acetylcysteine/hemorrhage

BACKGROUND Experimental hemorrhagic shock (HS) is based on controlling bleeding and the treatment of fluid resuscitation to restore tissue oxygenation and perfusion. The HS could promote ischemia/reperfusion injury, which induces a general exacerbation of the inflammatory process, initially

OBJECTIVE To evaluate the effect of N-acetylcysteine (NAC) combined with fluid resuscitation on pulmonary cell death in rats induced with controlled hemorrhagic shock (HS). METHODS Two arteries (MAP calculation and exsanguination) and one vein (treatments) were catheterized in 22 anesthetized rats.

BACKGROUND The underpinning pathophysiology, prevalence, and clinical relevance particular to hemorrhagic shock-induced liver damage have been explored only recently. Importantly, several investigators have revealed that an aberrant periportal endothelial response, characterized by the early release

Vasospasm remains an extremely serious complication that affects patients presenting with subarachnoid hemorrhage (SAH) due to ruptured intracranial aneurysms. The current therapeutic armamentarium is still insufficient in many cases, and the search for new therapies is necessary. In this study, we

OBJECTIVE N-acetylcysteine (NAC) has been investigated to attenuate organ injury in various experimental and clinical studies. However, results in hemorrhagic shock (HS) were controversial. We determined the effects of continuous administration of NAC on acute lung injury (ALI) and acute kidney

Warfarin-related nephropathy (WRN) occurs under conditions of overanticoagulation with warfarin. WRN is characterized by glomerular hemorrhage with occlusive tubular red blood cell (RBC) casts and acute kidney injury (AKI). Herein we test the hypothesis that oxidative stress plays a role in the AKI

This article seeks to standardize an experimental model of liver ischemia-reperfusion in rats following hemorrhagic shock modulated by N-acetylcysteine (NAC). Twenty-seven adult Wistar rats were randomized into three groups: the HS-IR-Garm underwent hemorrhagic shock with selective hepatic ischemia

OBJECTIVE To investigate the pulmonary oxidative stress and possible protective effect of N-Acetylcysteine (NAC) and Desferoxamine (DFX)in a porcine model subjected to hemorrhagic shock. METHODS Twenty-one pigs were randomly allocated to Group-A (sham, n = 5), Group-B (fluid resuscitation, n = 8)

Cyclophosphamide, an alkylating agent used in the chemotherapeutic treatment of neoplasias, is metabolized into active substances capable of damaging the urothelium when in contact with some enzymes. Amongst several alternative proposals for the treatment and prevention of hemorrhagic cystitis

Purpose. To determine if recent preoperative exposure to n-acetylcysteine (NAC), Mucomyst, increases postoperative blood loss in cardiac surgery patients. Methods. Retrospective review of cardiac surgery patients who underwent a cardiac catheterization within four days of surgery and whose serum

Renal ischemia/reperfusion injury induced by hemorrhagic shock (HS) and subsequent fluid resuscitation is a common cause of acute renal failure. The objective of this study was to evaluate the effect of combining N-acetylcysteine (NAC) with fluid resuscitation on renal injury in rats that underwent

BACKGROUND The drugs N-acetylcysteine and erdosteine were used to evaluate their protective effects in hemorrhagic shock-induced acute lung injury in an animal model. METHODS Forty rats were used and randomly allocated into four groups (n=10). Animals in group III were fed with water containing 1

OBJECTIVE When used to prevent perioperative inflammation and ischemia-reperfusion injury, N-acetylcysteine may inadvertently impair hemostasis. We, therefore, performed a post hoc analysis of a recent randomized controlled trial in cardiac surgery to determine whether N-acetylcysteine was

The neuroprotective effect of N-acetylcysteine (NAC), a sulfhydryl-containing antioxidant, on experimentally induced subarachnoid hemorrhage (SAH) in rats was assessed. NAC was administered to rats after the induction of SAH. Neurological deficits and brain edema were investigated. The activity of

BACKGROUND Pharmacological therapy is a strategy for the prevention of complications associated with ischemia and reperfusion injury that occurs after volume replacement in the treatment of hemorrhagic shock. OBJECTIVE The aim of this study was to evaluate the effect of N-acetylcysteine associated