Pinsky M R, Summer W R, Wise R A, Permutt S, Bromberger-Barnea B
J Appl Physiol Respir Environ Exerc Physiol. 1983 Apr;54(4):950-5. doi: 10.1152/jappl.1983.54.4.950.
We studied the cardiovascular effects of increasing intrathoracic pressure in an acute pentobarbital-anesthetized canine model of acute ventricular failure induced by large doses of propranolol. Left ventricular (LV) function curves were generated by volume loading from LV filling pressures of 5-20 Torr. The animals were ventilated by using intermittent positive-pressure ventilation with large tidal volumes (30 ml/kg). Chest and abdominal pneumatic binders were used to increase intrathoracic pressure. When compared with the control state, acute ventricular failure was associated with a decrease in the slope of the LV function curves (P less than 0.01). After binding the increase in intrathoracic pressure (1.1 +/- 1.6 to 12.1 +/- 2.4 Torr, P less than 0.01) was associated with an improvement in both right ventricular and LV function. Our study demonstrates that in this model of acute ventricular failure, increasing intrathoracic pressure improves cardiac function. We postulate that this observed improvement with increased intrathoracic pressure is due to reduced LV wall stress in a manner analogous to that seen with arterial vasodilator therapy in congestive heart failure.
我们在大剂量普萘洛尔诱发急性心室衰竭的急性戊巴比妥麻醉犬模型中,研究了增加胸内压的心血管效应。通过将左心室(LV)充盈压从5-20托进行容量负荷来生成左心室功能曲线。动物采用大潮气量(30 ml/kg)的间歇正压通气进行通气。使用胸部和腹部气动束缚带增加胸内压。与对照状态相比,急性心室衰竭与左心室功能曲线斜率降低相关(P<0.01)。束缚后胸内压升高(从1.1±1.6升至12.1±2.4托,P<0.01)与右心室和左心室功能改善相关。我们的研究表明,在这个急性心室衰竭模型中,增加胸内压可改善心脏功能。我们推测,观察到的胸内压升高带来的改善是由于左心室壁应力降低,其方式类似于充血性心力衰竭中动脉血管扩张剂治疗所见。