Pre-existing inflammatory state compromises heat tolerance in rats exposed to heat stress

Abstract

This study investigated the roles of endotoxemia and heat-induced tissue damage in the pathology of heat stroke. In groups of eight, male Wistar rats were treated with heat exposure only (HE), or heat exposure with turpentine (TϩHE), dexamethasone (DϩHE), and turpentine and dexamethasone combined (TDϩHE). The rats remained sedated for 2 h after receiving the respective treatments, followed by heat exposure until the core temperature (T c) was 42°C for 15 min; control rats received turpentine (T), dexamethasone (D), and turpentine and dexamethasone (TD) without heat stress. Blood samples were collected before treatment (baseline I), after 2 h of passive rest (baseline II), at T c 40°C (T40), and 15 min after achieving T c 42°C (T42). No rats died in the nonheat-stressed groups. Survival rate was lowest in the TDϩHE rats (37.5%), followed by the HE (62.5%), TϩHE (75%), and DϩHE (100%) rats (P Ͻ 0.05). The duration of survival at T42°C was shortest in the TDϩHE rats (9.9 Ϯ 6.2 min) (P Ͻ 0.01), followed by the TϩHE (11.3 Ϯ 6.1 min) and the HE (12.2 Ϯ 4 min) (P Ͻ 0.05) rats. The increase in plasma IL-6 concentrations was highest in the TϩHE (352%) and HE (178%) rats (P Ͻ 0.05). DϩHE treatment suppressed the increases in plasma aspartate transaminase, alanine aminotransferase, and IL-6 and LPS concentrations during severe heat stress. Heat stroke can be triggered by endotoxemia or heat-induced tissue damage, and preexisting inflammation compromises heat tolerance, whereas blocking endotoxemia increases heat tolerance.

Effect of housing conditions (clean vs. dirty) on growth performance and feeding behavior in growing pigs in a tropical climate

“…According to Renaudeau et al (2005), the capacity to eat during the hottest period of the day is an indicator of the ability to cope with heat stress. Based on this result and in agreement with studies made on rodents (Lim et al 2007), it could be hypothesised that bad sanitary status would negatively affect thermal tolerance in pigs.…”

Schisandra chinensis Prevents Hepatic Lipid Peroxidation and Oxidative Stress in Rats Subjected to Heat Environmental Stress

“…Changes in gene expression, which occur from a reaction to an environmental stressor, involve acute responses at the cellular level as well as changes in gene expression across a variety of organs and tissues associated with the acclimation response (Jian et al, 2008;Yan et al, 2009). In addition, exaggerated heat stress can lead to heat stroke, heat exhaustion, heat syncope and heat cramps (Kilbourne, 1997;Bouchama et al, 2005;Lim et al, 2007). Therefore, the control of the transcription factors in lipid metabolism and oxidative stress has been shown to be important in the treatment of heat stress and the prevention of disease induced by heat.…”

Cytokines and their role in hyperthermia and heat stroke

“…In turn, increased gut permeability gives rise to infiltration of endotoxins such as LPS from the digestive system into the blood, generating endotoxemia -a major contributor to the propagation of the inflammatory response in the event of heat stroke [61] , which underlies the production of pro-and anti-inflammatory cytokines such as TNF α , IL1 β , IL18, IL6, and IL1RA [25, 68 -70] . The inflammatory response to endotoxemia can be enhanced by pre-existing inflammation, as was demonstrated during lethal heat stroke in rats [79,80] .…”