Chronic Hypoxia Preconditioning Increases Survival In Rats Suffering From Heatstroke

Abstract

1. In the present study, we assessed the protective effects of chronic hypoxia preconditioning against heatstroke-induced injury in urethane-anaesthetized rats. Heatstroke was induced by exposing the animals to an ambient temperature of 42 degrees C. The time at which both the mean arterial pressure (MAP) and local cerebral blood flow (CBF) in the striatum began to decrease from peak levels was taken as the onset of heatstroke. Control rats were exposed to a temperature of 24 degrees C. 2. Mean arterial pressure, CBF, blood pH, PaO2, PaCO2 and survival time (the interval between onset of heatstroke and cardiac arrest) after heat stress were all lower than in control rats (in which 'survival time' was defined as > 360 min). However, blood lactate concentrations were greater in rats exposed to heat. Rats placed at high altitude (HA), when exposed to the same heat stress (42 degrees C) survived much longer (113 +/- 26 min; n = 8) than rats maintained at sea level (SL; 20 +/- 2 min; n = 8). 3. After the onset of heatstroke, blood pH and lactate concentrations were found to be significantly higher and lower, respectively, in HA rats than in SL rats. 4. Western blot assay revealed that chronic hypoxia preconditioning induced heat shock protein (HSP) 72 expression in both the kidneys and lungs. 5. Thus, it appears that the observed benefit of chronic hypoxia preconditioning is related to attenuation of tissue acidification and elevations of HSP72 expression in both kidneys and lungs during heatstroke.

Cross tolerance to environmental stressors: Effects of hypoxic acclimation on cardiovascular responses of channel catfish (Ictalurus punctatus) to a thermal challenge

“…Previous studies have shown cross tolerance between hypoxia/anoxia and high temperature stress in a variety of taxa: mammals (rats) (Wen et al, 2002; Tetievsky et al, 2008), insects ( Locusta migratoria ) (Wu et al, 2002), nematodes ( C. elegans ) (Treinin et al, 2003) and plants ( Arabidopsis ) (Banti et al, 2008). Although cross tolerance appears to be a widespread phenomenon, similarities and/or differences in the physiological mechanisms across different organisms have yet to be determined.…”

“…It has been shown in diverse organisms, from plants to vertebrates, that HIF (hypoxia-inducible factor) and HSP (heat shock proteins) are generically activated by either stress, and exposure to one often confers increased resistance to the other (Wen et al, 2002; Wu et al, 2002; Banti et al, 2008; Tetievsky et al, 2008). This suggests that HSP and HIF are probably part of a more generalized response to stress and not specific to either hypoxia or temperature.…”

CEREBROVASCULAR DYSFUNCTION IS AN ATTRACTIVE TARGET FOR THERAPY IN HEAT STROKE¶

“…During heat stroke, rodents display hyperthermia, arterial hypotension, intracranial hypertension, cerebral ischaemia, neuronal damage and overproduction of inflammatory cytokines (including TNF‐α and IL‐1) 16 . The above‐mentioned heat stroke syndromes can be attenuated by induction of HSP72 in multiple organs (including the heart and brain) with external heat shock, 130–133 chronic hypoxia 133 or regular exercise 134 . Preconditioning with HSP72 conferred significant protection against hyperthermia, arterial hypotension, decreased cardiac output, decreased stroke volume, decreased peripheral vascular resistance and increased levels of serum or tissue TNF‐α during heat stroke 130–135 .…”

Hypobaric hypoxia preconditioning attenuates acute lung injury during high-altitude exposure in rats via up-regulating heat-shock protein 70

“…In addition, brief hypoxia causes the overexpression of HSP (heat-shock protein)-70 as well as tolerance to focal cerebral hypoxia in rats [18]. Our previous results have shown that the observed benefit of HHP (hypobaric hypoxia preconditioning) was related to an increase in HSP70 overexpression in both the kidneys and lungs during heatstroke [19]. However, whether HHP protects against pulmonary vasoconstriction and systemic accumulation of oxidative/nitrosative/inflammatory stress biomarkers at high altitude via promoting the appearance of HSP70 in lungs prior to the onset of HAE (high-altitude exposure) remains unknown [20].…”