Connolly M W, Lim K H, Rose D M, Tan I P, Grossi E A, Baumann G F, Jacobowitz I J, Cunningham J N
Surgery. 1986 Aug;100(2):143-9.
This investigation examined the efficacy of right atrial-pulmonary artery bypass (RA-PA) during acute ischemia of the right ventricle. The right coronary artery (RCA) was ligated in 25 open chest, open pericardium sheep. Control animals (n = 15) were resuscitated with only intravenous fluids. In the experimental animals (n = 10) RA-PA bypass was initiated 5 minutes after right coronary occlusion. Sixty percent (9/15) of the control animals died within 90 minutes of RCA occlusion from refractory ventricular arrhythmia or right ventricular failure. Four of 10 RA-PA animals died within 2 hours of RCA occlusion from severe pulmonary hemorrhage and arterial oxygen desaturation when high flow rates (2.5 to 3.5 L/min) were initially instituted. In these animals, lung histologic findings demonstrated extensive hemorrhage into the alveolar spaces. After 6 hours of RCA occlusion in the six surviving control animals, there were significant increases in central venous pressure and right ventricular end-diastolic cord length (relative ventricular volume change measured by ultrasonic crystal analysis), and a significant decrease in the cardiac output. In contrast, during RCA occlusion in the six surviving animals on RA-PA bypass, cardiac output was well maintained, and there was a significant decrease in central venous pressure and end-diastolic length. The percent of change from baseline in end-diastolic length correlated inversely with the percent of change from baseline in cardiac output (r = -0.81, p less than 0.01). By crystal violet and triphenyltetrazolium chloride dye techniques, the mean percentage area of necrosis to area of risk was significantly less for the RA-PA group compared with the control group (5.6% versus 67.1%, p less than 0.0001). In this experimental model, RA-PA bypass effectively unloaded the acutely ischemic right ventricle, maintained systemic cardiac output, and significantly reduced right ventricular infarction size. Further investigations with this ventricular support modality are needed to determine its effects on pulmonary pathophysiology.
本研究检测了右心房-肺动脉旁路（RA-PA）在右心室急性缺血期间的疗效。对25只开胸、打开心包的绵羊结扎右冠状动脉（RCA）。对照组动物（n = 15）仅通过静脉输液进行复苏。在实验动物（n = 10）中，右冠状动脉闭塞5分钟后开始进行RA-PA旁路。60%（9/15）的对照组动物在RCA闭塞后90分钟内死于难治性室性心律失常或右心室衰竭。10只接受RA-PA的动物中有4只在RCA闭塞后2小时内死于严重肺出血和动脉血氧饱和度降低，这是由于最初设定了高流速（2.5至3.5升/分钟）。在这些动物中，肺组织学检查结果显示肺泡腔内有广泛出血。在6只存活的对照组动物RCA闭塞6小时后，中心静脉压和右心室舒张末期索长度（通过超声晶体分析测量的相对心室容积变化）显著增加，而心输出量显著降低。相比之下，在6只接受RA-PA旁路的存活动物RCA闭塞期间，心输出量得到良好维持，中心静脉压和舒张末期长度显著降低。舒张末期长度相对于基线的变化百分比与心输出量相对于基线的变化百分比呈负相关（r = -0.81，p < 0.01）。通过结晶紫和氯化三苯基四氮唑染色技术，与对照组相比，RA-PA组坏死面积与危险面积的平均百分比显著更小（5.6%对67.1%，p < 0.0001）。在这个实验模型中，RA-PA旁路有效地减轻了急性缺血右心室的负荷，维持了全身心输出量，并显著减小了右心室梗死面积。需要对这种心室支持方式进行进一步研究，以确定其对肺病理生理学的影响。
