Nitric oxide mediates lung injury induced by ischemia-reperfusion in rats

Kao, Shang Jyh; Peng, Tai-Chu; Lee, Ru Ping; Hsu, Kang; Chen, Chao-Fuh; Hung, Yu-Kuen; Wang, David; Chen, Hsing I.

doi:10.1007/bf02255998

Cited by 32 publications

(27 citation statements)

References 21 publications

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“…Isolation and perfusation of the lungs in situ Isolated perfused lungs were prepared according to the procedures described in previous studies [3,4]. A vertical incision was made along the midline of the thorax.…”

Section: Experimental Modelsmentioning

confidence: 99%

“…Weight changes were pre-calibrated on the electronic balance before preparation for the experiment. In the isolated lung in situ preparation, the changes in body weight (BW) reflected the changes in lung weight (LW) [3,4].…”

Section: Experimental Modelsmentioning

confidence: 99%

“…The slow component of the weight gain was plotted on a semi-log scale as a function of time. The capillary filtration rate was obtained by extrapolating the slow component of the weight gain back to zero time [3,4].…”

Section: Microvascular Permeabilitymentioning

confidence: 99%

“…Ischaemia causes lung injury through a temporary interruption of blood flow to the lungs followed by reperfusion, which is evidenced by increases in lung weight, microvascular permeability, pulmonary arterial pressure and lung pathology [3,4]. The current authors have provided evidence to indicate that endogenous and exogenous nitric oxide (NO) are detrimental to I/R lung injury [3], but that static inflation exerts protective effects [4].…”

mentioning

confidence: 98%

“…Studies from the present authors' laboratory have investigated the pathogenic mechanisms and potential therapeutic regimen on ALI induced by endotoxin [12,13] and I/R [3,4]. The present study was designed to evaluate the protective effect of nicotinamide on ALI caused by I/R in isolated perfused lungs.…”

mentioning

confidence: 99%

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Nicotinamide abrogates acute lung injury caused by ischaemia/reperfusion

Su¹,

Liu²,

Kao³

et al. 2007

European Respiratory Journal

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Poly (ADP-ribose) synthase or polymerase (PARS and PARP, respectively) is a cytotoxic enzyme which causes cellular damage. Nicotinamide, a compound of vitamin B complex, has been reported to exert an inhibitory effect on PARS or PARP. The present study tests the effects of nicotinamide on acute lung injury and associated alterations following ischaemia/reperfusion (I/R) of the isolated perfused rat's lung.I/R increased the lung weight (LW) to body weight ratio, LW gain, protein and dye tracer leakage, pulmonary arterial pressure and capillary permeability. The insult also increased nitrate/ nitrite, methyl guanidine, tumour necrosis factor-a and interleukin-1b in lung perfusate, while it decreased adenosine triphosphate content with an increase in PARP activity in lung tissue.Most of the I/R-induced changes were abrogated by post-treatment (30 min after I/R) with nicotinamide (100 mg?kg -1 body weight). However, the increase in pulmonary arterial pressure was enhanced by nicotinamide post-treatment. Following I/R, the inducible nitric oxide synthase (iNOS) mRNA expression was enhanced. Nicotinamide reduced the iNOS expression. The results suggest that nicotinamide exerted a protective effect on the acute lung injury caused by ischaemia/reperfusion. The mechanisms may be mediated through the inhibition on the poly (adenosine diphosphate-ribose) polymerase activity, inducible nitric oxide synthase expression and the subsequent suppression of nitric oxide, free radicals and pro-inflammatory cytokines with restoration of adenosine triphosphate.

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Section: Experimental Modelsmentioning

confidence: 99%

Section: Experimental Modelsmentioning

confidence: 99%

Section: Microvascular Permeabilitymentioning

confidence: 99%

mentioning

confidence: 98%

mentioning

confidence: 99%

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Nicotinamide abrogates acute lung injury caused by ischaemia/reperfusion

Su¹,

Liu²,

Kao³

et al. 2007

European Respiratory Journal

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Biomedical vignette

2003

J Biomed Sci

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Acute respiratory distress syndrome

Chen

Kao²,

Wang

et al. 2003

J Biomed Sci

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Acute respiratory distress syndrome (ARDS) can be associated with various disorders. Among these, coronavirus infection may cause life-threatening severe acute respiratory syndrome (SARS). In this review, we present animal models and techniques for the study of ARDS, and discuss the roles and possible mechanisms of various chemical factors, including nitric oxide (NO). Our early work revealed that cerebral compression elicits severe hemorrhagic pulmonary edema (PE), leading to central sympathetic activation that results in systemic vasoconstriction. The consequence of systemic vasoconstriction is volume and pressure loading in the pulmonary circulation. Vasodilators, but not oxidant radical scavengers, are effective in the prevention of centrogenic PE. In isolated perfused lung, exogenous and endogenous NO enhances lung injury following air embolism and ischemia/reperfusion. In contrast, NO synthase (NOS) inhibitors reverse such lung injury. Although NO is important in maintaining vasodilator tone, hypoxiainduced pulmonary vasoconstriction is accompanied by an increase instead of a decrease in NO release. In animal and isolated lung studies, endotoxin produces acute lung injury that is associated with increases in cytokines and inducible NOS mRNA expression, suggesting that NO is toxic to the lung in endotoxin shock. Recently, we reported several rare cases that indicate that ARDS in patients with Japanese B encephalitis, lymphangitis with breast cancer and fat embolism is caused by different mechanisms. Our early and recent studies on ARDS and PE may provide information for clinical practice and the understanding of the pathogenesis of SARS.

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Nitric oxide mediates lung injury induced by ischemia-reperfusion in rats

Cited by 32 publications

References 21 publications

Nicotinamide abrogates acute lung injury caused by ischaemia/reperfusion

Nicotinamide abrogates acute lung injury caused by ischaemia/reperfusion

Biomedical vignette

Acute respiratory distress syndrome

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