Role of nitric oxide and peroxynitrite anion in lung injury induced by intestinal ischemia-reperfusion in rats

Zhou, Jun; Jin, Guo Hua; Yi, Yi Ling; Zhang, Jun Lan; Huang, Xin

doi:10.3748/wjg.v9.i6.1318

Cited by 45 publications

(48 citation statements)

References 35 publications

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“…The ischemia-reperfusion lesion may complicate many clinical conditions and plays an important role in the pathogenesis and survival following mesenteric blood flow reduction [3][4][5] , and an extensive research approach have been done [6][7][8][9][10] to understand the mechanisms of ischemia-reperfusion intestinal injury to obtain the best protection. The occlusion by selective clamping of the cranial mesenteric artery and the one hour ischemic time used being the routine procedure until now in most reported research but not comparatively studied until now the importance of different collateral blood supply due to anatomic variations specie dependents.…”

Section: Discussionmentioning

confidence: 99%

Ischemia-reperfusion histopathology alterations of the rabbit intestinal wall with and without exclusion of the collateral mesenteric circulation supply

Gomes¹,

Filho

Porto

et al. 2010

Acta Cir. Bras.

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Purpose:To evaluate the histopathology alterations of the intestinal mucosa of rabbits submitted to different times of mesenteric artery ischemia and reperfusion with and without celiac artery collateral circulation supply. Methods: Two groups of eight male New Zealand white rabbits (weight 2.2-3.5 kg) were used in this study. In the Group 1 animals, the proximal mesenteric artery was occluded for 60 min with an atraumatic vascular clamp, followed by reperfusion for 60 min. In the Group 2 animals the small bowel and mesentery were cut 30cm and 60cm far from the gastroduodenal pyloric transition before the proximal mesenteric artery occlusion. Small bowel biopsies were obtained before ischemia (control), after 30 min and 60 min of mesenteric ischemia and at 30 and 60 min. of mesenteric artery reperfusion. Results: In the Group I animals, the followings histopathology grade results were observed: t1, mean 0.4 + 0.29; t2, mean 1.9 ± 0.38; t3, 1.9 ± 0.33; t4, 1.2 ± 0.36 and t5, 1.2 ± 0.32. Differences between t0 and t2 and between t3 and t4 were statistically significant (p<0.05). Differences between t2 and t3 and t4 and t5 were not significant (p>0.5). In the Group II animals, it was observed: t1, mean 1.6 ± 0.33; t2, 2.4 ± 0.36; t3, 3.0 ± 0.35; t4 3.4 ± 0.31; t5, 3 ± 031. Differences between t0 and t1, t1 and t2, and t2 and t3 were significant (p<0.05). Differences between histopathology grades results of samples t1 to t5 in Group 1 and 2 were statistically significant (p<0.5). Conclusion: Microscopic examination of the biopsies revealed significant evidence of worse small bowel wall ischemiareperfusion lesions by exclusion of the celiac artery collateral circulation supply. Key words: Mesenteric Vascular Occlusion. Vascular Diseases. Splanchnic Circulation. Rabbits. RESUMOObjetivo: Avaliar as alterações histopatológicas da mucosa intestinal de coelhos submetidos à isquemia-reperfusão com e sem exclusão da circulação mesentérica colateral. Métodos: Foram estudados dois grupos de oito coelhos Nova Zelândia machos com pesos variáveis entre 2,2 e 3,5 kg de peso corpóreo. Nos animais do Grupo 1, a artéria mesentérica proximal foi ocluida por pinçamento atraumático durante 60 min, seguido de reperfusão por 60 min. No Grupo 2 o intestino delgado e o mesentério foram seccionados 30 cm e 60 após a transição pilórica gastroduodenal antes da oclusão da artéria mesentérica cranial. Biópsias da parede intestinal foram obtidas antes da isquemia (controle), após 30 e 60 min. de isquemia. Resultados: No Grupo I foram observados os seguintes graus de lesões: t1,média de 0.4 + 0.29; t2, média 1.9 ± 0.38; t3, 1.9 ± 0.33; t4, 1.2 ± 0.36 e t5, 1.2 ± 0.32. As diferenças entre t0 e t2 e entre t3 e t4 foram significantes (p<0.05). As diferenças entre t2 e t3 e t4 e t5 não foram significantes (p>0.5). No Group II observou-se: t1, média de 1.6 ± 0.33; t2, 2.4 ± 0.36; t3, 3.0 ± 0.35; t4 3.4 ± 0.31; t5, 3 ± 031. As diferenças entre t0 e t1, t1 e t2, e t2 e t3 foram significantes (p<0.05). As diferenças entre os resultados histopato...

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Section: Discussionmentioning

confidence: 99%

Ischemia-reperfusion histopathology alterations of the rabbit intestinal wall with and without exclusion of the collateral mesenteric circulation supply

Gomes¹,

Filho

Porto

et al. 2010

Acta Cir. Bras.

