Malik A B, Geha A S
Cardiovasc Res. 1977 Jul;11(4):310-6. doi: 10.1093/cvr/11.4.310.
Myocardial function, flow and O2 consumption were compared in cardiac hypertrophy induced by pressure-loading (P) and by volume overloading (V). Increases in LV-to-body weight ratios in P and V hypertrophied hearts were comparable. Indices of LV function such as cardiac output, stroke volume, stroke work, minute work, peak LV dP/dt, ratio of peak LV dP/dt-to-isovolumic pressure and -to-LVEDP, and Vmax were significantly reduced from normal only in hypertrophy induced by V. Left ventricular coronary flow was reduced from 167.1 +/- 27.2 in normal dogs to 146.2 +/- 17.1 cm3/min-100 g-1 in P hypertrophy, and was reduced further to 82.5 +/- 8.2 cm3/min-100 g-1 in V hypertrophy. Flows decreased similarly in epicardium and endocardium in both hypertrophied hearts. Cardiac O2 extraction in P and V hearts was greater than in control hearts. Myocardial O2 consumption was maintained at control values in P hypertrophy, and decreased by 54 +/- 3% in V hypertrophy. These findings indicate that LV function is impaired at rest in hypertrophy induced by V and is normal in hypertrophy induced by P.
对压力负荷（P）和容量负荷（V）诱导的心肌肥厚模型的心肌功能、血流及氧耗进行了比较。P组和V组肥厚心脏的左心室与体重比值增加程度相当。仅在V诱导的肥厚模型中，左心室功能指标如心输出量、每搏量、每搏功、分钟功、左心室最大dp/dt、左心室最大dp/dt与等容压力及左心室舒张末期压力的比值以及Vmax较正常显著降低。左心室冠状动脉血流在正常犬为167.1±27.2，在P组肥厚时降至146.2±17.1cm³/min/100g，在V组肥厚时进一步降至82.5±8.2cm³/min/100g。在两种肥厚心脏中，心外膜和心内膜的血流均以相似方式降低。P组和V组心脏的心肌氧摄取均高于对照心脏。P组肥厚时心肌氧耗维持在对照值，而V组肥厚时心肌氧耗降低了54±3%。这些发现表明，V诱导的肥厚在静息时左心室功能受损，而P诱导的肥厚时左心室功能正常。
