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Protective Effects of Ischemic Preconditioning on Donor Lung in Canine Lung Transplantation FREE TO VIEW

Guohu Li; Shengxi Chen; Wanzhong Lou; ErXiong Lu
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From the Department of Cardiothoracic Surgery, Xiangya Hospital, Hunan Medical University, Hunan, PR China

1998 by the American College of Chest Physicians

Chest. 1998;113(5):1356-1359. doi:10.1378/chest.113.5.1356
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Background: Myocardial ischemic preconditioning has been found to protect the myocardium. We hypothesized that lung ischemic preconditioning might enhance canine lung preservation and reduce allograft lung dysfunction after transplantation.

Methods: Ten pairs of adult canines underwent left lung allotransplantation. Five donors were treated with ischemic preconditioning (their left hilus clamped for 10 min and released for 15 min [group IP]), and five donors were not treated with ischemic preconditioning (group C). The donor lungs were flushed with 4°C Euro-Collins solution (ECS) and stored in the same solution for 2½ h, then transplanted to the recipient canines. The animals were observed for 1 to 2 h after transplantation. The lung venous blood of the recipient and donor lung tissue was collected just after thoractomy and 1 h after reperfusion of the transplanted lung in both groups.

Results: The numbers of polymorphonuclear leukocytes (PMNs) in the pulmonary venous blood after reperfusion were significantly higher in group IP than in group C (p<0.05). However, the numbers of PMNs in lung interstitium under microscopy were less in group IP than in group C. The thromboxane B2, malondialdehyde, and mean pulmonary artery pressure contents were significantly lower in group IP than in group C (p<0.05), and the superoxide dismutase and mixed venous oxygen tension values were significantly higher in group IP than in group C (p<0.05). Histologic findings show less damage in group IP than in group C.

Conclusions: The protective effects of ischemic preconditioning in conjunction with ECS flush and storage were superior to using ECS alone. The possible mechanisms were that ischemic preconditioning inhibited the accumulation and activation of PMNs in lung tissue and reduced the production of oxygen-free radicals.




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