Brooks H, Kirk E S, Vokonas P S, Urschel C W, Sonnenblick E H
J Clin Invest. 1971 Oct;50(10):2176-83. doi: 10.1172/JCI106712.
Right ventricular performance was studied relative to right coronary artery flow in the chloralose-anesthetized, open chest dog. The right coronary artery was cannulated for measurement and control of flow and pressure. Under control conditions, right coronary artery occlusion caused no change in cardiac output, or right and left ventricular pressures, although right ventricular contractile force fell markedly. With right coronary artery flow intact, incremental pulmonary artery obstruction caused a corresponding decline in cardiac output and elevation of right ventricular end-diastolic pressure with eventual total right ventricular failure and systemic shock. With right coronary artery occlusion, identical degrees of pulmonary artery obstruction resulted in more pronounced changes in cardiac output and right ventricular end-diastolic pressure with right ventricular failure occurring at a much lower level of right ventricular stress.However, with right coronary artery flow intact, the right ventricular decompensation induced by pulmonary artery obstruction, could be reversed by raising right coronary artery perfusion to levels above normal, thus increasing right ventricular performance and restoring cardiac output. We conclude that right ventricular failure and resultant systemic hypotension due to severe pulmonary artery obstruction can be reversed simply by right coronary artery hyperperfusion, and that, although a normally contractile right ventricular free wall is not essential to maintain cardiac performance at rest, during right ventricular systolic stress, over-all cardiac performance becomes increasingly dependent on the right ventricle. The data further imply that increased myocardial impingement on right coronary artery flow during systole in right ventricular hypertension may be an important factor leading to right ventricular failure.
在水合氯醛麻醉、开胸的犬身上,研究了右心室功能与右冠状动脉血流的关系。将右冠状动脉插管以测量和控制血流及压力。在对照条件下,右冠状动脉闭塞时,心输出量、左右心室压力均无变化,尽管右心室收缩力明显下降。在右冠状动脉血流正常时,肺动脉逐渐梗阻会导致心输出量相应下降,右心室舒张末期压力升高,最终导致右心室完全衰竭和全身休克。在右冠状动脉闭塞时,相同程度的肺动脉梗阻会导致心输出量和右心室舒张末期压力出现更明显的变化,且右心室衰竭在右心室压力低得多的水平时就会发生。然而,在右冠状动脉血流正常时,肺动脉梗阻引起的右心室失代偿可通过将右冠状动脉灌注提高到正常水平以上而逆转,从而提高右心室功能并恢复心输出量。我们得出结论,严重肺动脉梗阻导致的右心室衰竭和由此产生的全身低血压可通过右冠状动脉过度灌注简单逆转,并且,尽管正常收缩的右心室游离壁对于维持静息时的心功能并非必不可少,但在右心室收缩应激期间,整体心功能越来越依赖于右心室。数据进一步表明,右心室高血压时收缩期心肌对右冠状动脉血流的冲击增加可能是导致右心室衰竭的一个重要因素。