Impact of passive heat stress and passive heat acclimation on circulating extracellular vesicles: An exploratory analysis

Ravanelli, Nicholas; Barry, Hadiatou; Bain, Anthony R.; Vachon, Laurent; Martel, Catherine; Gagnon, Daniel

doi:10.1113/ep090823

Cited by 1 publication

(6 citation statements)

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Section: Discussionsupporting

confidence: 89%

“…In the cerebral venous circulation, we found no change in circulating endothelial microvesicles (either activated or apoptotic) with poikilocapnic hyperthermia. This is in line with all other studies performed in healthy young participants (Coombs et al, 2019;Ravanelli et al, 2023;Wilhelm et al, 2017) where endothelial microvesicles were collected from the peripheral venous circulation. Interestingly, however, Coombs et al (2019) reported reductions in activated endothelial microvesicles in the venous circulation with passive heating in patients with spinal cord injury, probably attributable to the higher baseline values of venous endothelial microvesicles in this demographic.…”

Section: Microvesicles In Passive Poikilocapnic Hyperthermiasupporting

confidence: 89%

“…Broadly, across all studies and subsets of microvesicles (i.e. from all cell sources and vascular beds), passive heat stress can cause no change (Coombs et al., 2019; Ravanelli et al., 2023; Wilhelm et al., 2017), an increase (Ravanelli et al., 2023; Wilhelm et al., 2017) or even a slight decrease in microvesicles (Bain et al., 2017). However, a more nuanced (and appropriate) analysis suggests that the ‘noise’ relates to: (i) differences in thermal strain (e.g.…”

Section: Discussionmentioning

confidence: 99%

“…However, the effect of hyperthermia on microvesicle release is difficult to ascertain. For example, many factors appear to impact their concentrations in hyperthermia, including the magnitude of the increase in temperature, the location (venous or arterial) and the cellular origin of the microvesicle (Bain et al., 2017; Coombs et al., 2019; Ravanelli et al., 2023; Wilhelm et al., 2017).…”

Section: Introductionmentioning

confidence: 99%

“…Arterial pH might therefore be a factor in the alterations in microvesicle concentrations in heat stress. The respiratory‐induced alkalosis might counter a thermally mediated increase in microvesicle release (as observed in cancer cells; Otsuka et al., 2020), perhaps explaining why microvesicles derived from endothelial cells are typically unchanged (Coombs et al., 2019; Ravanelli et al., 2023) with passive alkalotic hyperthermia.…”

Section: Introductionmentioning

confidence: 99%

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Cerebral uptake of microvesicles occurs in normocapnic but not hypocapnic passive hyperthermia in young healthy male adults

Parikh,

Shepley,

Tymko

et al. 2023

The Journal of Physiology

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Passive hyperthermia causes cerebral hypoperfusion primarily from heat‐induced respiratory alkalosis. However, despite the cerebral hypoperfusion, it is possible that the mild alkalosis might help to attenuate cerebral inflammation. In this study, the cerebral exchange of extracellular vesicles (microvesicles), which are known to elicit pro‐inflammatory responses when released in conditions of stress, were examined in hyperthermia with and without respiratory alkalosis. Ten healthy male adults were heated passively, using a warm water‐perfused suit, up to core temperature + 2°C. Blood samples were taken from the radial artery and internal jugular bulb. Microvesicle concentrations were determined in platelet‐poor plasma via cells expressing CD62E (activated endothelial cells), CD31+/CD42b− (apoptotic endothelial cells), CD14 (monocytes) and CD45 (pan‐leucocytes). Cerebral blood flow was measured via duplex ultrasound of the internal carotid and vertebral arteries to determine cerebral exchange kinetics. From baseline to poikilocapnic (alkalotic) hyperthermia, there was no change in microvesicle concentration from any cell origin measured (P‐values all >0.05). However, when blood CO2 tension was normalized to baseline levels in hyperthermia, there was a marked increase in cerebral uptake of microvesicles expressing CD62E (P = 0.028), CD31+/CD42b− (P = 0.003) and CD14 (P = 0.031) compared with baseline, corresponding to large increases in arterial but not jugular venous concentrations. In a subset of seven participants who underwent hypercapnia and hypocapnia in the absence of heating, there was no change in microvesicle concentrations or cerebral exchange, suggesting that hyperthermia potentiated the CO2/pH‐mediated cerebral uptake of microvesicles. These data provide insight into a potential beneficial role of respiratory alkalosis in heat stress. imageKey points The hyperthermia‐induced hyperventilatory response is observed in most humans, despite causing potentially harmful reductions in cerebral blood flow. We tested the hypothesis that the respiratory‐induced alkalosis is associated with lower circulating microvesicle concentrations, specifically in the brain, despite the reductions in blood flow. At core temperature + 2°C with respiratory alkalosis, microvesicles derived from endothelial cells, monocytes and leucocytes were at concentrations similar to baseline in the arterial and cerebral venous circulation, with no changes in cross‐brain microvesicle kinetics. However, when core temperature was increased by 2°C with CO2/pH normalized to resting levels, there was a marked cerebral uptake of microvesicles derived from endothelial cells and monocytes. The CO2/pH‐mediated alteration in cerebral microvesicle uptake occurred only in hyperthermia. These new findings suggest that the heat‐induced hyperventilatory response might serve a beneficial role by preventing potentially inflammatory microvesicle uptake in the brain.

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Section: Discussionsupporting

confidence: 89%