Kapel'ko V I, Lakomkin V L, Konovalova G G, Tsyplenkova V G, Tikhaze A K, Lankin V Z
Kardiologiia. 2010;50(12):45-51.
Functional, biochemical and morphological studies of rat cardiac muscle after single injection of adriamycin (2.2 mg/kg) were carried out. The myocardium was taken for studies in 2 hours and in 2-3 weeks after adriamycin injection. The isolated heart was perfused retrogradely with Krebs solution and left ventricular isovolumic pressure and perfusion pressure were continuously monitored. Two-fold increase in perfusion rate was accompanied by raised developed pressure, heart rate and perfusion pressure which in the given conditions reflected a tone of coronary vessels. The cardiac contractile function of rats that received adriamycin 2 hours before, remained unaltered as compared to control group, however, perfusion pressure was raised by 26%. These hearts responded to H2O2 introduction (100 microM) into coronary vessels by more profound fall in developed pressure, which fell to 31 +/- 8% after 40 minutes vs. 61 +/- 5% in the control group (p<0.01). In two-three weeks after adriamycin injection, both cardiac contractile function and its responsiveness to oxidative stress induced by H2O2 introduction did not differ from the control, however, perfusion pressure remained elevated and this was accompanied by slowed myocardial relaxation. The myocardial concentration of malonic dialdehyde was moderately increased in adriamycin-treated group in both terms while the activity of antioxidant enzymes (SOD, GPHx and catalase) remained unaltered. Results showed an absence of the direct connection between myocardial antioxidant status and the contractile function changes at adriamycin action.
对单次注射阿霉素(2.2毫克/千克)后的大鼠心肌进行了功能、生化和形态学研究。在注射阿霉素后2小时以及2至3周取心肌进行研究。将离体心脏用克雷布斯溶液逆行灌注,并持续监测左心室等容压力和灌注压力。灌注速率增加两倍伴随着舒张压力、心率和灌注压力升高,在给定条件下这反映了冠状血管的张力。与对照组相比,在注射阿霉素2小时前给药的大鼠心脏收缩功能未发生改变,然而,灌注压力升高了26%。这些心脏在向冠状血管中注入过氧化氢(100微摩尔)后,舒张压力下降更为明显,40分钟后降至31±8%,而对照组为61±5%(p<0.01)。在注射阿霉素后两到三周,心脏收缩功能及其对注入过氧化氢诱导的氧化应激的反应性与对照组无差异,然而,灌注压力仍然升高,并且伴随着心肌舒张减慢。在两个时间段内,阿霉素治疗组心肌丙二醛浓度适度增加,而抗氧化酶(超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶)的活性保持不变。结果表明,在阿霉素作用下,心肌抗氧化状态与收缩功能变化之间不存在直接联系。