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 ; P < 0.05) and apoptosis-derived EMPs by ∼45% (from 46 ± 7 to 23 ± 3 microparticles μl ; P < 0.05). Likewise, circulating PMPs were reduced by ∼75% in response to hyperthermia (from 256 ± 43 to 62 ± 14 microparticles μl ). 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.

Cerebral metabolism, oxidation and inflammation in severe passive hyperthermia with and without respiratory alkalosis

“…Indeed, we have previously demonstrated that acute passive hyperthermia of +2°C core temperature causes a reduction in the concentration of circulating pro‐oxidative microparticles (Bain et al . ). Moreover, although IL‐6 is generally considered a sign of neural inflammation (Erta et al .…”

Passive heat therapy protects against endothelial cell hypoxia‐reoxygenation via effects of elevations in temperature and circulating factors

“…In addition, a recent study reported that acute passive heat stress reduces circulating levels of endothelial‐ and platelet‐derived microparticles (Bain et al . ). Elevated circulating levels of these particles are known to promote endothelial oxidative stress (Burger et al .…”

Whole‐body heat stress and exercise stimulate the appearance of platelet microvesicles in plasma with limited influence of vascular shear stress

“…A recent publication, however, reported reductions in arterial [PMV] (CD62P + – P‐selectin) in young men exposed to acute whole‐body passive heat stress, which elevated core temperature by +2°C (Bain et al. ). Currently, it is difficult to identify the reasons for such contradictory findings, but it may relate to the different sample preparation and storing protocols, distinct flow cytometer size resolution differences between studies, and the specificity of markers used for microvesicle population identification.…”

“…To adequately determine the impact of heat stress upon circulating [PMV], future studies need to assess the PMV time course with passive heat stress to establish whether the PMV concentrations increase initially, and then decline with higher levels of hyperthermia as suggested by Bain et al. ().…”

“…Our current experiments assessed MVs across both venous and arterial vessels show no decline with heat stress, but a possible increase in PMV concentration in the circulation. To adequately determine the impact of heat stress upon circulating [PMV], future studies need to assess the PMV time course with passive heat stress to establish whether the PMV concentrations increase initially, and then decline with higher levels of hyperthermia as suggested by Bain et al (2017).…”