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，腹主动脉瘤切除术（AAAectomy，腹主动脉瘤切除术）中主动脉交叉夹持（cross-clamp， XC）和解夹持（unclamp， XU）后，血流动力学会发生突变。一些报道表明，徐诱导肺动脉压显著升高。在AAAectomy中进行血流动力学管理的基本原理是有争议的。血管扩张剂不仅会降低肺血管阻力（PVR），还会降低全身血管阻力（SVR），导致动脉压下降。一氧化氮（NO）已被确定为强大的内皮源性松弛因子（EDRF）。吸入NO可降低PVR，但对SVR无影响或影响甚微。在IRB批准后，29只杂种狗建立动物模型，验证吸入NO对XC后XU后心脏功能的影响。用戊巴比妥麻醉，插管和机械通气。通过肱动脉和股动脉插管监测全身动脉压。将肺动脉导管推进至肺动脉主干，采用热稀释法测定心输出量。麻醉维持在芬太尼、咪达唑仑和吸入百分之五十的含氧氧化亚氮。开胸后，显露降主动脉于横膈膜正上方交叉夹持。所有犬的降主动脉交叉夹夹30分钟后解除夹夹。麻醉犬29只，按徐前处理分为4组。7只犬（第一组），不经任何处理，直接解除降主动脉夹夹。2组在开腹前给予乳酸林格氏液额外体积负荷。第三组的狗从XD后到研究结束时吸入浓度为20ppm的NO。第4组犬从XD中吸入40ppm的NO。在以下六个时间点记录血流动力学变量：XC前（XC前）、XU前（XU前）、XU后5分钟（5分钟）、XU后15分钟（15分钟）、XU后30分钟（30分钟）和XU后60分钟（60分钟）。虽然在1、2、3组中，平均肺动脉压（MPAP）在5 min时显著升高，但在4组中，MPAP与预XU值相比无显著升高。15min时，虽然1、3、4组的MPAP值有所恢复，但2组的MPAP值未恢复。在整个研究过程中，平均动脉压、中心静脉压、肺动脉楔压、心率和心输出量的值没有明显变化。经食管脉冲多普勒超声心动图显示，第1组和第3组经食管脉冲多普勒超声心动图显示，第1组和第3组经食管脉冲多普勒超声心动图显示，第1组和第3组经食管脉冲多普勒超声心动图显示，第5分钟舒张早期流波峰值速度下降。这些结果表明，XU前的容量负荷可能并不总是预防XU后的低血压，并且可能对肺动脉高压有不利影响。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