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Review
. 2013:2013:957054.
doi: 10.1155/2013/957054. Epub 2013 Dec 2.

Oxidative stress and antioxidant activity in hypothermia and rewarming: can RONS modulate the beneficial effects of therapeutic hypothermia?

Norma Alva  1 , Jesús Palomeque  1 , Teresa Carbonell  1
Affiliations
Review

Oxidative stress and antioxidant activity in hypothermia and rewarming: can RONS modulate the beneficial effects of therapeutic hypothermia?

Norma Alva et al. Oxid Med Cell Longev. 2013.

Abstract

Hypothermia is a condition in which core temperature drops below the level necessary to maintain bodily functions. The decrease in temperature may disrupt some physiological systems of the body, including alterations in microcirculation and reduction of oxygen supply to tissues. The lack of oxygen can induce the generation of reactive oxygen and nitrogen free radicals (RONS), followed by oxidative stress, and finally, apoptosis and/or necrosis. Furthermore, since the hypothermia is inevitably followed by a rewarming process, we should also consider its effects. Despite hypothermia and rewarming inducing injury, many benefits of hypothermia have been demonstrated when used to preserve brain, cardiac, hepatic, and intestinal function against ischemic injury. This review gives an overview of the effects of hypothermia and rewarming on the oxidant/antioxidant balance and provides hypothesis for the role of reactive oxygen species in therapeutic hypothermia.

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Figures

Figure 1
Figure 1
Portal vein flow (PVF) versus body temperature in anesthetized rats during cooling. After induction of anesthesia, animals were placed on a cooling/rewarming table. Animals were cooled at a mean rate of −0.25°C/min. Rats (n = 6) were intubated through the trachea and mechanically ventilated with room air. The portal vein circulation was analyzed using a laser-doppler blood flow meter by means of a fiberoptic probe positioned around the portal vein. The curve was calculated by taking the mean of PVF values of all the animals (referred to as a percentage of the starting point) at 5 min intervals and plotting each of these as one point. Note that blood flow is kept close to basal value during the beginning of the cooling (unshaded area) but it dropped drastically under 30 degrees of body temperature (shaded area) [33].
Figure 2
Figure 2
Modulation of apoptosis by hypothermia. After a serious insult the cell can trigger apoptosis, a highly regulated cell death mechanism. Intrinsic Pathway. Hypothermia increases ATP stores and slows ion channels then maintaining the integrity of the membranes. Hypothermia applied together or immediately after injury decreases the production of ROS. These events limit the rupture of the outer mitochondrial membrane and the release of proapoptotic molecules like cytochrome c into the cytosol. The hypothermia-induced increase in nitric oxide also avoids cytochrome c release and it is even reported that early NO production can exert a negative feedback regulation of iNOS [34]. Moreover, iNOS transcription activated by NFκB was diminished after hypothermia [35]. Since catalase is absent in mitochondria, maintaining GSH redox cycle is critical to avoid H2O2 accumulation. There is abundant evidence that hypothermia keeps GSH pool. Extrinsic Pathway. It was found that hypothermia decreases the affinity of the death ligands-death receptors, with the consequent inhibition of the initiator caspases like caspase-8 or the NFκB-family molecules.
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