Kapelko V I, Veksler V I, Gorina M S, Golikov M A
Institute of Experimental Cardiology, USSR Cardiology Research Center, Moscow.
Acta Physiol Pol. 1988 May-Jun;39(3):166-74.
The contractile function of hearts and atria isolated from rats treated with adriamycin (ADM, total cumulative dose 16-20 mg/kg for 8-10 weeks) was moderately lower as compared to control preparations. However, the former exhibited a relatively higher positive inotropic response to an elevation of Ca++ concentration in the perfusate of isolated hearts or paired pulse stimulation of atria so that maximally attainable values were similar in both groups. On the contrary, the depression of ADM-treated atrial contractile amplitude became even more prominent at moderate increase in stimulation rate and was associated with the apparent incomplete relaxation. Chemically skinned fibers from ADM-treated hearts began to develop force at lower Ca++ concentration and exhibited higher Ca++-sensitivity in pCA range 5.8-5.4. Results suggest that long-term ADM-treatment may be associated with a functional deficiency of Ca++-transporting mechanisms in myocardial cells which may contribute to the depression of the cardiac contractile function.
与对照制剂相比，从接受阿霉素（ADM，总累积剂量为16 - 20mg/kg，持续8 - 10周）治疗的大鼠分离出的心脏和心房的收缩功能适度降低。然而，前者在离体心脏灌流液中Ca++浓度升高或心房成对脉冲刺激时表现出相对较高的正性肌力反应，使得两组的最大可达到值相似。相反，在刺激频率适度增加时，ADM处理的心房收缩幅度的降低变得更加明显，并且与明显的不完全舒张有关。来自ADM处理心脏的化学去表皮纤维在较低的Ca++浓度下开始产生张力，并且在pCa范围5.8 - 5.4内表现出更高的Ca++敏感性。结果表明，长期ADM治疗可能与心肌细胞中Ca++转运机制的功能缺陷有关，这可能导致心脏收缩功能的降低。
