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，在腹主动脉瘤切除术(AAA)中，主动脉阻断(XC)和解除阻断(XU)后，血流动力学会发生突变。一些报道表明，徐引起了肺动脉压的显着上升。AAA切除术中血流动力学管理的理论基础是有争议的。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)，从而导致动脉压下降。一氧化氮(NO)被认为是一种强大的内皮源性松弛因子(EDRF)。吸入NO虽可降低PVR，但对SVR无影响或几乎不影响SVR。在IRB批准后，29只杂种犬用于动物模型，以验证吸入NO对XC后心脏功能的影响。通过臂动脉和股动脉插管监测全身动脉压。TH…将更多的肺动脉导管插入主肺动脉，采用热稀释法测定心输出量。麻醉维持使用芬太尼、咪达唑仑和吸入50%一氧化二氮氧气。开胸手术后，在横隔膜上方暴露降主动脉进行交叉夹闭。在所有的狗身上，降主动脉被交叉夹闭30分钟，然后解除夹闭。麻醉犬29只，随机分为4组。其中7只犬(第1组)单纯开放降主动脉，不作任何处理。第2组狗在XD前给予额外容量的乳酸林格氏溶液，第3组狗从XD后开始吸入20ppm的NO，直到研究结束。第1、2、3组分别于XC前(Pre-XC)、XU前(Pre-Xu)、XC后5min(5min)、Xh后15min(15min)、Xh后30min(30min)、Xu后60min(60min)6个时间点记录血流动力学参数。第1、3、4组MPAP均恢复正常，第2组未见恢复。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没有显示出显著的变化。经食道脉冲多普勒超声心动图测定的二尖瓣血流舒张期早期峰值速度在5min时下降。结果表明，冠脉前容量负荷并不一定能预防冠脉舒张期后的低血压，这可能对肺动脉高压有不良影响。虽然吸入20ppm的NO可能不能预防XU后的肺动脉高压，但吸入40ppm的NO可以在不降低MAP的情况下预防肺动脉高压。较少

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