McDonald K M, Francis G S, Carlyle P F, Hauer K, Matthews J, Hunter D W, Cohn J N
Department of Medicine, University of Minnesota Medical School, Minneapolis.
J Am Coll Cardiol. 1992 Feb;19(2):460-7. doi: 10.1016/0735-1097(92)90506-i.
Transmyocardial direct-current (DC) shock produces localized left ventricular myocardial necrosis without obstruction to coronary blood flow. In 43 dogs sequential measurements of hemodynamic, neuroendocrine and myocardial structural changes were made at baseline and for 16 weeks after DC shock. Six dogs (14%) died in the peri-shock period. By 1 week after shock, left ventricular mass, as measured by nuclear magnetic resonance imaging, had increased from a mean value +/- SD of 67.9 +/- 10.1 to 82.5 +/- 12.9 g (p = 0.0001). Left ventricular end-diastolic volume was unchanged at 1 week but increased at 16 weeks from 56.1 +/- 10.3 to 70.3 +/- 10.7 ml (p = 0.0003). Left ventricular mass demonstrated a further increase at 12 months (107.8 +/- 14.8 g). Rest cardiac output was significantly decreased at 4 months (3.67 +/- 1.23 to 3.18 +/- 0.81 liters/min, p less than 0.01) as was stroke volume (43 +/- 9 to 37 +/- 7 ml, p less than or equal to 0.01). Left ventricular ejection fraction decreased progressively from 73% to 38% at 1 year. At 4 months there were increases in mean pulmonary artery pressure (18 +/- 4 to 23 +/- 4 mm Hg, p less than 0.01), pulmonary capillary wedge pressure (9 +/- 3 to 15 +/- 3 mm Hg, p less than 0.01) and right atrial pressure (5 +/- 4 to 9 +/- 3 mm Hg, p less than 0.01). Plasma norepinephrine was increased at 4 months (318 +/- 190 to 523 +/- 221 pg/ml, p = 0.0003), whereas plasma renin activity was not significantly changed (4.3 +/- 2.6 vs. 5.2 +/- 3.4 ng/ml per h). Microsphere regional blood flow studies demonstrated a 50% reduction in skeletal muscle blood flow at 4 months (0.06 +/- 0.06 ml/min per g compared with 0.12 +/- 0.09 in normal dogs, p = 0.05), and a reduction in the endocardial/epicardial blood flow ratio (1.11 +/- 0.13 compared with 1.24 +/- 0.13 in normal dogs, p = 0.02). Therefore, in this model of acute left ventricular damage, left ventricular hypertrophy precedes progressive left ventricular dilation.(ABSTRACT TRUNCATED AT 250 WORDS)
经心肌直流电（DC）电击可产生局限性左心室心肌坏死，而不阻碍冠状动脉血流。对43只犬在基线时以及DC电击后16周连续测量血流动力学、神经内分泌和心肌结构变化。6只犬（14%）在电击周围期死亡。电击后1周，通过核磁共振成像测量，左心室质量从平均值±标准差67.9±10.1克增加到82.5±12.9克（p = 0.0001）。左心室舒张末期容积在1周时未改变，但在16周时从56.1±10.3毫升增加到70.3±10.7毫升（p = 0.0003）。左心室质量在12个月时进一步增加（107.8±14.8克）。静息心输出量在4个月时显著降低（从3.67±1.23升/分钟降至3.18±0.81升/分钟，p<0.01），每搏输出量也降低（从43±9毫升降至37±7毫升，p≤0.01）。左心室射血分数在1年时从73%逐渐降至38%。4个月时平均肺动脉压升高（从18±4毫米汞柱升至23±4毫米汞柱，p<0.01），肺毛细血管楔压升高（从9±3毫米汞柱升至15±3毫米汞柱，p<0.01），右心房压升高（从5±4毫米汞柱升至9±3毫米汞柱，p<0.01）。4个月时血浆去甲肾上腺素升高（从318±190皮克/毫升升至523±221皮克/毫升，p = 0.0003），而血浆肾素活性无显著变化（4.3±2.6对5.2±3.4纳克/毫升每小时）。微球区域血流研究表明，4个月时骨骼肌血流减少50%（0.06±0.06毫升/分钟每克，正常犬为0.12±0.09，p = 0.05），心内膜/心外膜血流比值降低（1.11±0.13，正常犬为1.24±0.13，p = 0.02）。因此，在这种急性左心室损伤模型中，左心室肥厚先于左心室逐渐扩张。（摘要截短于250字）
