Review paperTemperature regulation in laboratory mammals following acute toxic insult
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Role of TRPA1 in acute cardiopulmonary toxicity of inhaled acrolein
2017, Toxicology and Applied PharmacologyCitation Excerpt :The systemic benefit of the combined TRPA1 + V1 antagonist treatment (as used herein) also is described in a model of pancreatic cancer pain (Schwartz et al., 2011). Nonetheless, the specific mechanism and site of protection of TRPA1 or combined TRPA1 + TRPV1 antagonism remain to be elucidated although it does not appear to be due to stimulation of an increased breathing rate or inhibition of the well-known, robust rodent ‘hypothermic response’ (Gordon et al., 1988) or hyperthermia (see Suppl. Figs. 6 & 7). Because the TRPA1 antagonist was administered intraperitoneally, we infer the treatment primarily targeted pulmonary vascular TRPA1 more so than other sites, e.g., airway sensory fiber or CNS TRPA1 (see Graphical abstract).
Modification of the effects of air pollutants on mortality by temperature: A systematic review and meta-analysis
2017, Science of the Total EnvironmentCitation Excerpt :Heat may promote thrombosis through increasing blood viscosity and cholesterol levels secondary to dehydration and salt depletion (Bouchama and Knochel, 2002; McGeehin and Mirabelli, 2001). Similarly, the weaker effects of PM10 on cardiovascular mortality on low temperature days may result from slower physiological functions at lower temperature attenuating the toxicity of environmental pollutants (Gordon et al., 1988; Watkinson et al., 2003). We found a non-monotonic effect of ozone with increasing temperature, that is, both extreme high and low temperature enhanced the effect of O3 on non-accidental and cardiovascular mortality.
Risk assessment in combustion toxicology: Should carbon dioxide be recognized as a modifier of toxicity or separate toxicological entity?
2016, Toxicology LettersCitation Excerpt :The resultant hypothermia would be advantageous to an animal living in a poorly ventilated burrow or any other hostile environment. Hence, amongst the most important rodent-specific response to such stressors is hypothermia that decreases metabolism resulting in less O2 demand and CO2 production (for details see Gordon, 1990, 1993, 2005; Gordon et al., 1988. Due to their smaller thermal inertia, mice may attain hypothermia even faster than rats (Gordon et al., 2007).
Therapeutic hypothermia after cardiac arrest caused by self-inflicted intoxication: A multicenter retrospective cohort study
2014, American Journal of Emergency MedicineAcute inhalation toxicity of ammonia: Revisiting the importance of RD<inf>50</inf> and LCT<inf>01/50</inf> relationships for setting emergency response guideline values
2013, Regulatory Toxicology and PharmacologyCitation Excerpt :Due to their small thermal inertia, unlike humans, small laboratory rodents undergo a typical hypothermic response when exposed to this type of respiratory tract irritants. Consequently, the ten-fold lower body weights makes mice even more thermolabile than rats (Gordon et al., 1988; Gordon, 1993; Pauluhn and Mohr, 2000). Hence, mice appear to be the least suitable species to extrapolate from to man because of their extreme hypothermic response and associated physiological response when exposed to sensory irritants (Gordon et al., 2008) superimposed by the alkalinity of ammonia.