title: Passive heat stress reduces circulating endothelial and platelet microparticles.
abstract: What is the central question of this study? Does passive heat stress of +2°C oesophageal temperature change concentrations of circulating arterial endothelial- and platelet-derived microparticles in healthy adults? What is the main finding and its importance? Concentrations of circulating endothelial- and platelet-derived microparticles were markedly decreased in heat stress. Reductions in circulating microparticles might indicate favourable vascular changes associated with non-pathological hyperthermia. Interest in circulating endothelial- and platelet-derived microparticles (EMPs and PMPs, respectively) has increased because of their potential pathogenic role in vascular disease and as biomarkers for vascular health. Hyperthermia is commonly associated with a pro-inflammatory stress but might also provide vascular protection when the temperature elevation is non-pathological. Circulating microparticles might contribute to the cellular adjustments and resultant vascular impacts of hyperthermia. Here, we determined whether circulating concentrations of arterial EMPs and PMPs are altered by passive heat stress (+2°C oesophageal temperature). Ten healthy young men (age 23 ± 3 years) completed the study. Hyperthermia was achieved by circulating ∼49°C water through a water-perfused suit that covered the entire body except the hands, feet and head. Arterial (radial) blood samples were obtained immediately before heating (normothermia) and in hyperthermia. The mean ± SD oesophageal temperature in normothermia was 37.2 ± 0.1°C and in hyperthermia 39.1 ± 0.1°C. Concentrations of circulating EMPs and PMPs were markedly decreased in hyperthermia. Activation-derived EMPs were reduced by ∼30% (mean ± SD; from 61 ± 8 to 43 ± 7 microparticles μl-1; P < 0.05) and apoptosis-derived EMPs by ∼45% (from 46 ± 7 to 23 ± 3 microparticles μl-1; P < 0.05). Likewise, circulating PMPs were reduced by ∼75% in response to hyperthermia (from 256 ± 43 to 62 ± 14 microparticles μl-1). These beneficial reductions in circulating EMPs and PMPs in response to a 2°C increase in core temperature might partly underlie the reported vascular improvements following therapeutic bouts of physiological hyperthermia.
authors.affiliation: Department of Integrative Physiology, Integrative Vascular Biology Laboratory, University of Colorado, Boulder, CO, USA.|Faculty of Health and Social Development, Centre for Heart, Lung & Vascular Health, University of British Columbia, Kelowna, BC, Canada.
authors.forename: Anthony R
authors.identifier: 0000-0001-7910-6921
authors.initials: AR
authors.lastname: Bain
authors.affiliation: Faculty of Health and Social Development, Centre for Heart, Lung & Vascular Health, University of British Columbia, Kelowna, BC, Canada.
authors.forename: Philip N
authors.initials: PN
authors.lastname: Ainslie
authors.affiliation: Department of Integrative Physiology, Integrative Vascular Biology Laboratory, University of Colorado, Boulder, CO, USA.
authors.forename: Tyler D
authors.initials: TD
authors.lastname: Bammert
authors.affiliation: Department of Integrative Physiology, Integrative Vascular Biology Laboratory, University of Colorado, Boulder, CO, USA.
authors.forename: Jamie G
authors.initials: JG
authors.lastname: Hijmans
authors.affiliation: Faculty of Health and Social Development, Centre for Heart, Lung & Vascular Health, University of British Columbia, Kelowna, BC, Canada.|Division of Critical Care Medicine and Department of Medicine, University of British Columbia, Vancouver, BC, Canada.
authors.forename: Mypinder
authors.initials: M
authors.lastname: Sekhon
authors.affiliation: Faculty of Health and Social Development, Centre for Heart, Lung & Vascular Health, University of British Columbia, Kelowna, BC, Canada.
authors.forename: Ryan L
authors.identifier: 0000-0002-5657-0059
authors.initials: RL
authors.lastname: Hoiland
authors.affiliation: Faculty of Health and Social Development, Centre for Heart, Lung & Vascular Health, University of British Columbia, Kelowna, BC, Canada.
authors.forename: Daniela
authors.initials: D
authors.lastname: Flück
authors.affiliation: Brain Physics Laboratory, Division of Academic Neurosurgery, Department of Clinical Neurosciences, Addenbrookes Hospital, University of Cambridge, Cambridge, UK.
authors.forename: Joseph
authors.identifier: 0000-0002-6502-8069
authors.initials: J
authors.lastname: Donnelly
authors.affiliation: Department of Integrative Physiology, Integrative Vascular Biology Laboratory, University of Colorado, Boulder, CO, USA.
authors.forename: Christopher A
authors.identifier: 0000-0001-9372-5083
authors.initials: CA
authors.lastname: DeSouza
mesh_terms: D000328:Adult; D017209:Apoptosis / Q000502:physiology; D001792:Blood Platelets / Q000502:physiology*; D055252:Cell-Derived Microparticles / Q000502:physiology*; D004730:Endothelium, Vascular / Q000502:physiology*; D005334:Fever / Q000503:physiopathology; D006358:Hot Temperature; D006801:Humans; D008297:Male; D013312:Stress, Physiological / Q000502:physiology*; D055815:Young Adult
keywords: Hyperthermia; Microvesicles; Vascular Physiology; Vascular inflammation