Abstract

Although acute hypoxia is of utmost pathophysiologic relevance in health and disease, studies on its effects on both the macro- and microcirculation are scarce. Herein, we provide a comprehensive analysis of the effects of acute normobaric hypoxia on human macro- and microcirculation. 20 healthy participants were enrolled in this study. Hypoxia was induced in a normobaric hypoxia chamber by decreasing the partial pressure of oxygen in inhaled air stepwisely (pO2; 21.25 kPa (0 k), 16.42 kPa (2 k), 12.63 kPa (4 k) and 9.64 kPa (6 k)). Macrocirculatory effects were assessed by cardiac output measurements, microcirculatory changes were investigated by sidestream dark-field imaging in the sublingual capillary bed and videocapillaroscopy at the nailfold. Exposure to hypoxia resulted in a decrease of systemic vascular resistance (p < 0.0001) and diastolic blood pressure (p = 0.014). Concomitantly, we observed an increase in heart rate (p < 0.0001) and an increase of cardiac output (p < 0.0001). In the sublingual microcirculation, exposure to hypoxia resulted in an increase of total vessel density, proportion of perfused vessels and perfused vessel density. Furthermore, we observed an increase in peripheral capillary density. Exposure to acute hypoxia results in vasodilatation of resistance arteries, as well as recruitment of microvessels of the central and peripheral microcirculation. The observed macro- and microcirculatory effects are most likely a result from compensatory mechanisms to ensure adequate tissue oxygenation.

Highlights

  • LLS Lake Louise Score NC Number of crossings NIRS Near-infrared spectroscopy PCD Peripheral capillary recruitment pCO2 Partial pressure of carbon dioxide perfused number of crossings (PNC) Perfused number of crossings pO2 Partial pressure of oxygen proportion of perfused vessels (PPV) Proportion of perfused vessels perfused vessel density (PVD) Perfused vessel density systolic blood pressure (SBP) Systolic blood pressure stroke volume (SV) Stroke volume SVR Systemic vascular resistance total hemoglobin concentration (THb) Total hemoglobin concentration tissue saturation index (TSI) Tissue saturation index total vessel density (TVD) Total vessel density

  • Hypoxic stress initiates a transcriptional response by hypoxia inducible factors (HIF; during intermittent hypoxia predominately HIF-1α10–12), which leads to a reduction of cellular energy consumption, a secretion of pro-angiogenic and survival ­factors[10], and qualitative changes in mitochondrial ­function[13], which in turn results in alterations of the cardiovascular, haematological and even urinary ­physiology[14,15]

  • We enrolled 20 healthy subjects in this study, who had no significant experience in climbing or competitive sports

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Summary

Introduction

LLS Lake Louise Score NC Number of crossings NIRS Near-infrared spectroscopy PCD Peripheral capillary recruitment pCO2 Partial pressure of carbon dioxide PNC Perfused number of crossings pO2 Partial pressure of oxygen PPV Proportion of perfused vessels PVD Perfused vessel density SBP Systolic blood pressure SV Stroke volume SVR Systemic vascular resistance THb Total hemoglobin concentration TSI Tissue saturation index TVD Total vessel density. Since the microcirculation constitutes one of the central components where hypoxia mediates its unfavourable effects in critically ill patients, a thorough investigation of the effects of normobaric hypoxia on the microcirculatory system, with regards to its interplay with larger vessels, is of interest. To further elucidate this matter, we conducted an altitude simulation test and investigated both the macro- and microcirculatory effects of acute normobaric hypoxia (Fig. 1 provides an overview of the conducted measurements)

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