Intestinal reperfusion-induced pulmonary edema is related to increased pulmonary inducible nitric oxide synthase activity

Turnage, Richard H.; Wright, Joseph K.; Iglesias, J.; LaNoue, John L.; Nguyen, Hao G.; Kim, Lawrence; Myers, Stuart I.

doi:10.1067/msy.1998.91182

Cited by 7 publications

(8 citation statements)

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“…Constitutive NOS is protective in IRI, whereas inducible NOS is responsible for lung dysfunction [34]. Turnage et al [37,38] demonstrated the deleterious role of inducible NOS in the lung after intestinal IRI. Matsuyama et al [39] and Kosaka et al [40] reported that COX-2 and iNOS are up-regulated and have deleterious effects on renal IRI, which is in agreement with the present results.…”

Section: Discussionmentioning

confidence: 99%

Modulation of Lung Allergic Response by Renal Ischemia and Reperfusion Injury

Campanholle

Silva

Martins

et al. 2012

Cell Physiol Biochem

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The Th1/Th2 balance represents an important factor in the pathogenesis of renal ischemia-reperfusion injury (IRI). In addition, IRI causes a systemic inflammation that can affect other tissues, such as the lungs. To investigate the ability of renal IRI to modulate pulmonary function in a specific model of allergic inflammation, C57Bl/6 mice were immunized with ovalbumin/albumen on days 0 and 7 and challenged with an ovalbumin (OA) aerosol on days 14 and 21. After 24 h of the second antigen challenge, the animals were subjected to 45 minutes of ischemia. After 24 h of reperfusion, the bronchoalveolar lavage (BAL) fluid, blood and lung tissue were collected for analysis. Serum creatinine levels increased in both allergic and non-immunized animals subjected to IRI. However, BAL analysis showed a reduction in the total cells (46%) and neutrophils (58%) compared with control allergic animals not submitted to IRI. In addition, OA challenge induced the phosphorylation of ERK and Akt and the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in lung homogenates. After renal IRI, the phosphorylation of ERK and expression of COX-2 and iNOS were markedly reduced; however, there was no difference in the phosphorylation of Akt between sham and ischemic OA-challenged animals. Mucus production was also reduced in allergic mice after renal IRI. IL-4, IL-5 and IL-13 were markedly down-regulated in immunized/challenged mice subjected to IRI. These results suggest that renal IRI can modulate lung allergic inflammation, probably by altering the Th1/Th2 balance and, at least in part, by changing cellular signal transduction factors.

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Section: Discussionmentioning

confidence: 99%

Modulation of Lung Allergic Response by Renal Ischemia and Reperfusion Injury

Campanholle

Silva

Martins

et al. 2012

Cell Physiol Biochem

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“…Numerous clinical studies have clarified that perioperative hypovolemia, hemodynamic instability, and/or low cardiac output syndrome predicts morbidity and mortality following CPB 71,72 . Experimental splanchnic ischemia–reperfusion has been shown to induce lung recruitment and sequestration of neutrophils, 73 free radical injury, and increased pulmonary iNOS expression, while cytokines, and in particular TNF‐α, seem to play a central role to this process 74 . In addition, translocation of toxins and microbial flora may occur following intestinal ischemia leading to ischemic compromise of the integrity of the mucosal barrier 75 …”

Section: Pathophysiology Of Lung Dysfunction Following Open Heart Surmentioning

confidence: 99%

Lung Dysfunction Following Cardiopulmonary Bypass

Apostolakis

Filos

Koletsis

et al. 2010

Journal of Cardiac Surgery

244

195

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“…The resulting splanchnic ischemia and subsequent reperfusion can lead to both local intestinal and remote organ injury [1, 2, 3]. The mechanisms underlying the pathological changes in nonischemic organs are very complex and to date not fully understood, though evidence for the involvement of a number of inflammatory mediators is emerging, such as cytokines, arachidonic acid products, phagocytic cells, reactive oxygen species and also it seems that NO generated by inducible nitric oxide (iNOS) is involved [2, 4, 5, 6, 7, 8]. It has been shown in clinical studies as well as in animal models that intestinal ischemia-reperfusion (I/R) may lead to damage to the pulmonary function [2, 3, 4].…”

Section: Introductionmentioning

confidence: 99%

Effects of N-Acetylcysteine on Pulmonary Macrophage Activity after Intestinal Ischemia and Reperfusion in Rats / with Invited Commentaries

et al. 2000

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Background/Aims: Intestinal ischemia and reperfusion (I/R) is considered to be a critical and triggering event in the development of distal organ dysfunction after a variety of insults. It appears that activated leukocytes, especially polymorphonuclear granulocytes (PMNs), and reactive oxygen species are important mediators in the process. In the present study, the aim was to evaluate the behavior of pulmonary macrophages, acute lung injury and pulmonary endothelial permeability after intestinal I/R, together with potential alterations in pulmonary endothelial and epithelial ultrastructure and cellular membrane system integrity. Methods: Intestinal ischemia for 40 min was followed by reperfusion for 12 h in the rat. Macrophage uptake of radiolabeled bacteria, levels of pulmonary blood content assessed by radiolabeled red blood cells and pulmonary endothelial permeability of radiolabeled albumin, as well as pulmonary endothelial and epithelial ultrastructure and cellular membrane system integrity by the use of scanning electron microscopy and a tracer was evaluated after 12 h reperfusion. Treatment with the free radical scavenger N-acetylcysteine (NAC) administered prior to reperfusion was evaluated. Results: Overactivation of pulmonary macrophages was noted after intestinal I/R, as was a significant decrease in pulmonary blood content. No increase in pulmonary albumin leakage or increase in pulmonary water content was found after intestinal I/R as compared to controls. Treatment with NAC prevented against intestinal I/R-induced overactivation of pulmonary macrophages and a decrease in pulmonary blood content. Conclusion: Reactive oxygen species may be involved in the regulation of pulmonary macrophage function and pulmonary circulation after intestinal I/R.

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Intestinal reperfusion-induced pulmonary edema is related to increased pulmonary inducible nitric oxide synthase activity

Abstract: These data are consistent with the hypothesis that the release of nanomolar quantities of nitric oxide generated by iNOS contributes to IR-induced pulmonary microvascular dysfunction.

Cited by 7 publications

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Modulation of Lung Allergic Response by Renal Ischemia and Reperfusion Injury

Modulation of Lung Allergic Response by Renal Ischemia and Reperfusion Injury

Lung Dysfunction Following Cardiopulmonary Bypass

Effects of N-Acetylcysteine on Pulmonary Macrophage Activity after Intestinal Ischemia and Reperfusion in Rats / with Invited Commentaries

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