Schmeling D J, Caty M G, Oldham K T, Guice K S, Hinshaw D B
Department of Surgery, University of Michigan Medical School, Ann Arbor 48109.
Surgery. 1989 Aug;106(2):195-201; discussion 201-2.
Intestinal ischemia-reperfusion injury is a common and important clinical event associated with the activation of an endogenous inflammatory response. Some of the mediators of this response may be involved in the pathogenesis of multiple organ system failure. The purpose of this study was to determine whether remote organ dysfunction--specifically, acute lung injury--occurs after intestinal ischemia-reperfusion injury. After an ischemia-reperfusion event in rat intestine, whole lungs were obtained for measurement of tissue adenosine triphosphate (ATP) and myeloperoxidase values, and evaluation of histologic condition. In addition, lung microvascular permeability was assessed by determination of the rate at which iodine 125-labeled bovine serum albumin sequestration in the extravascular compartment occurred. Lung tissue ATP levels were no different in sham-operated animals than in those that had undergone 120 minutes of intestinal ischemia. Within 15 minutes of gut reperfusion, however, lung ATP decreased from 3.82 +/- 0.27 to 1.53 +/- 0.90 x 10(-7) moles/50 mg tissue, p less than 0.05. Neutrophil accumulation in the lungs, estimated by tissue myeloperoxidase determination, increased sevenfold (0.13 +/- 0.02 to 0.97 +/- 0.25 units/gm, p less than 0.05) after 120 minutes of ischemia and 15 minutes of reperfusion. Lung microvascular permeability increased threefold after 120 minutes of intestinal ischemia and 120 minutes of reperfusion (0.10 +/- 0.01 vs. 0.35 +/- 0.05 [lung/blood counts per minute], p less than 0.05). Intestinal ischemia followed by reperfusion is associated with acute lung injury characterized by increased microvascular permeability, histologic evidence of alveolar capillary endothelial cell injury, reduced lung tissue ATP levels, and the pulmonary sequestration of neutrophils. These data confirm an acute lung injury associated with intestinal ischemia-reperfusion and suggest a possible pathogenic role for the neutrophil.
肠缺血再灌注损伤是一种与内源性炎症反应激活相关的常见且重要的临床事件。这种反应的一些介质可能参与多器官系统功能衰竭的发病机制。本研究的目的是确定肠缺血再灌注损伤后是否会发生远隔器官功能障碍，特别是急性肺损伤。在大鼠肠道发生缺血再灌注事件后，获取整个肺脏以测量组织三磷酸腺苷（ATP）和髓过氧化物酶值，并评估组织学状况。此外，通过测定血管外腔中125碘标记的牛血清白蛋白的潴留率来评估肺微血管通透性。假手术动物的肺组织ATP水平与经历120分钟肠缺血的动物相比无差异。然而，在肠道再灌注后15分钟内，肺ATP从3.82±0.27降至1.53±0.90×10⁻⁷摩尔/50毫克组织，p<0.05。通过组织髓过氧化物酶测定估计，缺血120分钟和再灌注15分钟后，肺中中性粒细胞积聚增加了7倍（0.13±0.02至0.97±0.25单位/克，p<0.05）。肠缺血120分钟和再灌注120分钟后，肺微血管通透性增加了3倍（0.10±0.01对0.35±0.05[肺/血每分钟计数]，p<0.05）。肠缺血后再灌注与急性肺损伤相关，其特征为微血管通透性增加、肺泡毛细血管内皮细胞损伤的组织学证据、肺组织ATP水平降低以及中性粒细胞在肺中的潴留。这些数据证实了与肠缺血再灌注相关的急性肺损伤，并提示中性粒细胞可能具有致病作用。
