Fessler H E, Brower R G, Wise R, Permutt S
Department of Medicine, Johns Hopkins Medical Institutions, Francis Scott Key Medical Center, Baltimore, Maryland 21224.
Am J Physiol. 1990 Mar;258(3 Pt 2):H814-20. doi: 10.1152/ajpheart.1990.258.3.H814.
Pressure surrounding the heart (PSH) rises with maneuvers that increase pleural pressure. This may decrease left ventricular (LV) oxygen demand by reducing LV afterload. However, positive PSH may also directly impede coronary flow. To study the effects of positive PSH on coronary perfusion, PSH was increased in 10-mmHg increments from 0 to 60 mmHg in an isolated canine heart-lung preparation with constant venous return, arterial pressure, and lung volume. Increased PSH caused a rapid significant (P less than 0.001) fall in left atrial transmural pressure (PLATM) of up to 1.28 +/- 0.31 mmHg. With constant venous return and lung volume, this was interpreted to reflect decreased LV afterload. However, at levels of PSH greater than 30 mmHg, initial decreases in PLATM were followed by sustained increases, suggesting that there was a deterioration in cardiac function despite the lower level of afterload. Increased PSH was also associated with decreases in circumflex coronary artery flow [flow (ml/min) = 52.4 - 0.4PSH, P less than 0.01]. Moreover, when the circumflex coronary artery was maximally dilated with adenosine, the effects of PSH were amplified [flow (ml/min) = 137.9 - 1.78PSH, P less than 0.001], indicating that positive PSH mechanically impeded coronary flow. When PSH was raised to 60 mmHg for 90 s, the aortic-coronary sinus lactate concentration difference fell from 0.71 +/- 0.09 to 0.10 +/- 0.21 mM (mean +/- SE, P less than 0.001, n = 8), suggesting myocardial ischemia. We conclude that positive PSH directly decreases myocardial perfusion. This may lead to ischemic cardiac dysfunction, especially in patients with low arterial pressure or coronary artery disease.
心脏周围压力（PSH）会随着增加胸膜压力的操作而升高。这可能通过降低左心室（LV）后负荷来减少左心室的氧需求。然而，正性PSH也可能直接阻碍冠状动脉血流。为了研究正性PSH对冠状动脉灌注的影响，在一个具有恒定静脉回流、动脉压和肺容积的离体犬心肺制备模型中，将PSH以10 mmHg的增量从0升高至60 mmHg。PSH升高导致左心房跨壁压（PLATM）迅速显著下降（P<0.001），下降幅度高达1.28±0.31 mmHg。在静脉回流和肺容积恒定的情况下，这被解释为反映了左心室后负荷的降低。然而，当PSH水平高于30 mmHg时，PLATM最初下降后接着持续升高，这表明尽管后负荷水平较低，但心脏功能仍在恶化。PSH升高还与回旋支冠状动脉血流减少有关[血流（ml/min）=52.4 - 0.4PSH，P<0.01]。此外，当用腺苷使回旋支冠状动脉最大程度扩张时，PSH的影响被放大[血流（ml/min）=137.9 - 1.78PSH，P<0.001]，表明正性PSH机械性地阻碍了冠状动脉血流。当PSH升高至60 mmHg并持续90秒时，主动脉 - 冠状窦乳酸浓度差从0.71±0.09降至0.10±0.21 mM（均值±标准误，P<0.001，n = 8），提示心肌缺血。我们得出结论，正性PSH直接降低心肌灌注。这可能导致缺血性心脏功能障碍，尤其是在动脉压低或患有冠状动脉疾病的患者中。
