scholarly journals Propofol administration to the fetal–maternal unit reduces cardiac oxidative stress in preterm lambs subjected to prenatal asphyxia and cardiac arrest

2016 ◽  
Vol 79 (5) ◽  
pp. 748-753 ◽  
Author(s):  
Matthias Seehase ◽  
Patrick Houthuizen ◽  
Jennifer J. P. Collins ◽  
Luc J. Zimmermann ◽  
Boris W. Kramer
Keyword(s):  
Oxidative Stress ◽  
Cardiac Arrest ◽  
Prenatal Asphyxia

Normoxic resuscitation after cardiac arrest protects against hippocampal oxidative stress, metabolic failure, and neuronal death

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S42-S42
Author(s):  
Robert E Rosenthal ◽  
Viktoria Vereczki ◽  
Erica M Martin ◽  
Gary Fiskum
Keyword(s):  
Oxidative Stress ◽  
Cardiac Arrest ◽  
Neuronal Death

scholarly journals The roles of oxidative stress and Beclin-1 in the autophagosome clearance impairment triggered by cardiac arrest

2019 ◽  
Vol 136 ◽  
pp. 87-95 ◽  
Author(s):  
Xintao Wang ◽  
Dawei Sun ◽  
Yue Hu ◽  
Xiaotao Xu ◽  
Wei Jiang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Arrest ◽  
Beclin 1

scholarly journals Therapeutic hypothermia reduces inflammation and oxidative stress in the liver after asphyxial cardiac arrest in rats

2020 ◽  
Vol 35 (4) ◽  
pp. 286-295
Author(s):  
Yoonsoo Park ◽  
Ji Hyeon Ahn ◽  
Tae-Kyeong Lee ◽  
Bora Kim ◽  
Hyun-Jin Tae ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Arrest ◽  
Therapeutic Hypothermia ◽  
And Oxidative Stress ◽  
Asphyxial Cardiac Arrest

Abstract 508: Pyruvate Induction of Glyoxalase 1 in Porcine Brain Post-cardiac Arrest: Enhanced Methylglyoxal and Glutamate Detoxification

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Gary F Scott
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Cardiac Arrest ◽  
Cognitive Deficits ◽  
Cognitive Deficit ◽  
Gene Activation ◽  
Binding Activity ◽  
Enzyme Inactivation ◽  
Glyoxalase 1 ◽  
Glutamate Efflux

Background: After cardiac arrest (CA) and cardio-cerebral resuscitation (CCR), enhanced glycolysis elevates toxic methylglyoxal (MG) that contributes to carbonyl-exacerbated oxidative stress, enzyme inactivation and death of neurons and astroglia. Post cardiac arrest cognitive deficits may be prevented by pyruvate infusions that boost glyoxalase 1 (GLO1) detoxification of MG and brain glutamate efflux via Nrf2-regulated Phase II gene expression. Purpose: To define pyruvate-induced cytoprotective mechanisms that curtail brain injury and cognitive deficit after cardiac arrest and resuscitation in pigs. Methods: Pigs were subjected to CA/CCR, infused with 4 mM pyruvate or NaCl control, then carotid artery and frontal cortical lysates were assayed for Nrf2/ARE binding activity and GLO1 activity, while plasma glutamate concentrations were measured. Results: Compared with saline controls, pyruvate infused pigs demonstrated increased Nrf2/ARE binding activity and 3-fold higher GLO1 activity supporting MG detoxification. Plasma glutamate concentrations were substantially reduced by pyruvate, which would support greater brain efflux of excitotoxic glutamate. Conclusions: Intravenous pyruvate induces Nrf2-regulated gene activation for augmented GLO1 biological activity via mechanisms that may lower glutamate-inflicted excitotoxicity and the heretofore untreatable cognitive deficits.

THE EFFECT OF IMMATURITY AND PRENATAL ASPHYXIA ON THE LUNGS AND PULMONARY FUNCTION OF NEWBORN LAMBS: THE EXPERIMENTAL PRODUCTION OF RESPIRATORY DISTRESS

PEDIATRICS ◽  
1965 ◽  
Vol 35 (3) ◽  
pp. 382-392
Author(s):  
E. O. R. Reynolds ◽  
H. N. Jacobson ◽  
E. K. Motoyama ◽  
Y. Kikkawa, ◽  
J. M. Craig ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Gas Exchange ◽  
Pulmonary Function ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Human Infant ◽  
Experimental Production ◽  
Comparable Control ◽  
Prenatal Asphyxia ◽  
Experimental Disease

