Oliver R Gibson, Orlando Laitano, Kazuhito Watanabe, José González-Alonso
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引用次数: 0
Abstract
Hyperthermia can cause intestinal injury, facilitating endotoxin translocation and an inflammatory response that has been associated with heat illness. However, the potential occurrence of these responses has been incompletely reported during passive hyperthermia, and the independent effect of hyperthermia is equivocal. Furthermore, passive hyperthermia is a feature of heat therapy interventions, with mechanistic understanding developing. This experiment quantified the changes in intestinal fatty acid binding protein (iFABP), a marker of intestinal injury, and cytokine, chemokine and growth factor responses during three different prolonged passive hyperthermia protocols. Eight healthy males visited the laboratory on four counterbalanced occasions to undertake 2.5 h of rest (CON), one-leg heating (OLH), two-leg heating (TLH) and whole-body heating (WBH) via a garment circulating water at 50°C. Plasma concentrations of iFABP and 38 cytokines, chemokines and growth factors were quantified periodically, and core temperature (Tcore) was measured continuously. The Tcore increased from baseline in OLH, TLH and WBH (+0.4°C ± 0.2°C, +0.7°C ± 0.2°C and +2.3°C ± 0.4°C, respectively; P < 0.05) but remained unchanged in CON. iFABP increased from baseline in WBH only (∆587 ± 651 pg ml-1) and was different from CON and OLH in WBH after 2 h (P < 0.05). Increased iFABP (∆1085 ± 572 pg ml-1) was observed in 50% of participants at the end of WBH, with the other 50% demonstrating no change (∆89 ± 19 pg ml-1). All chemokines, cytokines and growth factors were unchanged in all protocols. These data indicate that passive whole-body hyperthermia, but not lower-limb hyperthermia, can cause intestinal injury in some individuals without a systemic inflammatory response.
期刊介绍:
Experimental Physiology publishes research papers that report novel insights into homeostatic and adaptive responses in health, as well as those that further our understanding of pathophysiological mechanisms in disease. We encourage papers that embrace the journal’s orientation of translation and integration, including studies of the adaptive responses to exercise, acute and chronic environmental stressors, growth and aging, and diseases where integrative homeostatic mechanisms play a key role in the response to and evolution of the disease process. Examples of such diseases include hypertension, heart failure, hypoxic lung disease, endocrine and neurological disorders. We are also keen to publish research that has a translational aspect or clinical application. Comparative physiology work that can be applied to aid the understanding human physiology is also encouraged.
Manuscripts that report the use of bioinformatic, genomic, molecular, proteomic and cellular techniques to provide novel insights into integrative physiological and pathophysiological mechanisms are welcomed.