兔肺缺血再灌注后中性粒细胞迁移的非CD18依赖性机制。

CD18-independent mechanism of neutrophil emigration in the rabbit lung after ischemia-reperfusion.

作者信息

Thomas D D, Sharar S R, Winn R K, Chi E Y, Verrier E D, Allen M D, Bishop M J

机构信息

Department of Cardiothoracic Surgery, University of Washington, Seattle, USA.

出版信息

Ann Thorac Surg. 1995 Nov;60(5):1360-6. doi: 10.1016/0003-4975(95)00546-W.

DOI:10.1016/0003-4975(95)00546-W

PMID:8526627

Abstract

BACKGROUND

Reperfusion of ischemic lung causes an inflammatory pulmonary vascular injury characterized by increased vascular permeability and migration of inflammatory cells into the alveoli. Migration of neutrophils into the alveolus during reperfusion after 24 hours of unilateral pulmonary artery occlusion has been shown to be in part dependent on the CD18 adhesion molecule on the cell surface. The current study investigated whether reperfusion lung injury after a 1-hour period of complete lung ischemia was CD18 dependent.

METHODS

Eighteen rabbits were assigned to one of three groups. Groups 1 and 2 were subjected to one hour of in situ right hilar occlusion followed by 2 hours of reperfusion. Group 3 was subjected to identical surgical dissection but the right hilum was never occluded. Group 1 rabbits received saline solution (1 mL/kg) before hilar occlusion and group 2 rabbits, monoclonal antibody 60.3, a blocking antibody for the CD18 adhesion molecule on the neutrophil surface (2 mg/kg). In 3 of the antibody-treated rabbits, flow cytometry was performed on blood neutrophils before and after administration of the antibody and 120 minutes after reperfusion.

RESULTS

The rabbits in groups 1 and 2 had significantly increased alveolar neutrophil infiltrate and increased pulmonary vascular resistance compared with the rabbits in group 3. However, there was no significant difference between group 1 (saline solution treated) and group 2 (antibody treated). Antibody treatment did not block migration of neutrophils into the alveoli. Flow cytometry of circulating neutrophils demonstrated that CD18 was upregulated after reperfusion and that CD18 was fully blocked after antibody treatment for the duration of the study.

CONCLUSIONS

We conclude that a 1-hour period of warm ischemia followed by reperfusion results in upregulation of CD18 but that emigration of the neutrophils into the alveoli is not CD18 dependent in this injury.

摘要

背景

缺血肺再灌注会导致炎症性肺血管损伤，其特征为血管通透性增加以及炎症细胞向肺泡内迁移。在单侧肺动脉闭塞24小时后的再灌注过程中，中性粒细胞向肺泡内的迁移已被证明部分依赖于细胞表面的CD18黏附分子。当前研究调查了完全性肺缺血1小时后的再灌注肺损伤是否依赖于CD18。

方法

18只兔子被分为三组。第1组和第2组接受1小时的原位右肺门闭塞，随后再灌注2小时。第3组接受相同的手术解剖，但右肺门从未闭塞。第1组兔子在肺门闭塞前接受生理盐水（1 mL/kg），第2组兔子接受单克隆抗体60.3，这是一种针对中性粒细胞表面CD18黏附分子的阻断抗体（2 mg/kg）。在3只接受抗体治疗的兔子中，在抗体给药前后以及再灌注120分钟后对血液中的中性粒细胞进行流式细胞术检测。