Zhang Chun-fang, Chen Sheng-xi, Guo Hai-zhou, Luo Wan-jun
Department of Cardiothoracic Surgery, Xiangya Hospital, Central South University, Changsha 410008, China.
Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2005 Feb;30(1):64-7.
To determine the protective mechanism of preconditioning to the lung injury induced by ischemia-reperfusion.
Twelve pigs were randomly divided into 2 groups: control group ( Group C) and ischemic preconditioning group ( Group IP). The concentration of superoxide distrautase (SOD) and malondialdehyde (MDA) in circuit were checked before and after the perfusion to reflect the lipid peroxidation in the lungs. Left lung biopsies were performed immediately after the perfusion and 1 hour postperfusion for histologic examination. The ICAM-1 expression was assessed by immunohistochemical analysis with Envision method and the mRNA expression of ICAM-1 was analyzed by RT-PCR.
SOD in Group IP was much higher than that in Group C (P < 0.01 ). MDA in Group IP was much lower than that in Group C ( P < 0.01 ). The lung histologic examination showed that Group C was significantly more serious than Group IP in pulmonary edema, inflammatory cell infiltration, mild focal hemorrhage, and alveolar disruption. The expression of ICAM-1 of lung tissue obviously decreased in Group IP than that in Group C (P <0.01 ). The expression of ICAM-1 mRNA of lung tissue was significantly lower in Group IP than that in Group C (P < 0.01 ).
Lung ischemic preconditioning can reduce the lung injury. The mechanisms of the protective effects of the IP may be related to the increase of SOD and the decrease of MDA. The preconditioning down-regulated the ICAM-1 expression is one of the mechanisms in reducing the lung injury.
确定预处理对缺血再灌注诱导的肺损伤的保护机制。
12只猪随机分为2组：对照组（C组）和缺血预处理组（IP组）。在灌注前后检测循环中超氧化物歧化酶（SOD）和丙二醛（MDA）的浓度，以反映肺组织中的脂质过氧化情况。灌注后立即及灌注后1小时取左肺组织进行活检，做组织学检查。采用Envision法免疫组化分析评估细胞间黏附分子-1（ICAM-1）的表达，并用逆转录聚合酶链反应（RT-PCR）分析ICAM-1的mRNA表达。
IP组的SOD水平显著高于C组（P<0.01）。IP组的MDA水平显著低于C组（P<0.01）。肺组织学检查显示，C组在肺水肿、炎性细胞浸润、轻度局灶性出血和肺泡破坏方面比IP组明显更严重。IP组肺组织中ICAM-1的表达明显低于C组（P<0.01）。IP组肺组织中ICAM-1的mRNA表达明显低于C组（P<0.01）。
肺缺血预处理可减轻肺损伤。IP组保护作用的机制可能与SOD升高和MDA降低有关。预处理下调ICAM-1表达是减轻肺损伤的机制之一。
