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[慢性阿霉素损伤中的心肌舒张弹性]

[Myocardial diastolic elasticity in chronic adriamycin lesion].

作者信息

Kapel'ko V I, Popovich M I, Golikov M A, Shul'zhenko V S, Gorina M S

出版信息

Biull Eksp Biol Med. 1987 Jan;103(1):17-9.

PMID:3801642
Abstract

Isolated hearts of the majority of rats receiving 20 mg/kg adriamycin for 10 weeks exhibited normal pump function. Left ventricular diastolic stiffness of these hearts was approximately 1.5 times higher, as compared to control hearts, with the filling pressure in the range of 5 to 20 cm H2O and diastolic pause 23% longer due to bradycardia. Pacing-induced increase in the heart rate up to the control level resulted in further increase in left ventricular diastolic stiffness due to the rise in myocardial stiffness, associated with a fall in cardiac output by 36%. The heart and right atrial compliance determined in separate experiments did not differ significantly from the control. The results suggest that increased left ventricular diastolic stiffness of adriamycin-treated rats seems to be rather due to energy-dependent disturbance in myofibril relaxation than to usually arising myocardial fibrosis.

摘要

大多数接受20mg/kg阿霉素治疗10周的大鼠离体心脏表现出正常的泵功能。与对照心脏相比,这些心脏的左心室舒张硬度大约高1.5倍,充盈压力在5至20cm H2O范围内,由于心动过缓舒张期停顿延长23%。起搏诱导心率增加至对照水平导致左心室舒张硬度进一步增加,这是由于心肌硬度增加,同时心输出量下降36%。在单独实验中测定的心脏和右心房顺应性与对照无显著差异。结果表明,阿霉素治疗大鼠左心室舒张硬度增加似乎更多是由于肌原纤维舒张的能量依赖性紊乱,而非通常出现的心肌纤维化。

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