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Prevention of contrast-induced nephropathy with N-acetylcysteine or sodium bicarbonate in patients with ST-segment-myocardial infarction: a prospective, randomized, open-labeled trial.

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BACKGROUND Contrast-induced nephropathy (CIN) is a serious condition in patients with ST-segment-elevation myocardial infarction treated with primary percutaneous coronary intervention. We compared the risk of acute CIN and the influence of preventive strategies in patients with ST-segment-elevation

Cardioprotective effects of N-acetylcysteine: the reduction in the extent of infarction and occurrence of reperfusion arrhythmias in the dog.

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We have studied the cardioprotective effect of N-acetylcysteine in the dog. In mongrel dogs of either sex, the left anterior descending coronary artery was ligated for a period of 2 hours behind the origin of its first diagonal branch. After this period, dogs in a treated group were administered 100

Protective Effects of Brain Infarction by N-Acetylcysteine Derivatives.

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OBJECTIVE We recently found that acrolein (CH2=CH-CHO) is more strongly involved in brain infarction compared with reactive oxygen species. In this study, we looked for acrolein scavengers with less side effects. METHODS Photochemically induced thrombosis model mice were prepared by injection of

Does N-acetylcysteine reduce the incidence of contrast-induced nephropathy and clinical events in patients undergoing primary angioplasty for acute myocardial infarction?

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OBJECTIVE We examined oral N-acetylcysteine effects on contrast-induced nephropathy (CIN) and clinical events in patients undergoing primary angioplasty for acute myocardial infarction. BACKGROUND Recent studies have reported that N-acetylcysteine reduces CIN and improves the clinical outcome in

Glutathione redox pathway and reperfusion injury. Effect of N-acetylcysteine on infarct size and ventricular function.

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Glutathione peroxidase is an important enzyme in the degradative cascade of reactive oxygen free radicals. N-Acetylcysteine (NAC) is a low molecular weight compound that has been used clinically to replenish glutathione. To assess the role of the glutathione redox pathway on reperfusion injury, 23

High dose intracoronary N-acetylcysteine in a porcine model of ST-elevation myocardial infarction.

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We sought to evaluate the safety and efficacy of N-acetylcysteine (NAC) on ischemia and reperfusion in a pig model focusing on cardio-renal protection. High doses of NAC may provide protection from contrast induced nephropathy (CIN). NAC has also been demonstrated to reduce myocardial infarction

N-acetylcysteine administration prevents nonthyroidal illness syndrome in patients with acute myocardial infarction: a randomized clinical trial.

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BACKGROUND The acute phase of the nonthyroidal illness syndrome (NTIS) is characterized by low T3 and high rT3 levels, affecting up to 75% of critically ill patients. Oxidative stress has been implicated as a causative factor of the disturbed peripheral thyroid hormone metabolism. OBJECTIVE The

N-acetylcysteine Plus Deferoxamine Improves Cardiac Function in Wistar Rats After Non-reperfused Acute Myocardial Infarction.

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The antioxidant N-acetycysteine can turn into a prooxidant molecule in presence of iron ions. Thus, our goal was to test if the association of N-acetylcysteine (NAC) and an iron chelator (deferoxamine--DFX) in a rodent model of acute myocardial infarction (AMI) improves cardiac function. Male Wistar

Effect of Oral N-Acetylcysteine Supplementation on the Immunity System in Patients with Acute Myocardial Infarction.

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inflammation, oxidative stress, and fibrosis play important roles after an acute myocardial infarction (AMI) event. The most studied inflammatory biomarker in cardiovascular disease is C-reactive protein (CRP). It has been demonstrated that myeloperoxidase (MPO) and Galectin-3 (Gal-3)

Effects of N-acetylcysteine on the cardiac remodeling biomarkers and major adverse events following acute myocardial infarction: a randomized clinical trial.

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OBJECTIVE The aims of this study were to evaluate the effects of N-acetylcysteine (NAC) on cardiac remodeling and major adverse events following acute myocardial infarction (AMI). METHODS In a prospective, double-blind, randomized clinical trial, the effect of NAC on the serum levels of cardiac

Impact of N-acetylcysteine on contrast-induced nephropathy defined by cystatin C in patients with ST-elevation myocardial infarction undergoing primary angioplasty.

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BACKGROUND The aim of this study was to assess the effects of N-acetylcysteine (N-ACC) on contrast-induced nephropathy (CIN) defined by Cystatin C (Cys-C) serum levels and to evaluate the influence of Cys-C on clinical outcome in patients with ST-elevation myocardial infarction (STEMI). METHODS In

Fatal myocardial infarction associated with intravenous N-acetylcysteine error.

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BACKGROUND N-acetylcysteine is used to treat acetaminophen toxicity and is available in both intravenous and oral formulations. Our report describes a patient treated with intravenous N-acetylcysteine for acetaminophen toxicity who died after an anaphylactoid reaction following initiation of the

N-acetylcysteine restores isoflurane-induced preconditioning against myocardial infarction during hyperglycemia.

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BACKGROUND Hyperglycemia generates reactive oxygen species and prevents isoflurane-induced preconditioning. The authors tested the hypothesis that scavenging reactive oxygen species with N-acetylcysteine will restore protection against myocardial infarction produced by isoflurane in

Effect of N-acetylcysteine on tissue necrosis during acute myocardial infarction in rabbits.

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This study examined whether N-acetylcysteine, a low molecular weight compound used clinically to replenish glutathione, could limit tissue necrosis during acute myocardial infarction in hearts with minimal coronary collateral flow. Fifty rabbits underwent 45 mins ischemia with and without coronary

Effect of N-acetylcysteine on myocardial infarct size following ischemia and reperfusion in dogs.

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The present study was designed to examine the role of N-acetylcysteine (NAC) on free radical mediated reperfusion injury in canine model. Fourteen dogs underwent 90 min of left anterior descending coronary artery (LAD) occlusion followed by 4 h of reperfusion. Treated animals received loading dose

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