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• 1
Electronic Resource
Oxford, UK : Munksgaard International Publishers
Indoor air 1 (1991), S. 0
ISSN: 1600-0668
Source: Blackwell Publishing Journal Backfiles 1879-2005
Topics: Architecture, Civil Engineering, Surveying , Medicine
Notes: Initation of the eyes and the upper respiratory tract (sensory irritation) in man due to the emission of vapours and gases from water-based indoor paints has been estimated from their ability to decrease the respiratory rate in mice (ASTM: E981-84, slightly modified). An acid-curing lacquer, known to give rise to sensory irritation during occupational exposure, was used as the positive control. In the bioassay the and-curing lacquer also gave rise to a pronounced sensory irritation, confirming that the ASTM method was applicable. Furthermore, the emission of formaldehyde, bases and acids was determined. The irritation within the first week was mainly due to the emission of organic solvents, but formaldehyde also played a role. Later the sensory irritation effect was caused mainly by the emission of formaldehyde. This indicates that the method revealed the different emission phases. None of the water-based paints (3 latex wall paints, 1 silicate paint and 1 distemper) gave rise to a biologically significant irritation effect. Nor did the water-based products emit formaldehyde or acids. However, varying degrees of emission of ammonia were observed. Taking into account the biological detection limits, no significant degree of sensory irritation can be expected in man 1-2 weeks after indoor painting with the tested water-based products.
Type of Medium: Electronic Resource
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• 2
Electronic Resource
Springer
European journal of applied physiology 68 (1994), S. 303-309
ISSN: 1439-6327
Keywords: Catecholamines ; Insulin ; Growth hormone ; ACTH ; Erythropoietin
Source: Springer Online Journal Archives 1860-2000
Topics: Medicine
Notes: Abstract To establish whether or not hypoxia influences the training-induced adaptation of hormonal responses to exercise, 21 healthy, untrained subjects [26 (2) years, mean (SE)] were studied in three groups before and after 5 weeks' training (cycle ergometer, 45 min· day−1, 5 days· week−1). Group 1 trained at sea level at 70% maximal oxygen uptake ( $$\dot V$$ O2max), group 2 in a hypobaric chamber at a simulated altitude of 2500 m at 70% of altitude $$\dot V$$ O2max, and group 3 at a simulated altitude of 2500 m at the same absolute work rate as group 1. Arterial blood was sampled before, during and at the end of exhaustive cycling at sea level (85% of pretraining of $$\dot V$$ O2max). $$\dot V$$ O2 increased by 12 (2)% with no significant difference between groups, whereas endurance improved most in group 1 (P 〈 0.05). Training-induced changes in response to exercise of noradrenaline, adrenaline, growth hormone, β-endorphin, glucagon, and insulin were similar in the three groups. Concentrations of erythropoietin and 2,3-diphosphoglycerate at rest did not change over the training period. In conclusion, within 5 weeks of training, no further adaptation of hormonal exercise responses takes place if intensity is increased above 70% $$\dot V$$ O2max. Furthermore, hypoxia per se does not add to the training-induced hormonal responses to exercise.
Type of Medium: Electronic Resource
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• 3
Electronic Resource
Springer
European journal of applied physiology 72 (1996), S. 297-302
ISSN: 1439-6327
Keywords: Altitude ; Diurnal ; Erythropoietin ; Haemoglobin oxygen affinity ; Hypoxia
Source: Springer Online Journal Archives 1860-2000
Topics: Medicine
Notes: Abstract This study tested the hypothesis that the diurnal variations of serum-erythropoietin concentration (serum-EPO) observed in normoxia also exist in hypoxia. The study also attempted to investigate the regulation of EPO production during sustained hypoxia. Nine subjects were investigated at sea level and during 4 days at an altitude of 4350 m. Median sea level serum-EPO concentration was 6 (range 6–13) U·l−1. Serum-EPO concentration increased after 18 and 42 h at altitude, [58 (range 39–240) and 54 (range 36–340) U·l−1, respectively], and then decreased after 64 and 88 h at altitude [34 (range 18–290) and 31 (range 17–104) U·l−1, respectively]. These changes of serum-EPO concentration were correlated to the changes in arterial blood oxygen saturation (r = −0.60,P = 0.0009), pH (r = 0.67,P = 0.003), and in-vivo venous blood oxygen half saturation tension (r = −0.68,P = 0.004) but not to the changes in 2, 3 diphosphoglycerate. After 64 h at altitude, six of the nine subjects had down-regulated their serum-EPO concentrations so that median values were three times above those at sea level. These six subjects had significant diurnal variations of serum-EPO concentration at sea level; the nadir occurred between 0800–1600 hours [6 (range 4–13) U·l−1], and peak concentrations occurred at 0400 hours [9 (range 8–14) U·l−1,P = 0.02]. After 64 h at altitude, the subjects had significant diurnal variations of serum-EPO concentration; the nadir occurred at 1600 hours [20 (range 16–26) U·l−1], and peak concentrations occurred at 0400 hours [31 (range 20–38) U·l−1,P = 0.02]. This study demonstrated diurnal variations of serum-EPO concentration in normoxia and hypoxia, with comparable time courses of median values. The results also suggested that EPO production at altitude is influenced by changes in pH and haemoglobin oxygen affinity.
