Bain Anthony R, Ainslie Philip N, Bammert Tyler D, Hijmans Jamie G, Sekhon Mypinder, Hoiland Ryan L, Flück Daniela, Donnelly Joseph, DeSouza Christopher A
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.
Exp Physiol. 2017 Jun 1;102(6):663-669. doi: 10.1113/EP086336.
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.
本研究的核心问题是什么？食管温度升高2°C的被动热应激是否会改变健康成年人循环动脉中内皮细胞衍生和血小板衍生的微粒浓度？主要发现及其重要性是什么？热应激时循环内皮细胞衍生和血小板衍生的微粒浓度显著降低。循环微粒的减少可能表明与非病理性体温过高相关的有利血管变化。由于循环内皮细胞衍生和血小板衍生的微粒（分别为EMPs和PMPs）在血管疾病中的潜在致病作用以及作为血管健康的生物标志物，人们对它们的兴趣增加了。体温过高通常与促炎应激相关，但当体温升高为非病理性时也可能提供血管保护。循环微粒可能有助于体温过高时的细胞调节和由此产生的血管影响。在此，我们确定被动热应激（食管温度升高2°C）是否会改变动脉EMPs和PMPs的循环浓度。10名健康年轻男性（年龄23±3岁）完成了该研究。通过使约49°C的水通过覆盖除手、脚和头部之外的整个身体的水灌注服来实现体温过高。在加热前（正常体温）和体温过高时立即采集动脉（桡动脉）血样。正常体温下食管温度的平均值±标准差为37.2±0.1°C，体温过高时为39.1±0.1°C。体温过高时循环EMPs和PMPs的浓度显著降低。激活衍生的EMPs减少了约30%（平均值±标准差；从61±8降至43±7个微粒/微升；P<0.05），凋亡衍生的EMPs减少了约45%（从46±7降至23±3个微粒/微升；P<0.05）。同样，响应体温过高，循环PMPs减少了约7５%（从256±43降至62±14个微粒/微升）。核心温度升高2°C时循环EMPs和PMPs的这些有益降低可能部分是治疗性生理性体温过高后报告的血管改善的基础。
