Pentoxifylline does not attenuate acute lung injury in the absence of granulocytes.
Pentoxifylline does not attenuate acute lung injury in the absence of granulocytes.
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在缺乏粒细胞的情况下，己酮可可碱不能减轻急性肺损伤。
DOI：
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发表时间：
1991
影响因子：
3.3
通讯作者：
T. Raffin
中科院分区：
文献类型：
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作者：
M. Yonemaru;J. Hatherill;H. Hoffmann;H. Zheng;K. Ishii;T. Raffin
戊茶碱（PTX）是一种甲基黄嘌呤，可抑制多形核白细胞（PMN）的活化，减轻脓毒症引起的急性肺损伤。我们研究了PTX是否能预防非PMN依赖性肺损伤。首先，我们研究了四组粒细胞缺失的豚鼠（对照组、PTX组、大肠杆菌组和大肠杆菌组）。coli + PTX）。通过肺湿重/干重（W/D）比和肺组织与血浆125 I-白蛋白比（白蛋白指数，AI）评估肺损伤。急诊与对照组和PTX组相比，大肠杆菌组肺W/D比值和AI显著增加。然而，PTX不能阻止E.大肠杆菌诱导的肺W/D比和AI增加。接下来，我们研究了PTX对内皮细胞单层通透性和环磷酸腺苷（cAMP）水平的影响。而E. LPS单独作用可增加内皮细胞的通透性，加入LPS的PMN可使内皮细胞通透性增加。PTX减弱了LPS暴露的PMN介导的通透性增加。PTX没有阻止LPS诱导的渗透性增加时，中性粒细胞不存在，虽然PTX增加内皮细胞cAMP水平。这些数据表明：1）PTX不能预防粒细胞耗竭豚鼠的肺损伤; 2）PTX不能预防LPS诱导的内皮细胞通透性增加，尽管cAMP水平增加; 3）PTX减弱内皮细胞通透性的PMN依赖性增加。
Pentoxifylline (PTX), a methylxanthine, can suppress polymorphonuclear leukocyte (PMN) activation and attenuate sepsis-induced acute lung injury. We investigated whether PTX prevents non-PMN-dependent lung injury. First we studied four groups of granulocyte-depleted guinea pigs (control, PTX, Escherichia coli, and E. coli + PTX). Lung injury was assessed by wet-to-dry lung weight (W/D) ratio and lung tissue-to-plasma 125I-albumin ratio (albumin index, AI). The E. coli group showed a significant increase in the lung W/D ratio and AI compared with the control and PTX groups. However, PTX did not prevent the E. coli-induced increase in the lung W/D ratio and AI. Next we investigated the effects of PTX on endothelial cell monolayer permeability and adenosine 3',5'-cyclic monophosphate (cAMP) levels. Whereas E. coli lipopolysaccharide (LPS) alone increased the endothelial permeability, PMNs added to the endothelial monolayers and exposed to LPS enhanced the increase. PTX attenuated the permeability increase mediated by LPS-exposed PMNs. PTX did not prevent the LPS-induced increase in permeability when PMNs were not present, although PTX increased endothelial cell cAMP levels. These data demonstrate that 1) PTX does not prevent lung injury in granulocyte-depleted guinea pigs; 2) PTX does not prevent LPS-induced increases in endothelial cell permeability, despite increased cAMP levels; and 3) PTX attenuates PMN-dependent increases in endothelial cell permeability.