Type of Medium: Electronic Resource
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• 4
Electronic Resource
Springer
European journal of applied physiology 74 (1996), S. 475-480
ISSN: 1439-6327
Keywords: Erythropoietin ; Carbon dioxide ; Haemoglobin oxygen affinity ; Human ; Hypoxia
Source: Springer Online Journal Archives 1860-2000
Topics: Medicine
Notes: Abstract This study investigated the human erythropoietin (EPO) response to short-term hypocapnic hypoxia, its relationship to a normoxic or hypoxic increase of the haemoglobin oxygen affinity, and its suppression by the addition of CO2 to the hypoxic gas. On separate days, eight healthy male subjects were exposed to 2 h each of hypocapnic hypoxia, normocapnic hypoxia, hypocapnic normoxia, and normal breathing of room air (control experiment). During the control experiment, serum-EPO showed significant variations (ANOVAP = 0.047) with a 15% increase in mean values. The serum-EPO measured in the other experiments were corrected for these spontaneous variations in each individual. At 2 h after ending hypocapnic hypoxia (10% O2 in nitrogen), mean serum-EPO increased by 28% [baseline 8.00 (SEM 0.84) U · 1−1, post-hypoxia 10.24 (SEM 0.95) U · 1−1, P = 0.005]. Normocapnic hypoxia was produced by the addition of CO2 (10% Co2 with 10% O2) to the hypoxic gas mixture. This elicited an increased ventilation, unaltered arterial pH and haemoglobin oxygen affinity, a lower degree of hypoxia than during hypocapnic hypoxia, and no significant changes in serum-EPO (ANOVAP 〉 0.05). Hypocapnic normoxia, produced by hyperventilation of room air, elicited a normoxic increase in the haemoglobin oxygen affinity without changing serum-EPO. Among the measured blood gas and acid-base parameters, only the partial pressures of oxygen in arterial blood during hypocapnic hypoxia were related to the peak values of serum-EPO (r = −0.81,P = 0.01). The present human EPO responses to hypoxia were lower than those which have previously been reported in rodents and humans. In contrast with the earlier rodent studies, it was found that human EPO production could not be triggered by short-term increases in pH and haemoglobin oxygen affinity per se, and the human EPO response to hypoxia could be suppressed by concomitant normocapnia without acidosis.
Type of Medium: Electronic Resource
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• 5
Electronic Resource
Springer
European journal of applied physiology 74 (1996), S. 475-480
ISSN: 1439-6327
Keywords: Key words Erythropoietin ; Carbon dioxide ; Haemoglobin oxygen affinity ; Human ; Hypoxia
Source: Springer Online Journal Archives 1860-2000
Topics: Medicine
Notes: Abstract  This study investigated the human erythropoietin (EPO) response to short-term hypocapnic hypoxia, its relationship to a normoxic or hypoxic increase of the haemoglobin oxygen affinity, and its suppression by the addition of CO2 to the hypoxic gas. On separate days, eight healthy male subjects were exposed to 2 h each of hypocapnic hypoxia, normocapnic hypoxia, hypocapnic normoxia, and normal breathing of room air (control experiment). During the control experiment, serum-EPO showed significant variations (ANOVA P=0.047) with a 15% increase in mean values. The serum-EPO measured in the other experiments were corrected for these spontaneous variations in each individual. At 2 h after ending hypocapnic hypoxia (10% O2 in nitrogen), mean serum-EPO increased by 28% [baseline 8.00 (SEM 0.84) U⋅1-1, post-hypoxia 10.24 (SEM 0.95) U⋅1-1, P=0.005]. Normocapnic hypoxia was produced by the addition of CO2 (10% Co2 with 10% O2) to the hypoxic gas mixture. This elicited an increased ventilation, unaltered arterial pH and haemoglobin oxygen affinity, a lower degree of hypoxia than during hypocapnic hypoxia, and no significant changes in serum-EPO (ANOVA P〉0.05). Hypocapnic normoxia, produced by hyperventilation of room air, elicited a normoxic increase in the haemoglobin oxygen affinity without changing serum-EPO. Among the measured blood gas and acid-base parameters, only the partial pressures of oxygen in arterial blood during hypocapnic hypoxia were related to the peak values of serum-EPO (r=−0.81, P=0.01). The present human EPO responses to hypoxia were lower than those which have previously been reported in rodents and humans. In contrast with the earlier rodent studies, it was found that human EPO production could not be triggered by short-term increases in pH and haemoglobin oxygen affinity per se, and the human EPO response to hypoxia could be suppressed by concomitant normocapnia without acidosis.
Type of Medium: Electronic Resource
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