Micheletti R, Di Paola E D, Schiavone A, English E, Benatti P, Capasso J M, Anversa P, Bianchi G
Prassis Istituto di Ricerche Sigma-Tau, Milano, Italy.
Am J Physiol. 1993 Apr;264(4 Pt 2):H1111-7. doi: 10.1152/ajpheart.1993.264.4.H1111.
To determine whether propionyl-L-carnitine (PLC) administration ameliorates ventricular remodeling after myocardial infarction, we performed coronary occlusion in rats and examined the long-term effects of the drug 19-24 wk after surgery. In view of the well-established role of angiotensin-converting enzyme (ACE) inhibitors in the reduction of ventricular dilation after infarction, the therapeutic impact of oral PLC (60 mg/kg) was compared with that of enalapril (1 mg/kg). Infarct size measured planimetrically was found to be comparable in untreated, PLC-treated, and enalapril-treated rats, averaging 40-46% of the left ventricular free wall. Heart weight was increased 14, 16, and 11% with no treatment, with PLC, and with enalapril, respectively. The relationship between left ventricular filling pressure and chamber volume demonstrated that PLC and enalapril significantly prevented the expansion in cavitary size after infarction. These protective influences were observed throughout the range of filling pressures measured, from 0 to 30 mmHg. At a uniform reference point of filling pressure of 4 mmHg, untreated infarcted hearts showed an expansion in ventricular volume of 2.17-fold (P < 0.0001). Corresponding increases in this parameter after PLC and enalapril were 36 and 43%, respectively, both not statistically significant. Moreover, PLC was capable of reducing the alterations in myocardial compliance associated with myocardial infarction. In conclusion, PLC reduces the magnitude of decompensated eccentric hypertrophy produced by myocardial infarction in a manner similar to that found with ACE inhibition.
为了确定给予丙酰-L-肉碱（PLC）是否能改善心肌梗死后的心室重构，我们对大鼠进行冠状动脉闭塞，并在术后19 - 24周检查该药物的长期效果。鉴于血管紧张素转换酶（ACE）抑制剂在减少梗死后心室扩张方面已确立的作用，将口服PLC（60 mg/kg）的治疗效果与依那普利（1 mg/kg）进行了比较。通过平面测量法测得的梗死面积在未治疗、PLC治疗和依那普利治疗的大鼠中相当，平均占左心室游离壁的40 - 46%。未治疗、接受PLC治疗和接受依那普利治疗的大鼠心脏重量分别增加了14%、16%和11%。左心室充盈压与心室容积之间的关系表明，PLC和依那普利显著防止了梗死后腔室大小的扩大。在测量的整个充盈压范围内（从0到30 mmHg）都观察到了这些保护作用。在充盈压为4 mmHg的统一参考点，未治疗的梗死心脏心室容积扩大了2.17倍（P < 0.0001）。PLC和依那普利治疗后该参数的相应增加分别为36%和43%，两者均无统计学意义。此外，PLC能够减少与心肌梗死相关的心肌顺应性改变。总之，PLC以类似于ACE抑制的方式降低了心肌梗死产生的失代偿性离心性肥大的程度。
