N-acetylcysteine-induced vasodilation involves voltage-gated potassium channels in rat aorta

Han, Weiqing; Zhu, Dingliang; Wu, Lin‐Sheng; Chen, Qi-Zhi; Guo, Shu-Jie; Gao, Pingjin

doi:10.1016/j.lfs.2009.02.023

Cited by 14 publications

(11 citation statements)

References 24 publications

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“…The beneficial effect of NAC could therefore be in part depends on this property. Although it has been reported evidence of NAC-induced vasodilation and hypotension [39,40], we didn’t found any systemic effect of NAC in our study.…”

Section: Discussioncontrasting

confidence: 80%

N-acetylcysteine improves established monocrotaline-induced pulmonary hypertension in rats

et al. 2014

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BackgroundThe outcome of patients suffering from pulmonary arterial hypertension (PAH) are predominantly determined by the response of the right ventricle to the increase afterload secondary to high vascular pulmonary resistance. However, little is known about the effects of the current available or experimental PAH treatments on the heart. Recently, inflammation has been implicated in the pathophysiology of PAH. N-acetylcysteine (NAC), a well-known safe anti-oxidant drug, has immuno-modulatory and cardioprotective properties. We therefore hypothesized that NAC could reduce the severity of pulmonary hypertension (PH) in rats exposed to monocrotaline (MCT), lowering inflammation and preserving pulmonary vascular system and right heart function.MethodsSaline-treated control, MCT-exposed, MCT-exposed and NAC treated rats (day 14–28) were evaluated at day 28 following MCT for hemodynamic parameters (right ventricular systolic pressure, mean pulmonary arterial pressure and cardiac output), right ventricular hypertrophy, pulmonary vascular morphometry, lung inflammatory cells immunohistochemistry (monocyte/macrophages and dendritic cells), IL-6 expression, cardiomyocyte hypertrophy and cardiac fibrosis.ResultsThe treatment with NAC significantly decreased pulmonary vascular remodeling, lung inflammation, and improved total pulmonary resistance (from 0.71 ± 0.05 for MCT group to 0.50 ± 0.06 for MCT + NAC group, p < 0.05). Right ventricular function was also improved with NAC treatment associated with a significant decrease in cardiomyocyte hypertrophy (625 ± 69 vs. 439 ± 21 μm2 for MCT and MCT + NAC group respectively, p < 0.001) and heart fibrosis (14.1 ± 0.8 vs. 8.8 ± 0.1% for MCT and MCT + NAC group respectively, p < 0.001).ConclusionsThrough its immuno-modulatory and cardioprotective properties, NAC has beneficial effect on pulmonary vascular and right heart function in experimental PH.

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Section: Discussioncontrasting

confidence: 80%

N-acetylcysteine improves established monocrotaline-induced pulmonary hypertension in rats

et al. 2014

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“…NAC has been shown to have anti-inflammatory and antioxidant properties 19,23,28 as well as to promote vasodilation. 20 This plethora of potentially beneficial actions makes the task of teasing out the exact mechanisms underlying the protective effects of this drug on skeletal muscle particularly difficult. Given the well-known antioxidant effects of NAC on skeletal muscle, 42 we anticipated that the observed beneficial effects of NAC on muscle regeneration and function would be accompanied by a reduction in markers of oxidative damage in the ischemic muscles.…”

Section: Discussionmentioning

confidence: 99%

“…The present study was designed to evaluate the impact of the compound N-acetylcysteine (NAC) on the structural and functional phenotype of different muscles in a mouse model of peripheral arterial insufficiency. We chose NAC because of the following reasons: first, NAC is a nonspecific antioxidant, 19 a vasodilator, 20 and has been consistently associated with improvements in fatigue resistance in a variety of animal preparations as well as in clinical populations 21,22 ; second, in diseases associated with myopathic changes, such as Duchenne muscular dystrophy, treatment with NAC has shown to abrogate adverse remodeling in both cardiac and skeletal muscle as evidenced by reduced fibrosis and reduced number of fibers with central nuclei. 23,24 Therefore, we tested the hypothesis that 2 weeks of daily administration of NAC would improve fatigue resistance, ameliorate the histopathological changes, and reduce oxidative damage in the skeletal muscle of mice subjected to bilateral ligation of the femoral artery.…”

mentioning

confidence: 99%

Effects of N-acetylcysteine on skeletal muscle structure and function in a mouse model of peripheral arterial insufficiency

Roseguini

Silva

Polotow

et al. 2015

Journal of Vascular Surgery

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Despite the increasing burden of peripheral arterial disease (PAD) and its detrimental consequences on the quality of life of the patients, few pharmacological therapies have shown to evoke meaningful effects on functional performance in these individuals. N-acetylcysteine is approved for clinical use, has minimal side effects and most important, has shown to consistently improve exercise performance in animals and humans. In this study, we showed, for the first time, that treatment with this drug at a dose amenable for clinical application evoked marked effects on fatigue resistance in the soleus muscle in a mouse model of PAD. These encouraging findings set the stage for translational studies to determine the acute and long-term impact of this drug on walking capacity in patients with PAD.

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“…In this study, IV‐NAC administration was an independent predictor of headache. It is true that NAC administration causes vasodilatation [14,15]. Headache induced by acute substance use is a common condition in which there is a clear relationship between the onset of symptoms and the intake of the drug for therapeutic purposes.…”

Section: Discussionmentioning

confidence: 99%

N‐acetylcysteine‐induced headache in hospitalized patients with acute acetaminophen overdose

Zyoud

Awang

Sulaiman

et al. 2011

Fundamemntal Clinical Pharma

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Intravenous N-acetylcysteine (IV-NAC) is usually regarded as a safe antidote to acetaminophen overdose. However, during infusion of the loading dose, adverse drug reactions such as a headache may occur. The objectives of this study were to investigate the prevalence of headache in patients presenting to hospital after acetaminophen overdose and to determine which clinical findings are most predictive of headache among these patients. This is a retrospective cohort study of hospital admissions for acute acetaminophen overdose that was conducted over a period of 4 years from January 1, 2005 to December 31, 2008. Demographic data, clinical characteristics, and predictors of headache were analyzed. spss 15 was used for data analysis. Two-hundred and fifty-five patients were studied; their mean age was 23.1 ± 1.6; 83.9% of them were women and 14.9% had a headache during hospitalization. Headache among patients was significantly associated with IV-NAC administration (P = 0.001), intentional ingestion of drug (P = 0.04), acetaminophen concentration above 'possible toxicity' treatment line (P = 0.04), a high acetaminophen concentration (P = 0.04), and a long hospital stay (P = 0.03). Multiple logistic regression showed a significant risk factor for headache in patients administered IV-NAC (P = 0.04). We recorded a high frequency of headache in patients with acute acetaminophen overdose in our geographical area. This study suggests that among those patients, the use of IV-NAC is associated with an increased risk of headache.

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N-acetylcysteine-induced vasodilation involves voltage-gated potassium channels in rat aorta

Cited by 14 publications

References 24 publications

N-acetylcysteine improves established monocrotaline-induced pulmonary hypertension in rats

N-acetylcysteine improves established monocrotaline-induced pulmonary hypertension in rats

Effects of N-acetylcysteine on skeletal muscle structure and function in a mouse model of peripheral arterial insufficiency

N‐acetylcysteine‐induced headache in hospitalized patients with acute acetaminophen overdose

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