Effect of N-Acetylcysteine in Attenuating Ischemic Reperfusion Injury in Patients Undergoing Coronary Artery Bypass Grafting with Cardiopulmonary Bypass

Prabhu, A.; Sujatha, D.; Kanagarajan, Nandhakumar; Vijayalakshmi, M. A.; Ninan, Benjamin

doi:10.1016/j.avsg.2008.12.005

Cited by 26 publications

(22 citation statements)

References 29 publications

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“…[24][25][26][27] However, at least in the present study, the use of NAC suppressed the progression of myocarditis in a rat EAM model. Theoretically, the primary antioxidant effects of NAC reduce the ROS production and inhibit the activation of nuclear factor-κ B (NFκB) by replenishing glutathione contents.…”

Section: Role Of Oxidative Stress In the Development Of Myocarditiscontrasting

confidence: 55%

N-Acetylcysteine Suppresses the Progression of Ventricular Remodeling in Acute Myocarditis - Studies in an Experimental Autoimmune Myocarditis (EAM) Model -

Niwano

Sasaki

et al. 2011

Circ J

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Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp lectrical and structural remodeling of the heart can develop in various pathological conditions, such as myocardial ischemia, 1-3 cardiomyopathy, 4,5 congestive heart failure, 3,6 hypertension 7 as well as myocarditis. 8, 9 In previous reports, we documented ventricular electrical and structural remodeling in an experimental autoimmune myocarditis (EAM) model in rats, 8,9 and it was characterized by prolongation in the effective refractory period (ERP) and monophasic action potential duration (MAPD) and downregulated expressions of the Kv4.2, Kv1.5, potassium channel interacting protein-2 (KChIP2) and sarcoplasmic reticulum Ca 2+ -ATPase 2a (SERCa2a). In this model, the overexpression of inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) or interferon-γ (IFN-γ) induces myocardial damage and possibly causes ventricular remodeling. 10, 11 We have also reported that TNF-α stimulation induces cellular hypertrophy as well as suppression of the Ito current and Kv4.2 expression in cultured neonatal rat myocytes. 12 Because TNF-α is a strong inducer of nitric oxide (NO) or reactive oxygen species (ROS), this inflammatory process may promote cardiac injury and electrical remodeling through a hyper-oxidative condition. Several studies have documented that antioxidant treatment using N-acetylcysteine (NAC), a thiol-containing radical scavenger and glutathione precursor, may attenuate the myocardial damage through in vitro and in vivo models of heart diseases, 13-15 so that the anti-remodeling effect of antioxidant therapy might be expected in myocarditis. In the present study, we evaluated the expression of inflammatory cytokines and ROS generation through the development of cardiac remodeling in an EAM rat model, and also evaluated the effect of NAC as an antioxidative therapy for ventricular electrical and structural remodeling. Background: Electrical and structural remodeling, characterized by prolonged action potential duration (APD), Kv4.2 downregulation and cellular infiltration were studied in rat experimental autoimmune myocarditis (EAM). Because the reactive oxygen species (ROS) has been speculated to play a role in the promotion of such remodeling, the effect of N-acetylcysteine (NAC) on the progression of ventricular remodeling was evaluated.

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Section: Role Of Oxidative Stress In the Development Of Myocarditiscontrasting

confidence: 55%

N-Acetylcysteine Suppresses the Progression of Ventricular Remodeling in Acute Myocarditis - Studies in an Experimental Autoimmune Myocarditis (EAM) Model -

Niwano

Sasaki

et al. 2011

Circ J

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“…Animals assigned to TBI-NAC received the drug at 30 minutes post-injury, injected at a dose of 50 mg/kg intraperitoneally (ip), and then once every 24 hours over the next three days, for a total of four doses based on previous reports [14], [15]. Animals in the Sham and TBI groups received i.p.…”

Section: Methodsmentioning

confidence: 99%

Efficacy of N-Acetyl Cysteine in Traumatic Brain Injury

et al. 2014

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In this study, using two different injury models in two different species, we found that early post-injury treatment with N-Acetyl Cysteine (NAC) reversed the behavioral deficits associated with the TBI. These data suggest generalization of a protocol similar to our recent clinical trial with NAC in blast-induced mTBI in a battlefield setting [1], to mild concussion from blunt trauma. This study used both weight drop in mice and fluid percussion injury in rats. These were chosen to simulate either mild or moderate traumatic brain injury (TBI). For mice, we used novel object recognition and the Y maze. For rats, we used the Morris water maze. NAC was administered beginning 30–60 minutes after injury. Behavioral deficits due to injury in both species were significantly reversed by NAC treatment. We thus conclude NAC produces significant behavioral recovery after injury. Future preclinical studies are needed to define the mechanism of action, perhaps leading to more effective therapies in man.

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“…36 Another study, however, found that NAC decreased oxidative stress in patients undergoing coronary artery bypass grafting using cardiopulmonary bypass. 37 A limitation of the present study is that we did not observe the animals for a longer period of time, but only 8 Figure 2 Bronchoalveolar lavage (BAL) neutrophil elastase (NE) baseline levels (BAL-1) did not differ significantly between the groups. The levels at BAL-2 were comparable between the N-acetylcysteine (NAC) and control (CON) groups.…”

Section: Discussionmentioning

confidence: 81%

Prevention of primary graft dysfunction in lung transplantation by N-acetylcysteine after prolonged cold ischemia

İnci

Erne

Arni

et al. 2010

The Journal of Heart and Lung Transplantation

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Effect of N-Acetylcysteine in Attenuating Ischemic Reperfusion Injury in Patients Undergoing Coronary Artery Bypass Grafting with Cardiopulmonary Bypass

Cited by 26 publications

References 29 publications

N-Acetylcysteine Suppresses the Progression of Ventricular Remodeling in Acute Myocarditis - Studies in an Experimental Autoimmune Myocarditis (EAM) Model -

N-Acetylcysteine Suppresses the Progression of Ventricular Remodeling in Acute Myocarditis - Studies in an Experimental Autoimmune Myocarditis (EAM) Model -

Efficacy of N-Acetyl Cysteine in Traumatic Brain Injury

Prevention of primary graft dysfunction in lung transplantation by N-acetylcysteine after prolonged cold ischemia

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