Chandra N C, Beyar R, Halperin H R, Tsitlik J E, Wurmb E, Rayburn B, Guerci A D, Weisfeldt M L
Peter Belfer Laboratory for Myocardial Research, Francis Scott Key Medical Center, Baltimore, MD 21224.
Circulation. 1991 Jul;84(1):279-86. doi: 10.1161/01.cir.84.1.279.
We have previously shown, in dogs with severe cardiac depression, that modest cyclic increases in intrathoracic pressure, starting synchronously with left ventricular isovolumic contraction, significantly increase aortic flow and pressure. However, little is known of changes in vital organ perfusion during this technique of assisted circulation.
We studied regional organ flow using radioactive labeled microspheres in 13 20-25-kg mongrel dogs. In the control group, after chemical induction of cardiac depression with verapamil and propranolol, coronary flow fell from 129.1 +/- 14.4 to 51.6 +/- 11.3 ml/100 g/min (p less than 0.005) and continued to decline over a 14-minute time period (flow was 32.2 +/- 11.5 ml/100 g/min at 7 minutes and 20.7 +/- 9.5 ml/100 g/min at 14 minutes [n = 6]; all p less than 0.05). In the intervention group, regional blood flow was evaluated before and after the induction of cardiac depression and also during assisted circulation using 400-msec, 20-25-mm Hg intrathoracic pressure increases delivered by a circumthoracic pneumatic vest, starting synchronously with left ventricular isovolumic contraction. In the intervention group, coronary flow fell from 119 +/- 26.7 to 47.9 +/- 13.1 ml/100 g/min 1 minute after the induction of cardiac depression (p less than 0.005). With the initiation of assisted circulation, coronary flow increased to 55.8 +/- 19.2 ml/100 g/min at 7 minutes and fell to 23.1 +/- 15.9 ml/100 g/min on termination of assisted circulation at 14 minutes (p less than 0.05 and p = NS versus control group flows at 1 and 14 minutes, respectively). During assisted circulation, cerebral, renal, and small intestinal flows also increased (all p less than 0.05 versus flows during myocardial depression). No significant increase in hepatic flow was observed.
In the canine model, manipulation of intrathoracic pressure appears to be an effective, short-term, noninvasive means of not only increasing aortic pressure but also increasing vital organ perfusion during cardiogenic shock. Further studies are needed to assess the usefulness of this technique of assisted circulation in humans.
我们之前已经表明,在患有严重心脏抑制的犬类中,从左心室等容收缩开始同步进行适度的胸内压周期性升高,可显著增加主动脉血流和压力。然而,对于这种辅助循环技术期间重要器官灌注的变化知之甚少。
我们使用放射性标记微球研究了13只体重20 - 25千克的杂种犬的局部器官血流。在对照组中,用维拉帕米和普萘洛尔化学诱导心脏抑制后,冠状动脉血流从129.1±14.4降至51.6±11.3毫升/100克/分钟(p<0.005),并在14分钟内持续下降(7分钟时血流为32.2±11.5毫升/100克/分钟,14分钟时为20.7±9.5毫升/100克/分钟[n = 6];所有p<0.05)。在干预组中,在诱导心脏抑制前后以及使用环绕胸部的气动背心进行辅助循环期间(从左心室等容收缩开始同步施加400毫秒、20 - 25毫米汞柱的胸内压升高)评估局部血流。在干预组中,诱导心脏抑制1分钟后冠状动脉血流从119±26.7降至47.9±13.1毫升/100克/分钟(p<0.005)。随着辅助循环的开始,冠状动脉血流在7分钟时增加到55.8±19.2毫升/100克/分钟,并在14分钟辅助循环结束时降至23.1±15.9毫升/100克/分钟(分别与对照组在1分钟和14分钟时的血流相比,p<0.05且p =无显著性差异)。在辅助循环期间,脑、肾和小肠血流也增加(与心肌抑制期间的血流相比,均p<0.05)。未观察到肝血流有显著增加。
在犬类模型中,操纵胸内压似乎是一种有效的短期非侵入性方法,不仅可增加主动脉压力,还可在心源性休克期间增加重要器官灌注。需要进一步研究以评估这种辅助循环技术在人类中的实用性。