1. The effect of immaturity on the lungs and pulmonary function of newborn lambs was assessed by delivering and observing 13 animals of varying gestational ages. In lambs of approximately 125-129 days gestation changes closely resembling those of human respiratory distress syndrome developed without asphyxia. These changes consisted of retraction of the chest wall, poor gas exchange, grossly liver-like lungs, reduced pulmonary surface activity, and, on histological examination, severe atelectasis, alveolar necrosis, and hyaline membranes. 2. Similar changes were found in 4 of 6 lambs subjected to severe prenatal asphyxia lasting for up to 4 hours which were between approximately 130-136 days gestation but not in three of four comparable control animals. 3. Prolonged prenatal asphyxia was followed by changes suggesting respiratory distress in only 1 of 6 lambs above 136 days gestation. One further lamb at 140 days gestation, acutely asphyxiated to the point of cardiac arrest, developed severe changes. 4. It is postulated that the experimental disease and the syndrome seen in the human infant are produced by similar mechanisms, and that the influence of prematurity is more important than that of asphyxia.

Abstract 361: The Augmentation of Oxygen-sensitive Generation of Oxygen Radicals in Mitochondria and the Attenuation of Hyperoxia-induced Oxidative Stress After Cardiac Arrest

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_4) ◽  
Author(s):  
Koichiro Shinozaki ◽  
Yu Okuma ◽  
Tomoaki Aoki ◽  
Mitsuaki Nishikimi ◽  
Kei Hayashida ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Arrest ◽  
Ex Vivo ◽  
Lung Injury Score ◽  
Ros Generation ◽  
Absolute Change ◽  
Isolated Mitochondria ◽  
Carbonyl Protein ◽  
Oxygen Sensitive ◽  
The Brain

Introduction: Hyperoxia can induce oxidative stress resulting in organ injuries after cardiac arrest (CA). Mitochondrial reactive oxygen species (ROS) are key to understanding its mechanism, however the augmentation of oxygen-sensitive ROS generation caused by CA ( Fig 1 ) has not been well described. Methods: Rats were assigned into: 1) sham with normoxia, 30% O2; 2) sham with hyperoxia, 100% O2; 3) CA with normoxia; and 4) CA with hyperoxia (n=15 for each group). CA was induced by 10-minute asphyxia and CPR was delivered. Neurological deficit score (NDS), histological lung injury score (LIS), survival time were obtained from the CA groups. Carbonyl protein as an oxidative stress indicator was measured at 2 hrs after resuscitation. H2O2 generation from isolated mitochondria were measured ex vivo at a normoxic and hyperoxic condition set up with nitrogen and air saturated medium. Results: Between the CA groups, the normoxia group had a higher 48hr-survival rate (77%), lower NDS (359±140), and lower LIS (4.3±2.9) compared to those (28%, 452±85, 14±2, respectively) of the hyperoxia group (p<0.01, p<0.05, and p<0.01, respectively). In the brain, lung, and kidney, CA augmented the hyperoxia-induced increase in carbonyl protein (absolute change: sham brain, 0.18 nmol/mg protein vs. CA brain, 0.61 nmol/mg protein; sham lung, 0.29 nmol/mg protein vs. CA lung, 0.72 nmol/mg protein; sham kidney, 0.04 nmol/mg protein vs. CA kidney, 0.55 nmol/mg protein, respectively). In the brain and kidney isolated mitochondria, CA augmented the hyperoxia-induced increase in H2O2 (absolute change: sham brain, 18 pmol/mg protein vs. CA brain, 60 pmol/mg protein; sham kidney, 16 pmol/mg protein vs. CA kidney, 45 pmol/mg protein, respectively). Conclusions: The normoxic therapy may attenuate organ damage and improve survival of CA. The reduction of augmented mitochondrial ROS generation, which is oxygen-sensitive, would be an important mechanism and therapeutic target of post-CA care.

scholarly journals Relationship between post-cardiac arrest myocardial oxidative stress and myocardial dysfunction in the rat

2014 ◽  
Vol 21 (1) ◽  
Author(s):  
Fernanda Schäfer Hackenhaar ◽  
Francesca Fumagalli ◽  
Giovanni Li Volti ◽  
Valeria Sorrenti ◽  
Ilaria Russo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Arrest ◽  
Myocardial Dysfunction ◽  
Myocardial Oxidative Stress
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