Abstract:Introduction: Adenosine is an ATP derivative that is strongly implicated in the cardiovascular adaptive response to exercise. In this study, we hypothesized that during exercise the hyperemia, commonly observed during exercise in air, was counteracted by the downregulation of the adenosinergic pathway during hyperoxic exposure.Methods: Ten healthy volunteers performed two randomized sessions including gas exposure (Medical air or Oxygen) at rest and during exercise performed at 40% of maximal intensity, accord… Show more
“…The vasoconstrictor effect of the decrease in APL was therefore implicated in hemodynamic differences and better tolerance to orthostatic stress during hyperoxic exposure [ 5 ]. These findings were supported by another study in healthy volunteers reporting that breathing pure oxygen at atmospheric pressure can increase peripheral vascular resistance associated with a decrease in APLs compared with the same session in air [ 48 ]. The differences remained significant between the two sessions when a low-intensity exercise was added to each experimental condition.…”
Section: Hyperoxiasupporting
confidence: 59%
“…The differences remained significant between the two sessions when a low-intensity exercise was added to each experimental condition. Meanwhile, hyperoxia did not suppress the increase in APL and the decrease in peripheral vascular resistance commonly recorded during exercise compared with resting reference [ 48 ]. In addition to various factors such as nitric oxide, prostacyclin (PGI2), and endothelium-derived hyperpolarizing factor [ 49 ], adenosine may be another important contributor involved in muscle hyperemia during exercise [ 50 ].…”
Climbers and aviators are exposed to severe hypoxia at high altitudes, whereas divers are exposed to hyperoxia at depth. The aim of this study was to report changes in the adenosinergic system induced by exposure to extreme oxygen partial pressures. At high altitudes, the increased adenosine concentration contributes to brain protection against hypoxia through various mechanisms such as stimulation of glycogenolysis for ATP production, reduction in neuronal energy requirements, enhancement in 2,3-bisphosphoglycerate production, and increase in cerebral blood flow secondary to vasodilation of cerebral arteries. In the context of mountain illness, the increased level of A2AR expression leads to glial dysfunction through neuroinflammation and is involved in the pathogenesis of neurological disorders. Nonetheless, a high level of adenosine concentration can protect against high-altitude pulmonary edema via a decrease in pulmonary arterial pressure. The adenosinergic system is also involved in the acclimatization phenomenon induced by prolonged exposure to altitude hypoxia. During hyperoxic exposure, decreased extracellular adenosine and low A2A receptor expression contribute to vasoconstriction. The resulting decrease in cerebral blood flow is considered a preventive phenomenon against cerebral oxygen toxicity through the decrease in oxygen delivery to the brain. With regard to lung oxygen toxicity, hyperoxia leads to an increase in extracellular adenosine, which acts to preserve pulmonary barrier function. Changes in the adenosinergic system induced by exposure to extreme oxygen partial pressures frequently have a benefit in decreasing the risk of adverse effects.
“…The vasoconstrictor effect of the decrease in APL was therefore implicated in hemodynamic differences and better tolerance to orthostatic stress during hyperoxic exposure [ 5 ]. These findings were supported by another study in healthy volunteers reporting that breathing pure oxygen at atmospheric pressure can increase peripheral vascular resistance associated with a decrease in APLs compared with the same session in air [ 48 ]. The differences remained significant between the two sessions when a low-intensity exercise was added to each experimental condition.…”
Section: Hyperoxiasupporting
confidence: 59%
“…The differences remained significant between the two sessions when a low-intensity exercise was added to each experimental condition. Meanwhile, hyperoxia did not suppress the increase in APL and the decrease in peripheral vascular resistance commonly recorded during exercise compared with resting reference [ 48 ]. In addition to various factors such as nitric oxide, prostacyclin (PGI2), and endothelium-derived hyperpolarizing factor [ 49 ], adenosine may be another important contributor involved in muscle hyperemia during exercise [ 50 ].…”
Climbers and aviators are exposed to severe hypoxia at high altitudes, whereas divers are exposed to hyperoxia at depth. The aim of this study was to report changes in the adenosinergic system induced by exposure to extreme oxygen partial pressures. At high altitudes, the increased adenosine concentration contributes to brain protection against hypoxia through various mechanisms such as stimulation of glycogenolysis for ATP production, reduction in neuronal energy requirements, enhancement in 2,3-bisphosphoglycerate production, and increase in cerebral blood flow secondary to vasodilation of cerebral arteries. In the context of mountain illness, the increased level of A2AR expression leads to glial dysfunction through neuroinflammation and is involved in the pathogenesis of neurological disorders. Nonetheless, a high level of adenosine concentration can protect against high-altitude pulmonary edema via a decrease in pulmonary arterial pressure. The adenosinergic system is also involved in the acclimatization phenomenon induced by prolonged exposure to altitude hypoxia. During hyperoxic exposure, decreased extracellular adenosine and low A2A receptor expression contribute to vasoconstriction. The resulting decrease in cerebral blood flow is considered a preventive phenomenon against cerebral oxygen toxicity through the decrease in oxygen delivery to the brain. With regard to lung oxygen toxicity, hyperoxia leads to an increase in extracellular adenosine, which acts to preserve pulmonary barrier function. Changes in the adenosinergic system induced by exposure to extreme oxygen partial pressures frequently have a benefit in decreasing the risk of adverse effects.
