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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Effect of moderate hypothermia on lipid peroxidation in canine brain tissue after cardiac arrest and resuscitation.

BACKGROUND AND PURPOSE--We sought to examine the effect of moderate hypothermia (30 degrees C to 32 degrees C) initiated after resuscitation on the scavenging systems of free radicals and lipid peroxidation in canine brain tissue after cardiac arrest and resuscitation. METHODS--Twenty-one dogs were divided into four groups: group A, nonischemic controls (shams) (n = 4); group B, 15-minute cardiac arrest without reperfusion (n = 4); group C, 15-minute cardiac arrest and standard resuscitation (n = 6); and group D, 15-minute cardiac arrest and hypothermic resuscitation (n = 7). During the period of 10 to 120 minutes after resuscitation, brain temperature and core temperature in group D remained at 30 degrees C to 32 degrees C and were 4 degrees C to 5 degrees C lower than in group C. For each dog, a sample of right parietal cerebral cortex was obtained from group A, group B, or from group C and group D at 2 hours after resuscitation. The sample was assayed for tissue malondialdehyde (MDA), the content of reduced glutathione (GSH), and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX). RESULTS--In group B, a 15-minute cardiac arrest induced an increase in MDA, a significant reduction of GSH, and no change in SOD and GSH-PX activities compared with group A. In group C, there were further increases in MDA and reductions in GSH content and GSH-PX activity compared with group A; SOD activity remained substantially unchanged. The content of MDA was higher in group D than in group A but less elevated in group D than in group C. The GSH content and SOD and GSH-PX activities were significantly higher in group D than in group C. CONCLUSIONS--Moderate hypothermia initiated after resuscitation can significantly inhibit the accumulation of lipid peroxidation products and the consumption of free radical scavengers in the brain tissue.[1]

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