Pulmonary impact of N-acetylcysteine in a controlled hemorrhagic shock model in rats

Saad, Karen Ruggeri; Saad, Paulo Fernandes; Filho, Luiz Dantas de Oliveira; Brito, Jôse Mára de; Koike, Márcia Kiyomi; Zanoni, Fernando Luiz; Dolhnikoff, Marisa; Montero, Edna Frasson de Souza

doi:10.1016/j.jss.2012.07.037

Cited by 10 publications

(11 citation statements)

References 45 publications

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“…; Saad et al . ). Ubiquinol is unique in that it is the only lipid‐soluble antioxidant synthesized endogenously (Bentinger et al .…”

Section: Discussionmentioning

confidence: 97%

“…Antioxidants have been used to minimize oxidative damage in a variety of diseases. Multiple compounds with antioxidant characteristics have been shown to reduce the negative effects of ischaemia-reperfusion injury following HS and fluid resuscitation Saad et al 2013). Ubiquinol is unique in that it is the only lipid-soluble antioxidant synthesized endogenously (Bentinger et al 2010).…”

Section: Discussionmentioning

confidence: 99%

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Effects of ubiquinol with fluid resuscitation following haemorrhagic shock on rat lungs, diaphragm, heart and kidneys

Bennetts

Shen

Thimmesch

et al. 2014

Experimental Physiology

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New Findings r What is the central question of this study?What are the effects of administering ubiquinol (reduced form of co-enzyme Q 10 ) following haemorrhagic shock on leucocyte mitochondrial superoxide, diaphragmatic hydrogen peroxide concentration and apoptosis in the lungs, diaphragm, heart and kidneys? r What is the main finding and its importance?The administration of ubiquinol attenuated damage to the lungs, diaphragm, heart and kidneys following haemorrhagic shock and fluid resuscitation. Leucocyte mitochondrial superoxide was reduced, while hydrogen peroxide and apoptosis in the diaphragm decreased, as did apoptosis in the lungs, heart and kidneys. These findings suggest that ubiquinol could be a potential antioxidant used to reduce the reperfusion injury following haemorrhagic shock.Haemorrhagic shock (HS) and fluid resuscitation can lead to increased reactive oxygen species (ROS), contributing to ischaemia-reperfusion injury and organ damage. Ubiquinol is a potent antioxidant that decreases ROS. This study examined the effects of ubiquinol administered with fluid resuscitation following controlled HS. Adult male Sprague-Dawley rats were randomly assigned to treatment [ubiquinol, 1 mg (100 g body weight)−1 ] or control groups. Rats were subjected to 60 min of HS by removing 40% of the total blood volume to a mean arterial pressure ß45-55 mmHg. The animals were resuscitated with blood and lactated Ringer solution, with or without ubiquinol, and monitored for 120 min. At the end of the experiments, the rats were killed and the lungs, diaphragm, heart and kidneys harvested. Leucocytes were analysed for mitochondrial superoxide at baseline, end of shock and 120 min following fluid resuscitation using MitoSOX Red. Diaphragms were examined for hydrogen peroxide using dihydrofluorescein diacetate and confocal microscopy. The apoptosis in lungs, diaphragm, heart and kidneys was measured using fluorescence microscopy with acridine orange and ethidium bromide. Leucocyte mitochondrial superoxide levels were significantly lower in rats that received ubiquinol than in the control animals. Production of hydrogen peroxide and apoptosis were significantly reduced in the organs of rats treated with ubiquinol. These findings suggest that ubiquinol, administered with fluid resuscitation after HS, attenuates ROS production and

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“…; Saad et al . ). Ubiquinol is unique in that it is the only lipid‐soluble antioxidant synthesized endogenously (Bentinger et al .…”

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Effects of ubiquinol with fluid resuscitation following haemorrhagic shock on rat lungs, diaphragm, heart and kidneys

Bennetts

Shen

Thimmesch

et al. 2014

Experimental Physiology

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“…Sigma Aldrich (UK), 150 mg/kg, i.p.) [30] for three consecutive days. The last injection of propofol occurred 12 h prior to operation.…”

