Hypothermic protection in an acute hypoxia model in rats: Acid-base and oxidant/antioxidant profiles.
OBJECTIVE
Recent works demonstrate the benefits of hypothermia when used to preserve brain, cardiac, hepatic, and intestinal function against hypoxic-ischemic injury. However, it is also known that hypothermia affects systemic parameters and also induces the generation of reactive oxygen species in cells and tissues. Here we studied the acid-base related parameters and the antioxidant-oxidant effects of deep hypothermia induction before an acute hypoxic insult in rats.


METHODS
Acid-base indicators and parameters related to oxidative stress were analyzed in hypothermic rats (21-22 degrees C) breathing room air during 2h (control hypothermia), and hypothermic animals switched to hypoxic air (10% O(2)) during the second hour (hypothermia hypoxia group), and they were compared with corresponding normothermia groups maintained at 37 degrees C (control normothermia and normothermia hypoxia groups).


RESULTS
Mild metabolic acidosis appeared early in arterial blood during hypothermia. After exposure to hypoxia, evidence of tissue injury (plasma transaminases and blood lactate) and oxidative stress (increase in lipid peroxidation, decrease in glutathione levels and in the glutathione reduction potential in liver) was found. In contrast, in the hypothermia hypoxia group, plasmatic parameters remained as the control values, and the hepatic glutathione reduction potential were significantly more negative when compared with the normothermia hypoxia group.


CONCLUSIONS
We propose that acidosis induced by hypothermia contributes to the maintenance of intracellular reduction potential in liver, regarding the GSSG/2GSH couple and may help to increase plasmatic antioxidant pool. Our findings provide new insights into the protective effects of hypothermia in vivo.
Alva
Norma
N
Departament de Fisiologia, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain. nvalva@ub.edu
Carbonell
Teresa
T
Palomeque
Jesús
J
D000136:Acid-Base Equilibrium / Q000502:physiology; D000138:Acidosis / Q000209:etiology / Q000378:metabolism*; D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001158:Arteries; D004195:Disease Models, Animal; D005978:Glutathione / Q000378:metabolism; D007035:Hypothermia / Q000150:complications / Q000378:metabolism*; D007036:Hypothermia, Induced; D000860:Hypoxia / Q000503:physiopathology / Q000628:therapy*; D007511:Ischemia / Q000503:physiopathology / Q000628:therapy; D019344:Lactic Acid / Q000097:blood; D015227:Lipid Peroxidation; D008099:Liver / Q000503:physiopathology*; D008297:Male; D016877:Oxidants / Q000378:metabolism*; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D051381:Rats; D000637:Transaminases / Q000097:blood
D000975:Antioxidants; D016877:Oxidants; D019344:Lactic Acid; D000637:Transaminases; D005978:Glutathione