Role of beta 2 integrins and ICAM-1 in lung injury following ischemia-reperfusion of rat hind limbs.

Role of beta 2 integrins and ICAM-1 in lung injury following ischemia-reperfusion of rat hind limbs.
复制标题

DOI:
--
复制
发表时间:
1993-08
期刊:
The American journal of pathology
影响因子:
--
通讯作者:
Andreas Seekamp;Michael S. Mulligan;Gerd O. Till;C. Smith;M. Miyasaka;T. Tamatani;rd R F Todd;P. Ward
Andreas Seekamp;Michael S. Mulligan;Gerd O. Till;C. Smith;M. Miyasaka;T. Tamatani;rd R F Todd;P. Ward
中科院分区:
其他
文献类型:
--
作者:
Andreas Seekamp;Michael S. Mulligan;Gerd O. Till;C. Smith;M. Miyasaka;T. Tamatani;rd R F Todd;P. Ward

文献摘要

被引文献

相似文献

涉及大鼠后肢的缺血/再灌注导致骨骼肌局部损伤以及肺损伤,如通过增加的血管通透性(125 I标记的牛血清白蛋白渗漏)和出血(51 Cr标记的大鼠红细胞外渗)所测量的。在当前的研究中,我们重点关注了后肢再灌注期间发生的肺部事件。再灌注后4小时获得的血液中性粒细胞的分析表明上调的CD 11b和CD 18,但不是CD 11 a。来自相同动物的血浆证明了在正常血液中性粒细胞中诱导类似效应的能力,表明血浆中存在嗜中性粒细胞活化剂。在再灌注过程中,肺损伤在4小时内逐渐发展,已被证明是嗜中性粒细胞依赖性的,需要CD 11 a/CD 18和CD 11b/CD 18以及细胞间粘附分子-1。这些数据表明,大鼠下肢缺血和再灌注损伤引起全身变化,导致嗜中性粒细胞依赖性肺损伤,即β 2整合素-(白细胞功能抗原-1,Mac-1)和细胞间粘附分子-1依赖性。
Ischemia/reperfusion involving the hind limbs of rats results in both local injury to skeletal muscle as well as injury to lungs, as measured by increased vascular permeability (125I-labeled bovine serum albumin leakage) and hemorrhage (extravasation of 51Cr-labeled rat erythrocytes). In the current study, we have focused on events in lungs occurring during reperfusion of hind limbs. Analysis of blood neutrophils obtained 4 hours after reperfusion has indicated up-regulation of CD11b and CD18 but not CD11a. Plasma from the same animals demonstrate the ability to induce similar effects in normal blood neutrophils, indicative of the presence of a neutrophil-activating agent in plasma. During reperfusion, lung injury, which develops progressively over a 4-hour period, has been shown to be neutrophil-dependent and requires CD11a/CD18 and CD11b/CD18 as well as intercellular adhesion molecule-1. These data suggest that ischemia and reperfusion injury of rat lower extremities causes systemic changes that result in neutrophil-dependent lung injury that is beta 2 integrin- (leukocyte function antigen-1, Mac-1) and intercellular adhesion molecule-1-dependent.