Nakano K, Corin W J, Spann J F, Biederman R W, Denslow S, Carabello B A
Department of Medicine, Medical University of South Carolina, Charleston 29425.
Circ Res. 1989 Dec;65(6):1555-64. doi: 10.1161/01.res.65.6.1555.
To detect the functional significance of subendocardial hypoperfusion in the pressure-overloaded left ventricle, we studied subendocardial and subepicardial function and subendocardial and subepicardial blood flow simultaneously in seven dogs with left ventricular hypertrophy (left ventricle/body weight ratio, 7.2 g/kg) produced by chronic aortic banding. Seven normal dogs served as controls. Subendocardial and subepicardial segment lengths were measured by ultrasonic dimension gauges, and myocardial blood flow was measured with radioactive microspheres. Atrial pacing (180-200 beats/min for 5 minutes) was used to produce a chronotropic stress. In dogs with left ventricular hypertrophy, the subendocardial blood flow failed to increase during pacing compared with the baseline state (1.21 +/- 0.17 vs. 1.22 +/- 0.17 ml/min/g). Subendocardial shortening fraction deteriorated with pacing stress (before pacing, 30.6 +/- 3.9%; after pacing, 24.2 +/- 3.7%; p less than 0.001). In controls, subendocardial blood flow increased from 1.32 +/- 0.19 to 1.80 +/- 0.19 ml/min/g during pacing, and shortening fraction was preserved (before pacing, 25.5 +/- 3.9%; after pacing, 25.9 +/- 3.3%). Subepicardial blood flow in dogs with hypertrophy increased from 1.54 +/- 0.24 to 2.32 +/- 0.34 ml/min/g, and subepicardial shortening fraction was maintained (before pacing, 10.4 +/- 1.0%; after pacing, 10.5 +/- 1.2%) as it was in controls (subepicardial blood flow, from 1.27 +/- 0.18 to 2.12 +/- 0.17 ml/min/g; shortening fraction, from 16.6 +/- 2.5% to 15.5 +/- 2.2%). We conclude that, with pacing stress in pressure-overload hypertrophy, subendocardial blood flow failed to increase. This abnormality corresponded with a deterioration in subendocardial contractile function.
为了检测心内膜下灌注不足在压力超负荷左心室中的功能意义，我们对7只通过慢性主动脉缩窄造成左心室肥厚（左心室/体重比为7.2 g/kg）的犬同时研究了心内膜下和心外膜下功能以及心内膜下和心外膜下血流。7只正常犬作为对照。使用超声尺寸测量仪测量心内膜下和心外膜下节段长度，并用放射性微球测量心肌血流。采用心房起搏（180 - 200次/分钟，持续5分钟）产生变时应激。在左心室肥厚的犬中，与基线状态相比，起搏期间心内膜下血流未能增加（1.21±0.17 vs. 1.22±0.17 ml/min/g）。心内膜下缩短分数在起搏应激下恶化（起搏前，30.6±3.9%；起搏后，24.2±3.7%；p＜0.001）。在对照组中，起搏期间心内膜下血流从1.32±0.19增加至1.80±0.19 ml/min/g，且缩短分数得以保留（起搏前，25.5±3.9%；起搏后，25.9±3.3%）。肥厚犬的心外膜下血流从1.54±0.24增加至2.32±0.34 ml/min/g，且心外膜下缩短分数得以维持（起搏前，10.4±1.0%；起搏后，10.5±1.2%），与对照组情况相同（心外膜下血流，从1.27±0.18增加至2.12±0.17 ml/min/g；缩短分数，从16.6±2.5%降至15.5±2.2%）。我们得出结论，在压力超负荷肥厚的情况下，随着起搏应激，心内膜下血流未能增加。这种异常与心内膜下收缩功能的恶化相对应。
