/千克/分钟,随后为2.0微克/千克/分钟)对部分闭塞(冠状动脉血流减少59.4%)和完全冠状动脉闭塞期间心外膜下和心内膜下缺血性功能障碍的影响。部分冠状动脉闭塞30分钟后,缺血区的心外膜收缩期缩短率从12.4±2.9%降至-0.4±0.9%(p<0.001),心内膜从18.9±3.1%降至-1.0±1.1%(p<0.001)。哇巴因输注使心外膜收缩期缩短率从-0.4±0.9%增加至10.6±3.1%(p<0.001),心内膜从-1.0±1.1%增加至17.2±3.4%(p<0.001)。舒张末期长度未改变。相比之下,完全冠状动脉闭塞30分钟后,心外膜和心内膜层的收缩期缩短均被收缩期延长所取代,且两层均不受哇巴因输注的影响。非缺血的心外膜和心内膜层的收缩期缩短持续增加。我们得出结论,哇巴因可改善部分冠状动脉闭塞后缺血的心外膜和心内膜层的收缩功能,且不会加重心内膜下缺血性功能障碍。然而,完全冠状动脉闭塞后,缺血区的收缩不受哇巴因影响。

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