Decreased heat tolerance is associated with hypothalamo-pituitary-adrenocortical axis impairment.
When rats are exposed to heat, they adapt themselves to the stressor with a wide inter-individual variability. Such differences in heat tolerance may be related to particularities in the hypothalamo-pituitary-adrenocortical (HPA) axis activation. To further this hypothesis, 80 rats instrumented with a telemetric device for abdominal temperature (Tabd) measurement were separated into two groups. Sixty-eight rats were exposed during 90 min at an ambient temperature of 40 degrees C, and 12 rats to an ambient temperature of 22 degrees C. Heat-exposed rats were then divided into three groups using the a posteriori k-means clustering method according to their Tabd level at the end of heat exposure. Heat tolerant rats (Tol, n=30) exhibiting the lowest Tabd showed a slight dehydration, a moderate triglyceride mobilization, but the highest plasma adrenocorticotropic-hormone (ACTH) and corticosterone levels. Conversely, heat exhausted rats (HE, n=14) presented the highest Tabd, a higher degree of dehydration, a greater metabolic imbalance with the lowest plasma triglyceride level and the highest lactate concentration, as well as a lowest plasma corticosterone and ACTH levels. The fact that the proopiomelanocortin (POMC) mRNA content within the pituitary was low despite of a high c-fos mRNA level is also relevant. Current inflammatory processes in HE rats were underlined by lower inhibitory factor kappaBalpha (IkappaBalpha) mRNA and higher tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) mRNA. In conclusion, data show that intolerance to heat exposure is associated to an HPA axis impairment, possibly related to changes occurring in the IkappaBalpha and TNF-alpha mRNA levels.
Michel
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Département des Facteurs Humains, Pôle de Neurophysiologie du Stress, Centre de Recherches du Service de Santé des Armées Emile Pardé, 24 Avenue des Maquis du Grésivaudan, F-38702 La Tronche Cédex, France. vmichel@crssa.net
Peinnequin
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Alonso
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Buguet
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Cespuglio
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Canini
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D000324:Adrenocorticotropic Hormone / Q000097:blood; D000818:Animals; D020013:Calcium Signaling / Q000502:physiology; D003345:Corticosterone / Q000097:blood; D003346:Corticotropin-Releasing Hormone / Q000096:biosynthesis / Q000235:genetics; D015870:Gene Expression / Q000502:physiology; D017781:Genes, Immediate-Early / Q000235:genetics; D018840:HSP70 Heat-Shock Proteins / Q000096:biosynthesis / Q000235:genetics; D018882:Heat Stress Disorders / Q000503:physiopathology*; D006400:Hematocrit; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology*; D018836:Inflammation Mediators / Q000378:metabolism; D047908:Intracellular Signaling Peptides and Proteins; D008297:Male; D010913:Pituitary-Adrenal System / Q000503:physiopathology*; D011333:Pro-Opiomelanocortin / Q000096:biosynthesis / Q000235:genetics; D012333:RNA, Messenger / Q000032:analysis / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013686:Telemetry; D014157:Transcription Factors / Q000096:biosynthesis / Q000235:genetics
D018840:HSP70 Heat-Shock Proteins; D018836:Inflammation Mediators; D047908:Intracellular Signaling Peptides and Proteins; C548050:RCAN1 protein, rat; D012333:RNA, Messenger; D014157:Transcription Factors; D011333:Pro-Opiomelanocortin; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone; D003345:Corticosterone