1998
DOI: 10.1006/jsre.1998.5435
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Physiologic Basis of Pulmonary Edema during Intestinal Reperfusion

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Cited by 34 publications
(24 citation statements)
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“…Mesenteric I/R injury has been reported to induce acute lung injury characterized by increased neut- rophil and cytokine activation and also accumulation of inflammatory infiltrates, alveolar capillary endothelial cell injury, increased microvascular permeability, and pulmonary edema (21). In this study, supporting the previous studies, histopathological scores of lung tissues showed correlation with intestinal injury.…”
Section: Resultssupporting
confidence: 90%
“…Mesenteric I/R injury has been reported to induce acute lung injury characterized by increased neut- rophil and cytokine activation and also accumulation of inflammatory infiltrates, alveolar capillary endothelial cell injury, increased microvascular permeability, and pulmonary edema (21). In this study, supporting the previous studies, histopathological scores of lung tissues showed correlation with intestinal injury.…”
Section: Resultssupporting
confidence: 90%
“…In this study, reperfusion without hIL-10 overexpression after 60 min of mesenteric ischemia led to neutrophil accumulation and increased MPO activity, which is consistent with previous studies (Iglesias et al 1998;Koksoy et al 2000). We measured neutrophil accumulation both by determining MPO concentration within the lung and histopathological counting.…”
Section: Discussionsupporting
confidence: 91%
“…There are several methods to evaluate the degree of pulmonary edema in literature (Iglesias et al 1998;Koike et al 2000;Koksoy et al 2001;Dowdall et al 2002). Lung tissue wet/dry ratio and Evans blue dye concentration were used in the current study to assess the changes in the pulmonary microvascular permeability.…”
Section: Discussionmentioning
confidence: 99%
“…Ultimately, multi-organ failure ensues and involves the liver [18] , heart [26] , kidneys [27] and lungs [28] . Acute pulmonary edema resulting from mesenteric ischemia/reperfusion is caused by an increase in pulmonary microvascular permeability to fluids and proteins, as well as smooth muscle dysfunction [29,30] .…”
Section: Pathophysiologymentioning
confidence: 99%