肠道缺血/再灌注诱导的急性肺损伤是一个依赖肺泡巨噬细胞的事件。
Gut ischemia/reperfusion induced acute lung injury is an alveolar macrophage dependent event.
作者信息
Moraes Luciana Borsoi, Murakami Abel Hiroshi F, Fontes Belchor, Poggetti Renato Sergio, van Rooijen Nico, Younes Riad Nain, Heimbecker Ana Maria Cattani, Birolini Dario
机构信息
Laboratory of Medical Investigation of the 3rd Division of Surgical Clinic, Hospital das Clinicas, University of Sao Paulo School of Medicine, Sao Paulo, Brazil.
出版信息
J Trauma. 2008 May;64(5):1196-200; discussion 1200-1. doi: 10.1097/TA.0b013e31816c5ca6.
BACKGROUND
Although the role of the lung alveolar macrophage (AM) as a mediator of acute lung injury (ALI) after lung ischemia/reperfusion (I/R) has been suggested by animal experiments, it has not been determined whether AMs mediate ALI after intestinal I/R. The objective of this study was to determine the effect of AM elimination on ALI after intestinal I/R in rats.
METHODS
Male Wistar rats (n = 90) were randomly divided into three groups: the clodronate-liposomes (CLOD-LIP) group received intratracheal treatment with CLOD-LIP; the liposomes (LIP) group received intratracheal treatment with LIP; and the nontreated (UNTREAT) group received no treatment. Twenty-four hours later each group was randomly divided into three subgroups: the intestinal I/R subgroup was subjected to 45-minute intestinal ischemia and 2-hour reperfusion; the laparotomy (LAP) subgroup was subjected to LAP and sham procedures; the control (CTR) subgroup received no treatment. At the end of reperfusion, ALI was quantitated in all the animals by the Evans blue dye (EBD) method.
RESULTS
ALI values are expressed as EBD lung leakage (microg EBD/g dry lung weight). EBD lung leakage values in the CLOD-LIP group were 32.59 +/- 12.74 for I/R, 27.74 +/- 7.99 for LAP, and 33.52 +/- 10.17 for CTR. In the LIP group, lung leakage values were 58.02 +/- 18.04 for I/R, 31.90 +/- 8.72 for LAP, and 27.17 +/- 11.48 for CTR. In the UNTREAT group, lung leakage values were 55.60 +/- 10.96 for I/R, 35.99 +/- 6.89 for LAP, and 30.83 +/- 8.41 for CTR. Within each group, LAP values did not differ from CTR values. However, in the LIP and UNTREAT groups, values for both the LAP and CTR subgroups were lower than values for the I/R subgroup (p < 0.001). The CLOD-LIP I/R subgroup value was less (p < 0.001) than the I/R subgroup values in the LIP and UNTREAT groups. These results indicated that I/R provokes ALI that can be prevented by CLOD-LIP treatment, and further suggested that AMs are essential for ALI occurrence induced by intestinal I/R in rats.
背景
尽管动物实验提示肺泡巨噬细胞（AM）在肺缺血/再灌注（I/R）后作为急性肺损伤（ALI）的介质发挥作用，但尚未确定AMs是否介导肠I/R后的ALI。本研究的目的是确定消除AMs对大鼠肠I/R后ALI的影响。
方法
将90只雄性Wistar大鼠随机分为三组：氯膦酸盐脂质体（CLOD-LIP）组经气管内给予CLOD-LIP治疗；脂质体（LIP）组经气管内给予LIP治疗；未治疗（UNTREAT）组未接受任何治疗。24小时后，每组再随机分为三个亚组：肠I/R亚组经历45分钟肠缺血和2小时再灌注；剖腹术（LAP）亚组进行剖腹术及假手术；对照组（CTR）亚组不接受任何治疗。再灌注结束时，采用伊文思蓝染料（EBD）法对所有动物的ALI进行定量。
结果
ALI值以EBD肺渗漏（μg EBD/克干肺重量）表示。CLOD-LIP组I/R时EBD肺渗漏值为32.59±12.74，LAP时为27.74±7.99，CTR时为33.52±10.17。LIP组I/R时肺渗漏值为58.02±18.04，LAP时为31.90±8.72，CTR时为27.17±11.48。UNTREAT组I/R时肺渗漏值为55.60±10.96，LAP时为35.99±6.89，CTR时为30.83±8.41。每组内，LAP值与CTR值无差异。然而，在LIP组和UNTREAT组中，LAP亚组和CTR亚组的值均低于I/R亚组的值（p<0.001）。CLOD-LIP I/R亚组的值低于LIP组和UNTREAT组的I/R亚组的值（p<0.001）。这些结果表明I/R可引发ALI，CLOD-LIP治疗可预防，进一步提示AMs对大鼠肠I/R诱导的ALI发生至关重要。
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