Proceedings of The Physiological Society

Europhysiology 2018 (London, UK) (2018) Proc Physiol Soc 41, PCA346

Poster Communications

Acute hypoxia decreases microvascular endothelium-dependent function in healthy men

G. M. Rossetti1, D. T. Jones1, T. van Riessen2,1, H. E. Davies1, P. G. Mullins3, S. J. Oliver1, J. H. Macdonald1, A. Sandoo1

1. School of Sport, Health, & Exercise Sciences, Bangor Univeristy, Bangor, Gwynedd, United Kingdom. 2. Faculty of Medicine, University van Amsterdam, Amsterdam, Netherlands. 3. Bangor Imaging Unit, School of Psychology, Bangor Univeristy, Bangor, United Kingdom.

  • Fig 1. Microvascular function following 30-min exposure to normoxia and hypoxia. (A) PEndothelium-dependent microvascular function determined by percentage change in perfusion in response to iontophoresis of acetylcholine (ACh; p = 0.04). (B) Endothelium-independent microvascular function determined by percentage change in perfusion in response to iontophoresis of sodium nitroprusside (SNP; p = 0.7).

Previous studies have shown that hypoxia (whether acute or chronic) impairs endothelium-dependent and endothelium-independent macrovascular function. However, at present the effects of hypoxia on the microvasculature in humans are unknown. In disease states microvascular dysfunction often precedes macrovascular dysfunction, suggesting a causative role. Assessment of microvascular endothelial function is therefore important to help uncover the complex mechanisms of endothelial dysfunction. Thus, we aimed to examine whether hypoxia differentially affects endothelium-dependent and endothelium-independent microvascular function in healthy men. We hypothesized that acute hypoxia would decrease microvascular function. Eleven healthy men (Age: 23 (2) years, Height: 184 (5) cm, Body Mass: 82 (14) kg, VO2max: 53 (8) ml/kg/min) completed this randomised, double-blind, crossover study. Participants were exposed to 30-min normoxia (FIO2 = 0.21, sea level) or 30-min hypoxia (FIO2 = 0.12; equivalent ~5000m) before undergoing assessment of microvascular endothelial function using laser doppler imaging with iontophoresis of acetylcholine (ACh - endothelium-dependent) and sodium nitroprusside (SNP - endothelium-independent). Microvascular endothelial function was determined by calculating the percentage change in perfusion relative to baseline perfusion. Statistical difference between normoxia and hypoxia was determined by a combination of Wilcoxon signed rank test and Hodges-Lehmen 95% confidence intervals. The hypoxic exposure induced moderate hypoxaemia (SpO2 mean (SD): 79 (4) %). Baseline perfusion was not different between conditions (p = 0.9). Thirty minutes of hypoxia significantly impaired endothelium-dependent microvascular function compared to normoxia (% change in perfusion after ACh administration (median [IQR]): normoxia = 600 [324] %, hypoxia = 191 [295] %; p = 0.04; 95% CI [-437, -24]; Fig 1A), but did not alter endothelium-independent microvascular function (% change in perfusion after SNP administration: normoxia = 626 [602] %, hypoxia = 405 [630] %; p = 0.7; 95% CI [-256, 265]; Fig 1B). In conclusion, acute hypoxia impaired endothelium-dependent microvascular function in healthy men but did not affect endothelium-independent microvascular function. These findings suggest that in clinical conditions characterised by hypoxia (i.e. obstructive sleep apnoea), loss of nitric oxide-mediated dilatation may contribute to impairment in microvascular health and excess cardiovascular disease risk. Further studies examining the chronic effects of hypoxia on microvascular endothelial function are warranted.

Where applicable, experiments conform with Society ethical requirements