Passive heat stress reduces circulating endothelial and platelet microparticles

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 degrees C oesophageal temperature). Ten healthy young men (age 23 +/- 3years) completed the study. Hyperthermia was achieved by circulating approximate to 49 degrees 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 degrees C and in hyperthermia 39.1 +/- 0.1 degrees C. Concentrations of circulating EMPs and PMPs were markedly decreased in hyperthermia. Activation-derived EMPs were reduced by approximate to 30% (mean +/- SD; from 61 +/- 8 to 43 +/- 7microparticlesl(-1); P<0.05) and apoptosis-derived EMPs by approximate to 45% (from 46 +/- 7 to 23 +/- 3microparticlesl(-1); P<0.05). Likewise, circulating PMPs were reduced by approximate to 75% in response to hyperthermia (from 256 +/- 43 to 62 +/- 14microparticlesl(-1)). These beneficial reductions in circulating EMPs and PMPs in response to a 2 degrees C increase in core temperature might partly underlie the reported vascular improvements following therapeutic bouts of physiological hyperthermia.