Resuscitation from experimental heatstroke by brain cooling therapy

Hsiao, Sheng-Huang; Chang, Ching‐Ping; Chiu, Tsai-Hsien; Lin, Mao‐Tsun

doi:10.1016/j.resuscitation.2006.11.003

Cited by 35 publications

(24 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our previous results [6] have also demonstrated that WBC or brain cooling improves the outcomes of heatstroke by attenuating microvascular injury, thrombosis, inflammation, and apoptosis in several vital organs [6, 42, 43]. Together, both of our previous and present results suggest that WBC may improve outcomes of heatstroke via attenuating multiple organs (including lungs) dysfunction or failure.…”

Section: Discussionsupporting

confidence: 80%

Attenuation of Acute Lung Inflammation and Injury by Whole Body Cooling in a Rat Heatstroke Model

Yang

Chang

Cheng

et al. 2009

BioMed Research International

Self Cite

View full text Add to dashboard Cite

Whole body cooling is the current therapy of choice for heatstroke because the therapeutic agents are not available. In this study, we assessed the effects of whole body cooling on several indices of acute lung inflammation and injury which might occur during heatstroke. Anesthetized rats were randomized into the following groups and given (a) no treatment or (b) whole body cooling immediately after onset of heatstroke. As compared with the normothermic controls, the untreated heatstroke rats had higher levels of pleural exudates volume and polymorphonuclear cell numbers, lung myloperoxidase activity and inducible nitric oxide synthase expression, histologic lung injury score, and bronchoalveolar proinflammatory cytokines and glutamate, and PaCO2. In contrast, the values of mean arterial pressure, heart rate, PaO2, pH, and blood HCO3− were all significantly lower during heatstroke. The acute lung inflammation and injury and electrolyte imbalance that occurred during heatstroke were significantly reduced by whole body cooling. In conclusion, we identified heat-induced acute lung inflammation and injury and electrolyte imbalance could be ameliorated by whole body cooling.

show abstract

Section: Discussionsupporting

confidence: 80%

Attenuation of Acute Lung Inflammation and Injury by Whole Body Cooling in a Rat Heatstroke Model

Yang

Chang

Cheng

et al. 2009

BioMed Research International

Self Cite

View full text Add to dashboard Cite

show abstract

“…In a previous report [36], an increase in oxidative stress in the hippocampus, as detected by an increase in free radical production and NO levels, was observed in rat exposed to a simulated high altitude equivalent to 6100 m in an animal decompression chamber for 3-7 days. Our present results also showed that the non-HHP rats had an increase in free radical production and NO x level in the BALF after a simulated HAE of 6000 m (9.8 % O 2 at 0.47 ATA) for 24 h. 2,3-DHBA and NO x are two well-known markers of cellular oxidative damage markers [37,38]. Again, the HAEinduced oxidative damage in lungs was significantly reduced by HHP in rats.…”

Section: Discussionsupporting

confidence: 77%

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

et al. 2011

Self Cite

View full text Add to dashboard Cite

HHP (hypobaric hypoxia preconditioning) induces the overexpression of HSP70 (heat-shock protein 70), as well as tolerance to cerebral ischaemia. In the present study, we hypothesized that HHP would protect against HAE (high-altitude exposure)-induced acute lung injury and oedema via promoting the expression of HSP70 in lungs prior to the onset of HAE. At 2 weeks after the start of HHP, animals were exposed to a simulated HAE of 6000 m in a hypobaric chamber for 24 h. Immediately after being returned to ambient pressure, the non-HHP animals had higher scores of alveolar oedema, neutrophil infiltration and haemorrhage, acute pleurisy (e.g. increased exudate volume, increased numbers of polymorphonuclear cells and increased lung myeloperoxidase activity), increased pro-inflammatory cytokines [e.g. TNF-α (tumour necrosis factor-α), IL (interleukin)-1β and IL-6], and increased cellular ischaemia (i.e. glutamate and lactate/pyruvate ratio) and oxidative damage [glycerol, NOx (combined nitrate+nitrite) and 2,3-dihydroxybenzoic acid] markers in the BALF (bronchoalveolar fluid). HHP, in addition to inducing overexpression of HSP70 in the lungs, significantly attenuated HAE-induced pulmonary oedema, inflammation, and ischaemic and oxidative damage in the lungs. The beneficial effects of HHP in preventing the occurrence of HAE-induced pulmonary oedema, inflammation, and ischaemic and oxidative damage was reduced significantly by pretreatment with a neutralizing anti-HSP70 antibody. In conclusion, HHP may attenuate the occurrence of pulmonary oedema, inflammation, and ischaemic and oxidative damage caused by HAE in part via up-regulating HSP70 in the lungs.

show abstract

“…Indeed, plasma or cerebral levels of NO are elevated in heatstroke rats (27,28; present results). Aminoguanidine, an inducible nitric oxide synthase (iNOS) inhibitor, improves heat tolerance in the rat by preserving the splanchnic blood flow (29) and reducing intracranial hypertension and cerebral ischemia and damage (30).…”

Section: Stress Accordingly Cd34supporting

confidence: 61%

“…On the other hand, IL-10 has been shown to possess important anti-inflammatory and immunosuppressive properties through attenuation of TNF-α and other proinflammatory cytokines (34). In the present results, like brain cooling therapy (28), CD34…”

Section: Or Cd34mentioning

confidence: 50%

Human Umbilical Cord Blood–Derived CD34+ Cells Can Be Used as a Prophylactic Agent for Experimental Heatstroke

Hwang¹,

Chen²,

Lin³

et al. 2008

J Pharmacol Sci

Self Cite

View full text Add to dashboard Cite

Abstract. We attempted to assess the prophylactic effect of human umbilical cord bloodderived CD34+ cells in experimental heatstroke. Anesthetized rats, 1 day before heat stress, were divided into 2 major groups and given CD34 − cells (defined by 1 × 10 6 human cord blood lymphocytes and monocytes that contained <0.2% CD34 + cells) or CD34 + cells (defined by 1 × 10 6 human cord blood lymphocytes and monocytes that contained >95% CD34 + cells). They were exposed to ambient temperature of 43°C for 70 min to induce heatstroke. When the CD34 − cells-treated or untreated rats underwent heat stress, their survival time values were found to be 20 -24 min. Pretreatment with CD34+ cells significantly increased survival time (123 -351 min). As compared with normothermic controls, all CD34− cells-treated heatstroke animals displayed hypotension, hepatic and renal failure, hypercoagulable state, activated inflammation, and cerebral ischemia and injury. However, these heatstroke reactions all were significantly suppressed by CD34 + cells pretreatment. In addition, the levels of interlukin-10 in plasma and glial cell line-derived neurotrophic factors in brain were all significantly increased after CD34 + cell administration during heatstroke. Our data indicate that human umbilical cord-derived CD34 + cells can be used as a prophylactic agent for experimental heatstroke.

show abstract

Resuscitation from experimental heatstroke by brain cooling therapy

Cited by 35 publications

References 22 publications

Attenuation of Acute Lung Inflammation and Injury by Whole Body Cooling in a Rat Heatstroke Model

Attenuation of Acute Lung Inflammation and Injury by Whole Body Cooling in a Rat Heatstroke Model

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

Human Umbilical Cord Blood–Derived CD34+ Cells Can Be Used as a Prophylactic Agent for Experimental Heatstroke

Contact Info

Product

Resources

About