Right and Left Ventricular Responses to Aortic Unclamping Following Aortic Cross-Clamping. -Effects of Nitric Oxide Inhalation on Cardiac Performance Assessed by Transesophageal Echocardiography

众所周知，腹主动脉切除术（AAA切除术）中，主动脉阻断（XC）和开放（XU）后可发生血液动力学的突然变化。一些报告表明XU引起肺动脉压显著升高。AAA切除术期间血流动力学管理的基本原理存在争议。血管扩张剂不仅能降低肺血管阻力（PVR），还能降低全身血管阻力（SVR），导致动脉压下降。一氧化氮（NO）是一种强有力的内皮源性舒张因子（EDRF）。经IRB批准，用29只杂种犬建立XC后XU的动物模型，观察吸入NO对心脏功能的影响。通过肱动脉和股动脉插管监测全身动脉压。日 关于我们 将肺动脉导管插入主肺动脉，用热稀释法测定心输出量。麻醉维持芬太尼，咪达唑仑和吸入百分之五十的一氧化二氮的氧气。开胸后，暴露降主动脉，于膈肌上方交叉夹闭，所有犬均交叉夹闭降主动脉30 min后松开。将29只麻醉犬随机分为4组，其中7只（组1）仅开放降主动脉，不作任何处理。第2组在XD前给予乳酸林格氏液超容量负荷，第3组在XD后即刻至实验结束吸入浓度为20ppm的NO。第4组犬吸入40ppm的XD NO，在以下6个时间点记录血流动力学参数：XC前、XU前、XU后5 min、XU后15 min、XU后30 min、XU后60 min。肺动脉平均压（MPAP）在5min时明显升高，第4组MPAP与术前相比无明显升高，第1、3、4组MPAP在15min时恢复，第2组MPAP未恢复。在整个研究方案中，平均动脉压、中心静脉压、肺动脉楔压、心率和心输出量的值未显示出显著变化。经食管脉冲多普勒超声心动图显示，第1组和第3组二尖瓣口舒张早期血流峰值速度在5min时降低。结果提示，术前容量负荷并不一定能预防术后低血压的发生，可能对肺动脉高压有不良影响。虽然吸入20 ppm的NO可能不能预防XU后的肺动脉高压，但吸入40 ppm的NO可以预防肺动脉高压而不会降低MAP。少

It is well known that abrupt changes in heumodynamics can occur after aortic cross-clamping (XC) and unclamping (XU) during abdominal aortic aneurysmectomy (AAAectomy). Several reports indicate that XU induces a significant rise in pulmonary arterial pressure. The rationale for hemodynamic management during AAAectomy is controversial. Vasodilators would decrease not only pulmonary vascular resistance (PVR), but also systemic vascular resistance (SVR), resulting in a fall in arterial pressure. Nitric oxide (NO) has been identified as the powerful endothelium-derived relaxing factor (EDRF). Although inhaled NO decreases PVR,it has no or little effect on SVR.Following approval of the IRB,29 mongrel dogs were used for animal models to validate the efficacy of inhaled NO on the cardiac performance following XU after XC.The dogs were anesthetized with pentobarbital, intubated and mechanically ventilated. Systemic arterial pressure was monitored via a brachial and femoral arterial cannula. Th … More e pulmonary artery catheter was advanced to the main pulmonary artery, cardiac output was measured with thermodilution technique. Anesthesia was maintained with fentanyl, midazoram and inhalation of fifty percent nitrous oxide in oxygen. After thoracotomy, descending aorta was exposed for cross-clamping at just above the diaphragm.In all dogs, descending aorta was cross-clamped for thirty minutes and was unclamped. Anesthetized dogs (n=29) were divided into four groups with respect to the treatment before XU.In seven dogs (Group1), descending aorta was simply unclamped without any treatment. Dogs in group 2 were given extra-volume loading of lactated Ringer's solution before XD.Dogs in group 3 inhaled NO in a concentration of 20 ppm from just after XD to the end of the study. Dogs in group 4 were treated with inhalation of NO at 40ppm from XD.Hemodynamic variables were recorded at the following six time-points : just before XC (pre-XC), just before XU (pre-XU), 5 min after XU (5 min), 15 min after XU (15 min), 30 min after XU (30 min), and 60 min after XU (60 min).Although in group 1,2 and 3, mean pulmonary arterial pressure (MPAP) significantly increased at 5 min, MPAP did not significantly increase in group 4 compared with the value of pre XU.At 15 min, although the values in MPAP were restored in group 1,3 and 4, the value in group 2 was not restored. The values in mean arterial pressure, central venous pressure, pulmonary arterial wedge pressure, heart rate and cardiac output did not show significant changes throughout the study protocol. Peak velocities of early diastolic flow wave in transmitral flow assessed by transesophageal pulsed Doppler echocardiography decreased at 5 min in group 1 and 3.These results indicate that volume loading before XU may not always prevent post-XU hypotension, and that may have adverse effect on pulmonary hypertension. Although inhalation of NO at 20 ppm may not prevent pulmonary hypertension following XU,inhalation at 40 ppm would prevent pulmonary hypertension without a fall in MAP. Less