Pulmonary Nitric Oxide Metabolism Following Infrarenal AorticCross-clamp-induced Ischaemia–Reperfusion Injury

Abstract

the reperfusion phase of infrarenal aortic cross-clamping provokes a significant increase in pulmonary NOS metabolism. The increase in plasma TNF-alpha and MPO activity suggests that this response may be secondary to inducible NOS expression. Manipulation of this response may benefit patients at risk of acute injury following infrarenal aortic reconstruction.

The Effect of Nω-Nitro-l-Arginine Methyl Ester and l-Arginine on Lung Injury Induced by Abdominal Aortic Occlusion–Reperfusion

“…13 Three different NO synthase isoforms have been identifi ed: two constitutive, Ca 2 + / calmodulin-dependent isoforms (c-NOS) and one Ca 2 + -independent isoform (i-NOS), which is inducible and regulated at the transcriptional level by cytokines and bacterial endotoxin. 8 The inducible isoform is particularly expressed when activated by proinfl ammatory cytokines.…”

“…28 Pararajasingam et al found the plasma level of tumor necrosis factor-α and lung tissue level of total NO synthase activity to significantly increase after aortic occlusion-reperfusion in the rat. 13 In isolated, blood-perfused rat lungs, Lu et al reported that IR alone can upregulate i-NOS mRNA and i-NOS enzyme activity. 29 We found increased NO levels in the aortic IR group, which can be partly explained by the induced i-NOS activity after aortic occlusion-reperfusion.…”

“…12 Pararajasingam et al also showed that the reperfusion phase of infrarenal aortic-cross-clamping provokes a signifi cant increase in pulmonary NO syntheses metabolism. 13 Reactive oxygen species and subsequent lipid peroxidation play an important role during aortic IR-induced lung injury. 4 Malondialdehyde (MDA) has been used as an indicator of both lipid peroxidation and oxidative stress in several studies.…”

“…,13 Ischemia-reperfusion of the lower extremities elicits an acute infl ammatory response characterized by activation of neutrophils. a Neutrophils within alveolar interstitium in aortic IR group (H&E, ×400).…”

Avaliação dos efeitos do 17beta-estradiol na lesão mesentérica pela oclusão da aorta descendente proximal em ratos machos

“…O excesso de produção de NO pela iNOS contribui para a fisiopatologia da lesão de isquemia e reperfusão. No entanto, o NO produzido pela eNOS exerce um efeito protetor meritório sobre o intestino delgado no início da lesão de isquemia e reperfusão (Durakbasa et al, 1998;Pararajasingam et al, 2000;Mallick et al, 2004;Cerqueira et al, 2005). O óxido nítrico atenua o desenvolvimento da aterosclerose através da prevenção da expressão de moléculas de adesão, agregação plaquetária e das interações leucócito-endotélio.…”