Inhaled nitric oxide improves lung allograft function after prolonged storage.
Inhaled nitric oxide improves lung allograft function after prolonged storage.
复制标题
吸入一氧化氮可改善长期储存后的肺同种异体移植功能。
DOI：
10.1016/s0022-5223(96)70252-0
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Patterson,GA
中科院分区：
文献类型：
--
作者：
Okabayashi,K;Triantafillou,AN;Yamashita,M;Aoe,M;DeMeester,SR;Cooper,JD;Patterson,GA
早期移植物功能障碍引起的死亡，表现为肺血管阻力的进行性增加和氧合的减少，仍然是肺移植中的一个严重问题。吸入一氧化氮，一种重要的体内平衡分子，已被证明对各种急性肺损伤有有益的作用。本研究旨在探讨吸入一氧化氮对犬左肺移植后肺功能的影响。14只犬进行了左肺移植。供体接受全身肝素和前列腺素E1，然后用改良的Euro-Collins溶液进行肺动脉冲洗。供体左肺在1 ℃下储存18小时，随后植入。再灌注后立即结扎对侧右主肺动脉和支气管。关闭胸部，接受者转为仰卧位进行6小时评估。在1.0和5 cm水呼气末正压的吸入氧分数下，以15分钟的间隔进行血液动力学和动脉和静脉血气分析。在评估结束时处死动物。进行同种异体移植物髓过氧化物酶活性测定和湿/干重比。在组I（n = 5）中，在再灌注前和整个6小时评估期间，连续给予浓度为60至70 ppm的一氧化氮气体。在第二组（n = 5），一氧化氮管理开始在再灌注损伤后，在相同的浓度。组III动物（n = 4）不接受一氧化氮。组I的气体交换明显改善。在6小时评估期结束时，组I和组III的平均动脉血氧分压分别为253.8 ± 44.7 mm Hg和114.9 ± 25.5 mm Hg（p < 0.05）。第二组动物没有改善氧与一氧化氮。全身血流动力学不受一氧化氮的影响。然而，观察到肺血管阻力立即降低。组I髓过氧化物酶活性显著低于对照组III（分别为0.24 ± 0.06和0.36 ± 0.04单位; p < 0.05）。（《胸血管外科杂志》1996;112：293-9）
Morbidity caused by early allograft dysfunction, manifested by a progressive increase in pulmonary vascular resistance and a decrease in oxygenation, remains a serious problem in lung transplantation. Inhalation of nitric oxide, an essential homeostatic molecule, has been shown to have beneficial effects on a variety of acute lung injuries. The purpose of the present study was to investigate the effect of inhaled nitric oxide on posttransplant function of canine left lung allografts. Fourteen dogs underwent left lung allotransplantation. Donors received systemic heparin and prostaglandin E1followed by pulmonary artery flush with modified Euro-Collins solution. Donor left lungs were stored for 18 hours at 1º C and subsequently implanted. Immediately after reperfusion, the contralateral right main pulmonary artery and bronchus were ligated. The chest was closed and recipients turned to the supine position for the 6-hour assessment period. Hemodynamic and arterial and venous blood gas analyses were made at 15-minute intervals at an inspired oxygen fraction of 1.0 and 5 cm of water positive end-expiratory pressure. Animals were killed at the end of the assessment. Allograft myeloperoxidase activity assays and wet/dry weight ratios were done. In group I ( n = 5), nitric oxide gas was administered continuously at concentrations of 60 to 70 ppm before reperfusion and throughout the 6-hour assessment period. In group II ( n = 5), nitric oxide administration was initiated at the same concentration after reperfusion injury had developed. Group III animals ( n = 4) received no nitric oxide. Significant improvement in gas exchange was apparent in group I. At the end of the 6-hour assessment period, mean arterial oxygen tension was 253.8 ± 44.7 mm Hg and 114.9 ± 25.5 mm Hg in groups I and III, respectively ( p < 0.05). Group II animals had no improvement in oxygenation with nitric oxide. Systemic hemodynamics were unaffected by nitric oxide. However, an immediate decrease in pulmonary vascular resistance was noted. Group I myeloperoxidase activity was significantly lower than that in control group III (0.24 ± 0.06 versus 0.36 ± 0.04 units, respectively; p < 0.05). (J Thorac Cardiovasc Surg 1996;112:293-9)