In early March 2015, the 19 th edition of the bi-annual International Hypoxia Symposia took place in the gorgeous winter settings of the Château Lake Louise in the Canadian Rockies. Some 190 scientists, doctors, students, and other interested people gathered to learn and exchange on the multiple facets of life’s fascinating relationship with the element oxygen. It was the late Charlie Houston who launched the International Hypoxia Symposia several decades ago, to the great satisfaction of an increasingly international audience. The symposia still continue, now organized by Rob Roach, with help from Peter Hackett and myself. Even if visa problems unfortunately prevented some prospective attendees to make it to Lake Louise, the 2015 symposium again brought together people from all around the world. The (informal) competition on who travelled the most miles to attend was close, with several attendees from places on the opposite side of the planet. The prize went to Keith Burgess who came all the way from Australia. As customary the symposium started on Tuesday at 6 PM with a welcome reception, the perfect occasion to meet many friends and colleagues again. On Wednesday the first session Hypoxia: From Microcirculation to Genetic Selection started off with Can Ince from Amsterdam, who reported some of his fascinating work on hypoxia in the intensive care settings. He introduced his talk with the paradoxical observation that patients with systemic circulatory problems, such as encountered in sepsis or major traumatic hemorrhage, once stabilized with regard their systematic hemodynamics, still show serious signs of tissue hypoxia. Ince underlined the important point that one cannot draw any conclusions on the state of the microcirculation looking only at systematic hemodynamics (Kanoore et al., 2015). Initially using NADH fluorescence and later porphyrin quenching techniques, Ince and colleagues have convincingly shown that hypoxic pockets in otherwise healthy tissue can exist because of changes on microcirculatory level. Ince and colleagues now have developed handheld microscopes to capture video of the microcirculation (e.g., under the tongue) to monitor the microcirculatory state in patients. Ince also reminded us that increasing Fio2 in patients does not necessarily lead to improved oxygenation there were needed, and that an increase in Po2 may even lead to microcirculatory vasoconstriction. Ince ended his presentation citing from his article in a Christmas issue of the British Medical Journal titled ‘Why Rudolph’s Nose is Red: Observational Study’ (Ince et al., 2012), in which he and Norwegian colleagues used handheld microscopes to image the microcirculation in reindeer in comparison to men, showing that reindeer have a higher microcirculatory density. Andy Lovering followed with the troubling observation that more than a third of the general population has a patent foramen ovale (PFO). Even if Claudius Galen already reported the existence of PFOs, it was Hagen who first quantified prevalence between 19% and 36%, based on cadaver observations (Hagen et al., 1984). The modern technique of saline contrast echocardiography has now led to estimations of PFO prevalence between 25% and 38%. This is troubling because such prevalence implies that much of what has been published to date on cardio-pulmonary gas exchange has not taken into account any effects of shunting through such a PFO. For example, PFO + subjects show widening of their alveolar-arterial O2 difference (AadO2) with exercise intensity. The size of the PFO matters, because the larger the PFO the greater the shunt. Thus, depending on size, PFOs have relevant effects, as also suggested by recent observations during the AltitudeOmics project (Elliott et al., 2015). In PFO subjects, acclimatization over 16 days improved the initially widened Alveolararterial O2 difference (AadO2), while in PFO + subjects the AadO2 did not improve. PFO + subjects further showed blunted ventilatory acclimatization as compared to PFO subjects for reasons that remain unknown. Lovering further presented some intriguing results on the effects of a PFO on thermoregulation. The idea is that the pulmonary circulation is important for cooling and that a right-left shunt through a PFO may impair this, leading to a measurable increase in body temperature in PFO + subjects. Lovering concluded by suggesting that the presence of a PFO confers an increased risk for AMS and HAPE. The first session was concluded by a fascinating talk given by Emilia Huerta on the presence of genes in the Tibetan genome coming from admixture with the Denisovans’ genome (Huerta-Sanchez et al., 2014). She started her talk by reminding us that there are three regions on earth in which humans have been exposed to lowered Pio2 for enough generations to have undergone selection pressure for adaptation: East-Africa, the Andes, and Tibet, even though the adaptations described for the populations living in these regions are not necessarily the same. The Tibetans do not show
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