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Biomedical subjects

Christian Schirlo

Publications and source records attributed to Christian Schirlo.

3 recordsLinked to original sources

Cognitive and emotional processing at high altitude.

INTRODUCTION: Exposure to altitude reduces oxygen supply to the central nervous system and may cause a variety of neuropsychological impairments. We investigated the relationship between certain cognitive functions and cardiovascular and respiratory variables during acute hypobaric hypoxia. METHODS: There were three groups of seven men who were each exposed to a 2-h altitude profile (AP) involving 30 min at each of the following simulated altitudes (m): AP1, 450-1500-3000; AP2, 450-1500-4500; Control 450-650-650. The neuropsychological tests included word fluency and three word-association tasks tapping processes of cognitive flexibility and emotion regulation. A lateralized tachistoscopic lexical decision task with high and low emotional target words was also administered to assess possible shifts in hemispheric superiorities for positive and negative affect. RESULTS: No significant differences in word fluency, word association, or lateralized lexical decision performances were found, despite a significant oxygen desaturation and a drop in diastolic BP at 4500 m, indicating the beginning of central hypoxia in terms of a functional impairment of the vasomotor center. CONCLUSION: During acute exposure to hypobaric hypoxia, selected cognitive and affective functions mediated by the frontal lobe were preserved. Functional hemispheric asymmetries for emotional processes remained unchanged.

Acclimatization↗

Influence of altitude exposure on coronary flow reserve.

BACKGROUND: Although no data exist on the effect of altitude exposure on coronary flow reserve (CFR), patients with coronary artery disease (CAD) are advised not to exceed moderate altitudes of approximately 2500 m above sea level. We studied the influence of altitude on myocardial blood flow (MBF) in controls and CAD patients. METHODS AND RESULTS: In 10 healthy controls and 8 patients with CAD, MBF was measured by positron emission tomography and 15O-labeled water at rest, during adenosine stress, and after supine bicycle exercise. This protocol was repeated during inhalation of a hypoxic gas mixture corresponding to an altitude of 4500 m (controls) and 2500 m (CAD). Workload was targeted to comparable heart rate-blood pressure products at normoxia and hypoxia. Resting MBF increased significantly in controls at 4500 m (+24%, P<0.01) and in CAD patients at 2500 m (+24%, P<0.05). Altitude had no influence on adenosine-induced hyperemia and CFR. Exercise-induced hyperemia increased significantly in controls (+38%, P<0.01) at 4500 m (despite a reduction in workload, -28%, P<0.0001) but not in CAD patients at 2500 m (moderate decrease in workload, -11%, P<0.05). Exercise-induced reserve was preserved in controls (+10%, P=NS) but decreased in CAD patients (-18%, P<0.005). CONCLUSIONS: At 2500 m altitude, there is a significant decrease in exercise-induced reserve in CAD patients, indicating that compensatory mechanisms might be exhausted even at moderate altitudes, whereas healthy controls have preserved reserve up to 4500 m. Thus, patients with CAD and impaired CFR should be cautious when performing physical exercise even at moderate altitude.

Adult↗

Characteristics of the ventilatory response in subjects susceptible to high altitude pulmonary edema during acute and prolonged hypoxia.

The present study compares the changes in ventilation in response to sustained hypobaric hypoxia and acute normobaric hypoxia between subjects susceptible to high altitude pulmonary edema (HAPE-S) and control subjects (C-S). Seven HAPE-S and five C-S were exposed to simulated high altitude of 4000 m for 23 h in a hypobaric chamber. Resting minute ventilation (V(E)), tidal volume (V(T)), and respiratory frequency (f(R)), as well as the end-tidal partial pressures of oxygen (P(ET(O2))) and carbon dioxide (P(ET(CO2))) were measured in all subjects sitting in a standardized position. Six measurement periods were recorded: ZH1 at 450 m at Zurich level, HA1 on attaining 3600 m altitude, HA2 after 20 min at 4000 m, HA3 after 21 h and HA4 after 23 h at 4000 m altitude, and ZH2 immediately after recompression to Zurich level. At ZH1 and HA3, the measurements were first done in lying, then in sitting, and afterwards in standing. Peripheral arterial oxygen saturation (Sa(O2)) was continuously recorded. All respiratory parameters were also measured during exercise lasting 30 min, the work load being 50% of maximal oxygen consumption (V(O2max)) at Zurich level and 26% of the Zurich V(O2max) at 4000 m. V(E), P(ET(O2)) and P(ET(CO2)) did not significantly differ between HAPE-S and C-S at rest and during exercise periods at Zurich level and at high altitude. However, Sa(O2) was significantly lower in HAPE-S than in C-S at rest and during exercise at 4000 m. Breathing through the mouthpiece during ventilation measurements increased significantly the Sa(O2) in HAPE-S in posture tests at HA3. This effect was most pronounced in the supine posture, in which HAPE-S had the lowest Sa(O2) values. These data provide evidence that (1) gas exchange might be impaired on the level of ventilation-perfusion mismatch or due to diffusion limitation in HAPE-S during the first 23 h of exposure to a simulated altitude of 4000 m, and (2) contrary to C-S, the Sa(O2) in HAPE-S is significantly affected by body position and by mouthpiece breathing.

Acute Disease↗