Cason B A, Hickey R F, Shnier C B
Department of Anesthesia, University of California, San Francisco.
J Card Surg. 1993 Mar;8(2 Suppl):295-9. doi: 10.1111/j.1540-8191.1993.tb01327.x.
In this study, we used a swine model to study coronary autoregulation in the stunned myocardium. In 18 domestic swine, the left anterior descending coronary artery was cannulated and flow to this artery controlled via an extracorporeal perfusion circuit. Stunning was induced by reducing pump flow to approximately 25% of the baseline value for 15 minutes followed by 1 hour of reperfusion. This ischemia/reperfusion protocol reduced systolic shortening to approximately 50% of control, at 1 hour of reperfusion. Neither the slope of the coronary pressure-flow relation (0.41 +/- 0.19 vs 0.48 +/- 0.26 mL/100 g per min per mmHg) nor an autoregulation index (0.43 +/- 0.16 vs 0.30 +/- 0.32) was significantly changed at 1 hour reperfusion (p > 0.05) compared to baseline. These findings argue against the hypothesis that the mechanical dysfunction of the stunned myocardium is due to suboptimal perfusion caused by poor coronary autoregulation.
在本研究中，我们使用猪模型来研究顿抑心肌中的冠状动脉自动调节。在18头家猪中，将左前降支冠状动脉插管，并通过体外灌注回路控制该动脉的血流。通过将泵流量降低至基线值的约25%并持续15分钟，随后再灌注1小时来诱导顿抑。在再灌注1小时时，这种缺血/再灌注方案使收缩期缩短降低至对照值的约50%。与基线相比，在再灌注1小时时，冠状动脉压力-血流关系的斜率（0.41±0.19对0.48±0.26 mL/100 g每分钟每毫米汞柱）和自动调节指数（0.43±0.16对0.30±0.3）均无显著变化（p>0.05）。这些发现与顿抑心肌的机械功能障碍是由于冠状动脉自动调节不良导致灌注不足这一假说相悖。