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“…NO's clinical effectiveness has been well documented (3)(4)(5)(6), although some reports suggest that it may exacerbate lung inflammation (7), raising the concern that it may have toxic properties in some clinical settings. Infants who receive inhaled NO for PPHN are often treated with high inspired oxygen, and in the O 2 -rich environment of the lung, higher oxides of nitrogen (NO x ) including peroxynitrite may form (8), which can cause hemorrhage, inflammation, and edema (9,10). Airways of animal and human subjects who have received inhaled NO showed the same patterns of oxidative injury found in animals and humans who were exposed to NO x or hyperoxia (11,12).…”

mentioning

confidence: 81%

A Novel Inhaled Organic Nitrate That Affects Pulmonary Vascular Tone in a Piglet Model of Hypoxia-Induced Pulmonary Hypertension

et al. 2005

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Persistent pulmonary hypertension of the newborn is characterized by elevated pulmonary vascular resistance after birth leading to right-to-left shunting and systemic arterial hypoxemia. Inhaled nitric oxide (NO) is effective in reducing the need for extracorporeal membrane oxygenation, but it has potential toxicities, especially in an oxygen-rich environment. A number of other NO-based molecules have been given by inhalation, but their structure-function relationships have not been established. Recent studies have raised the idea that toxic and beneficial properties can be separated. We synthesized a novel organic nitrate [ethyl nitrate (ENO 2 )], tested it in vitro, and administered it to hypoxic piglets. ENO 2 lowered pulmonary artery pressure and raised the PO 2 in arterial blood but did not alter systemic vascular resistance or methemoglobin levels. In addition, we tested the effect of ENO 2 in the presence of the thiol glutathione, both in vivo and in vitro, and found its action to be enhanced. Although ENO 2 is less potent than inhaled NO on a doseequivalency basis, pretreatment of hypoxic animals with glutathione, which may be depleted in injured lungs, led to a markedly enhanced effect (largely mitigating the difference in potency). The disease entity persistent pulmonary hypertension of the newborn (PPHN) is characterized by elevated pulmonary vascular resistance (PVR) after birth leading to extrapulmonary right-to-left shunting through the patent foramen ovale and patent ductus arteriosus with resulting systemic arterial hypoxemia. These patients are frequently treated with inhaled nitric oxide (NO) and may require extracorporeal membrane oxygenation; those with severe respiratory failure are at increased risk for neurodevelopmental impairment (1,2). NO's clinical effectiveness has been well documented (3-6), although some reports suggest that it may exacerbate lung inflammation (7), raising the concern that it may have toxic properties in some clinical settings. Infants who receive inhaled NO for PPHN are often treated with high inspired oxygen, and in the O 2 -rich environment of the lung, higher oxides of nitrogen (NO x ) including peroxynitrite may form (8), which can cause hemorrhage, inflammation, and edema (9,10). Airways of animal and human subjects who have received inhaled NO showed the same patterns of oxidative injury found in animals and humans who were exposed to NO x or hyperoxia (11,12).Inhaled, exogenous NO is delivered to well-ventilated parts of the lung and will stimulate guanylate cyclase activity, leading to vascular smooth muscle relaxation. Thus, NO has been effective in lowering pulmonary artery pressure (PAP)

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“…On the other hand, the mechanism of remote organ injury is poorly understood. Oxidant agents as well as inflammatory mediators such as tumor necrosis factor-α, interleukin-1 [24], and nitric oxide (NO) [25], adhesion molecules such as intercellular adhesion molecule 1 [24,26], and complement [27] have been implicated in the pathogenesis of remote organ injury [20]. The results of Es ' refog lu et al indicated that myocardial ischemia reperfusion induces severe testicular damage and antioxidant agents have protective effects on testicular injury after myocardial ischemia reperfusion.…”

Section: Discussionmentioning

confidence: 99%

“…Although there are limited experimental studies, it is known that ischemia reperfusion injury causes damage in organs not related to the initial ischemic tissues; this is termed "remote organ injury" [1][2][3][4][5]. As far as we know, there are only a few reports demonstrating remote organ injury following skeletal muscle ischemia reperfusion injury [6,7].…”

Section: Introductionmentioning

confidence: 99%

The antioxidant role of N-acetylcysteine on the testicular remote injury after skeletal muscle ischemia and reperfusion in rats

Takhtfooladi¹,

Jahanshahi²,

Sotoudeh³

et al. 2013

pjp

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It is known that ischemia reperfusion causes remote organ injury as well as local injury. The aim of this study was to investigate whether N-acetylcysteine has a protective effect against testicular injury after skeletal muscle ischemia reperfusion. Twenty male Wistar rats were allocated to two groups: ischemia reperfusion (control group) and ischemia reperfusion + N-acetylcysteine (treatment group). All animals underwent 2 h of ischemia by occlusion of the femoral artery and 24 h of reperfusion. Rats in treatment group received N-acetylcysteine (150 mg/kg IV) before the reperfusion period. After the reperfusion period, testes were removed for histopathological and biochemical studies. The blood samples were collected for evaluation of serum malondialdehyde (MDA) and nitric oxide (NO) production levels. The MDA levels in testes homogenates were found to be significantly decreased in treatment group (p < 0.05). Treatment of N-acetylcysteine significantly decreased serum MDA and NO levels compared to the control group (p < 0.05). In the control group, tissues showed histological changes. Histopathologically, there was a significant difference (p < 0.05) between two groups. According to histological and biochemical findings, we conclude that N-acetylcysteine has preventive effects in the testicular injury after skeletal muscle ischemia reperfusion.

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Role of nitric oxide and peroxynitrite anion in lung injury induced by intestinal ischemia-reperfusion in rats

Abstract: Intestinal IR increases NO and ONOO(-) production in the lung, which may be involved in intestinal IR-mediated lung injury.

Cited by 45 publications

References 35 publications

Ischemia-reperfusion histopathology alterations of the rabbit intestinal wall with and without exclusion of the collateral mesenteric circulation supply

Ischemia-reperfusion histopathology alterations of the rabbit intestinal wall with and without exclusion of the collateral mesenteric circulation supply

A Novel Inhaled Organic Nitrate That Affects Pulmonary Vascular Tone in a Piglet Model of Hypoxia-Induced Pulmonary Hypertension

The antioxidant role of N-acetylcysteine on the testicular remote injury after skeletal muscle ischemia and reperfusion in rats

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