Serraf A, Robotin M, Bonnet N, Détruit H, Baudet B, Mazmanian M G, Hervé P, Planché C
Laboratoire de Chirurgie Expérimentale, Hôpital Marie-Lannelongue, Le Plessis-Robinson, France.
J Thorac Cardiovasc Surg. 1997 Dec;114(6):1061-9. doi: 10.1016/S0022-5223(97)70020-5.
The purpose of this study was to analyze the mechanisms associated with lung injury after cardiopulmonary bypass and to propose strategies of prevention.
Thirty-two neonatal piglets underwent 90 minutes of hypothermic cardiopulmonary bypass without aortic cross-clamping. Five experimental groups were defined: group I had standard cardiopulmonary bypass (control), group II received continuous low-flow lung perfusion during cardiopulmonary bypass, group III treatment was similar to that of group I with maintenance of ventilation, group IV received pneumoplegia, and group V received nitric oxide ventilation (30 ppm) after cardiopulmonary bypass. Data drawn from hemodynamic and gas exchange values and muscular and pulmonary tissular levels of adenosine triphosphate (in micromoles per gram) and myeloperoxidase (in international units per 100 mg) were used for comparisons before and 30 and 60 minutes after cardiopulmonary bypass. Pulmonary and systemic vascular endothelial functions were assessed in vitro after cardiopulmonary bypass on isolated rings of pulmonary and iliac arteries.
Pulmonary vascular resistance index, cardiac index, and oxygen tension were better preserved in groups II, IV, and V. All groups disclosed a significant decrease in lung adenosine triphosphate levels and an increase in myeloperoxidase activity whereas these levels stayed within pre-cardiopulmonary bypass ranges in muscular beds. Endothelium-dependent relaxation was preserved in systemic arteries but was strongly affected in pulmonary arteries after cardiopulmonary bypass. None of the methods that aimed to protect the pulmonary vascular bed demonstrated any preservation of pulmonary endothelial function.
Cardiopulmonary bypass results in ischemia-reperfusion injury of the pulmonary vascular bed. Lung protection by continuous perfusion, pneumoplegia, or nitric oxide ventilation can prevent hemodynamic alterations after cardiopulmonary bypass but failed to prevent any of the biochemical disturbances.
本研究旨在分析体外循环后肺损伤的相关机制并提出预防策略。
32只新生仔猪接受了90分钟的低温体外循环且未进行主动脉交叉钳夹。定义了五个实验组:第一组进行标准体外循环(对照组),第二组在体外循环期间接受持续低流量肺灌注,第三组的处理与第一组相似并维持通气,第四组接受肺麻痹,第五组在体外循环后接受一氧化氮通气(30 ppm)。从血流动力学和气体交换值以及肌肉和肺组织中三磷酸腺苷(每克微摩尔数)和髓过氧化物酶(每100毫克国际单位数)水平获取的数据用于体外循环前以及体外循环后30分钟和60分钟的比较。体外循环后在离体的肺动脉和髂动脉环上评估肺和全身血管内皮功能。
第二组、第四组和第五组的肺血管阻力指数、心脏指数和氧分压得到了更好的维持。所有组均显示肺三磷酸腺苷水平显著降低且髓过氧化物酶活性增加,而这些水平在肌肉床中保持在体外循环前的范围内。全身动脉的内皮依赖性舒张功能得以保留,但体外循环后肺动脉的内皮依赖性舒张功能受到严重影响。旨在保护肺血管床的任何方法均未显示对肺内皮功能有任何保护作用。
体外循环导致肺血管床的缺血 - 再灌注损伤。通过持续灌注、肺麻痹或一氧化氮通气进行肺保护可预防体外循环后的血流动力学改变,但未能预防任何生化紊乱。