“…Adenosine is an inter-cellular modulator that signals altered cellular activity and metabolic stress within a tissue by activating adenosine receptors [ 1 ]. Acute exercise increases adenosine levels in human blood [ 2 , 3 ] and the rat brain [ 4 ]. Accordingly, adenosine contributes to exercise-induced vasodilation [ 5 ] and also causes drowsiness and tiredness at rest, being a candidate molecule to signal exercise fatigue [ 6 – 8 ].…”
Ecto-5′-nucleotidase or CD73 is the main source of extracellular adenosine involved in the activation of adenosine A
2A
receptors, responsible for the ergogenic effects of caffeine. We now investigated the role of CD73 in exercise by comparing female wild-type (WT) and CD73 knockout (KO) mice in a treadmill-graded test to evaluate running power, oxygen uptake (V̇O
2
), and respiratory exchange ratio (RER) — the gold standards characterizing physical performance. Spontaneous locomotion in the open field and submaximal running power and V̇O
2
in the treadmill were similar between CD73-KO and WT mice; V̇O
2
max also demonstrated equivalent aerobic power, but CD73-KO mice displayed a 43.7 ± 4.2% larger critical power (large effect size, P < 0.05) and 3.8 ± 0.4% increase of maximum RER (small effect size, P < 0.05). Thus, KO of CD73 was ergogenic; i.e., it increased physical performance.
“…There is compelling evidence that patients exposed to hyperoxia have an increased risk of both short- and long-term mortality [ 17 , 18 ]. This risk is related to both the extent and the duration of hyperoxia patients were exposed to, although recent in-vivo studies have demonstrated that even a short exposure to supra-physiological oxygen levels may result in haemodynamic changes (reduction in cardiac output and an increase in vascular resistance for example) that may contribute to a worse outcome [ 19 ].…”
Background
Previous studies have demonstrated an association between hyperoxia and increased mortality in various patient groups. Critically unwell and injured patients are routinely given high concentration oxygen in the pre-hospital phase of care. We aim to investigate the incidence of hyperoxia in major trauma patients receiving pre-hospital emergency anesthesia (PHEA) in the pre-hospital setting and determine factors that may help guide clinicians with pre-hospital oxygen administration in these patients.
Methods
A retrospective cohort study was performed of all patients who received PHEA by a single helicopter emergency medical service (HEMS) between 1 October 2014 and 1 May 2019 and who were subsequently transferred to one major trauma centre (MTC). Patient and treatment factors were collected from the electronic patient records of the HEMS service and the MTC. Hyperoxia was defined as a PaO2 > 16 kPA on the first arterial blood gas analysis upon arrival in the MTC.
Results
On arrival in the MTC, the majority of the patients (90/147, 61.2%) had severe hyperoxia, whereas 30 patients (20.4%) had mild hyperoxia and 26 patients (19.7%) had normoxia. Only 1 patient (0.7%) had hypoxia. The median PaO2 on the first arterial blood gas analysis (ABGA) after HEMS handover was 36.7 [IQR 18.5–52.2] kPa, with a range of 7.0–86.0 kPa. SpO2 pulse oximetry readings before handover were independently associated with the presence of hyperoxia. An SpO2 ≥ 97% was associated with a significantly increased odds of hyperoxia (OR 3.99 [1.58–10.08]), and had a sensitivity of 86.7% [79.1–92.4], a specificity of 37.9% [20.7–57.8], a positive predictive value of 84.5% [70.2–87.9] and a negative predictive value of 42.3% [27.4–58.7] for the presence of hyperoxemia.
Conclusion
Trauma patients who have undergone PHEA often have profound hyperoxemia upon arrival at hospital. In the pre-hospital setting, where arterial blood gas analysis is not readily available a titrated approach to oxygen therapy should be considered to reduce the incidence of potentially harmful tissue hyperoxia.
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