The physiological consequences of environment-induced heat stress (EIHS), caused by prolonged exposure to excess heat and humidity, are largely unknown. The purpose of this investigation was to determine the extent to which EIHS alters cardiac health. We hypothesized that 24 h of EIHS would cause cardiac injury and cellular dysfunction in a murine EIHS model. To test this hypothesis, 7-wk-old female mice were housed under thermoneutral (TN) conditions ( = 12; 31.2 ± 1.01°C, 35 ± 0.7% humidity) or EIHS conditions ( = 14; 37.6 ± 0.01°C, 42.0 ± 0.06% humidity) for 24 h. Environment-induced heat stress increased rectal temperature by 2.1°C ( < 0.01) and increased subcutaneous temperature by 1.8°C ( < 0.01). Body weight was decreased by 10% ( = 0.03), heart weight/body weight was increased by 26% ( < 0.01), and tissue water content was increased by 11% ( < 0.05) in EIHS compared with TN. In comparison with TN, EIHS increased protein abundance of heat shock protein (HSP) 27 by 84% ( = 0.01); however, HSPs 90, 60, 70, and phosphorylated HSP 27 were similar between groups. Histological inspection of the heart revealed that EIHS animals had increased myocyte vacuolation in the left ventricle ( = 0.01), right ventricle ( < 0.01), and septum ( = 0.01) compared with TN animals. Biochemical indices are suggestive of mitochondrial remodeling, increased autophagic flux, and robust activation of endoplasmic reticulum stress in hearts from EIHS mice compared with TN mice. These data demonstrate that 1 day of EIHS is sufficient to induce myocardial injury and biochemical dysregulation. The consequences of prolonged environment-induced heat stress (EIHS) on heart health are largely unknown. We discovered that a 24-h exposure to environmental conditions sufficient to cause EIHS resulted in cardiac edema and histopathologic changes in the right and left ventricles. Furthermore, among other biochemical changes, EIHS increased autophagic flux and caused endoplasmic reticulum stress. These data raise the possibility that thermic injury, even when insufficient to cause heat stroke, can damage the myocardium.
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http://dx.doi.org/10.1152/ajpheart.00180.2024 | DOI Listing |
Am J Physiol Heart Circ Physiol
October 2024
Department of Animal Science, Iowa State University, Ames, Iowa, United States.
The physiological consequences of environment-induced heat stress (EIHS), caused by prolonged exposure to excess heat and humidity, are largely unknown. The purpose of this investigation was to determine the extent to which EIHS alters cardiac health. We hypothesized that 24 h of EIHS would cause cardiac injury and cellular dysfunction in a murine EIHS model.
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April 2024
Department of Biology, McMaster University, Hamilton, ON, Canada, L8S 4K1.
During maximal cold challenge (cold-induced V̇O2,max) in hypoxia, highland deer mice (Peromyscus maniculatus) show higher rates of circulatory fatty acid delivery compared with lowland deer mice. Fatty acid delivery also increases with acclimation to cold hypoxia (CH) and probably plays a major role in supporting the high rates of thermogenesis observed in highland deer mice. However, it is unknown which tissues take up these fatty acids and their relative contribution to thermogenesis.
View Article and Find Full Text PDFPolymers (Basel)
February 2024
Key Laboratory of Enhanced Heat Transfer and Energy Conservation of Education Ministry, School of Chemistry and Chemical Engineering, South China University of Technology, Guangzhou 510640, China.
Natural environment hosts a considerable amount of accessible energy, comprising mechanical, thermal, and chemical potentials. Environment-induced nanogenerators are nanomaterial-based electronic chips that capture environmental energy and convert it into electricity in an environmentally friendly way. Polymers, characterized by their superior flexibility, lightweight, and ease of processing, are considered viable materials.
View Article and Find Full Text PDFJ Exp Zool A Ecol Integr Physiol
June 2024
Department of Convergence Study on the Ocean Science and Technology, Korea Maritime and Ocean University, Busan, Korea.
The effects of red light-emitting diode (LED) light irradiation (630 nm, 0.5 W/m) and melatonin (10 and 10M) on oxidative stress and physiological responses in abalones exposed to high temperatures (28°C) were investigated. Changes in messenger RNA (mRNA) expressions of melatonin receptor (MT-R), heat shock protein 70 (HSP70), and antioxidant enzymes, as well as alterations in HO levels in the hemolymph, were examined.
View Article and Find Full Text PDFExp Eye Res
March 2024
North Texas Eye Research Institute, University of North Texas Health Science Center, 3430 Camp Bowie Blvd, Fort Worth, TX, 76107, USA; Department of Pharmaceutical Sciences, University of North Texas Health Science Center, 3430 Camp Bowie Blvd, Fort Worth, TX, 76107, USA; Department of Pharmacology and Neuroscience, University of North Texas Health Science Center, 3430 Camp Bowie Blvd, Fort Worth, TX, 76107, USA. Electronic address:
Corneal dysfunctions associated with Diabetes Mellitus (DM), termed diabetic keratopathy (DK), can cause impaired vision and/or blindness. Hypoxia affects both Type 1 (T1DM) and Type 2 (T2DM) surprisingly, the role of hypoxia in DK is unexplored. The aim of this study was to examine the impact of hypoxia in vitro on primary human corneal stromal cells derived from Healthy (HCFs), and diabetic (T1DMs and T2DMs) subjects, by exposing them to normoxic (21% O) or hypoxic (2% O) conditions through 2D and 3D in vitro models.
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