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

Role of interleukin‐18 in the development of acute pulmonary injury induced by intestinal ischemia/reperfusion and its possible mechanism

“…Intestinal I/R induced the expression or increased activity of pulmonary iNOS and was related to pulmonary edema, and specific inhibition of iNOS greatly reduced the pulmonary microvascular leakage. 2,4,13,14,21 Our results gave further evidence that in vivo treatment of L-NIL reduced pulmonary microvascular permeability and lung injury in all experimental groups, including intestinal I/R mice, I/R mice treated with IL-18 and sham mice treated with IL-18. This also suggested that exogenous IL-18 enhanced pulmonary edema and was possibly mediated by the action of iNOS, although direct evidence such as the effect of IL-18 on the activity or expression of iNOS is needed.…”

“…Previous reports have suggested that iNOS may be involved in lung injury and specific inhibition of iNOS markedly reduces I/Rinduced pulmonary microvascular dysfunction. 2,4,14,21 Here we evaluated whether or not iNOS affected the function of IL-18 in intestinal I/R-induced lung injury. Animals were divided into either the sham group pretreated with IL-18, I/R group and I/R group pretreated with IL-18, and the sham group was taken as a negative control in the assessment of pulmonary microvascular leakage.…”

Lung Dysfunction Following Cardiopulmonary Bypass

“…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 Therapeutic strategies should aim to maintain perioperative hemodynamic stability, and therefore to minimize postoperative intestinal ischemia.…”

Lung inflammation is induced by renal ischemia and reperfusion injury as part of the systemic inflammatory syndrome

“…Although the role of NO in IRI is still controversial, previous studies have demonstrated that both NOS isoforms exert different modulator effects in lung after an intestinal IRI. The constitutive NOS is protective in intestinal IRI, whereas the inducible NOS is responsible for the lung dysfunction [30][31][32]. In addition, other authors have described that COX-2 and iNOS are up-regulated in ischemic kidneys and have a deleterious participation in renal IRI [33,34].…”