Section: Methodsmentioning

confidence: 99%

Propofol Activation of the Nrf2 Pathway Is Associated with Amelioration of Acute Lung Injury in a Rat Liver Transplantation Model

Yao

Luo

Zhu

et al. 2014

Oxidative Medicine and Cellular Longevity

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Objective. This study aimed to investigate whether propofol pretreatment can protect against liver transplantation-induced acute lung injury (ALI) and to explore whether Nrf2 pathway is involved in the protections provided by propofol pretreatment. Method. Adult male Sprague-Dawley rats were divided into five groups based on the random number table. Lung pathology was observed by optical microscopy. Lung water content was assessed by wet/dry ratio, and PaO2 was detected by blood gas analysis. The contents of H2O2, MDA, and SOD activity were determined by ELISA method, and the expression of HO-1, NQO1, Keap1, and nuclear Nrf2 was assayed by western blotting. Results. Compared with saline-treated model group, both propofol and N-acetylcysteine pretreatment can reduce the acute lung injury caused by orthotopic autologous liver transplantation (OALT), decrease the lung injury scores, lung water content, and H2O2 and MDA levels, and improve the arterial PaO2 and SOD activity. Furthermore, propofol (but not N-acetylcysteine) pretreatment especially in high dose inhibited the expression of Keap1 and induced translocation of Nrf2 into the nucleus to further upregulate the expression of HO-1 and NQO1 downstream. Conclusion. Pretreatment with propofol is associated with attenuation of OALT-induced ALI, and the Nrf2 pathway is involved in the antioxidative processes.

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“…For this matter, a series of active compounds [72−75] that can reduce the inflammations resulting from the fluids generated by resuscitation have been studies. The compounds that had a great contribution in the good post-resuscitation management are acid valproic [72], or N-acetylcysteine [73]. The complete impact of the oxidative stress and free radical on the pulmonary tissue and the biochemical and physiological explications Blocks the specific receptors -peroxisome proliferator IL -interleukine; TNF-α -tumor necrosis factor alfa; ICU -intensive care unit of all the clinical manifestation that appear in a patient with multiple traumas remain unclear and need further research.…”

Section: Biochemical Aspects Of Free Radicals and The Actions Of Oxidmentioning

confidence: 99%

Oxidative stress in severe pulmonary trauma in critical ill patients. Antioxidant therapy in patients with multiple trauma — a review

Bedreag¹,

Rogobete

Sărăndan³

et al. 2015

Anaesthesiol Intensive Ther

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Multiple trauma patients require extremely good management and thus, the trauma team needs to be prepared and to be up to date with the new standards of intensive therapy. Oxidative stress and free radicals represent an extremely aggressive factor to cells, having a direct consequence upon the severity of lung inflammation. Pulmonary tissue is damaged by oxidative stress, leading to biosynthesis of mediators that exacerbate inflammation modulators. The subsequent inflammation spreads throughout the body, leading most of the time to multiple organ dysfunction and death. In this paper, we briefly present an update of biochemical effects of oxidative stress and free radical damage to the pulmonary tissue in patients in critical condition in the intensive care unit. Also, we would like to present a series of active substances that substantially reduce the aggressiveness of free radicals, increasing the chances of survival.

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Pulmonary impact of N-acetylcysteine in a controlled hemorrhagic shock model in rats

Cited by 10 publications

References 45 publications

Effects of ubiquinol with fluid resuscitation following haemorrhagic shock on rat lungs, diaphragm, heart and kidneys

Effects of ubiquinol with fluid resuscitation following haemorrhagic shock on rat lungs, diaphragm, heart and kidneys

Propofol Activation of the Nrf2 Pathway Is Associated with Amelioration of Acute Lung Injury in a Rat Liver Transplantation Model

Oxidative stress in severe pulmonary trauma in critical ill patients. Antioxidant therapy in patients with multiple trauma — a review

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