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  • Alveolar-arterialPO2 difference  (1)
  • cytoprotection  (1)
  • 1
    ISSN: 1573-2568
    Keywords: esophagitis ; sucralfate ; prostaglandin ; cytoprotection ; acid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The cytoprotective effects of liquid sucralfate and a synthetic analog of prostaglandin E1 (PGE1) on acid-induced esophagitis in cats were studied. Esophagitis was induced in adult cats using a constant infusion of 0.1 N HCl at 1 ml/min for 20 min. Animals were infused for either one or three days. Mucosal lesions were evaluated by blinded investigators using both fiberoptic endoscopy and light microscopy. Histologic changes included basal cell hyperplasia, intraepithelial leukocytosis, and subepithelial leukocytosis. Liquid sucralfate given prior to acid infusion consistently prevented acid-induced lesions in both one- and three-day infusions, demonstrated by both endoscopy and quantitative histologic scoring. Indomethacin (200 μg/kg) given prior to sucralfate and acid did not affect sucralfate cytoprotection. Synthetic PGE1, given in doses of 5 μg/kg and 100 μg/kg, afforded no esophageal cytoprotection. These studies indicate that sucralfate is cytoprotective against acid-induced esophageal injury in cats, an effect that does not appear to be mediated by prostaglandin. In addition, synthetic PGE1 does not confer protection in this animal model.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    European journal of applied physiology 65 (1992), S. 37-42 
    ISSN: 1439-6327
    Keywords: Alveolar-arterialPO2 difference ; Pulmonary gas exchange ; VO2max ; Hypoxia ; Hyperoxia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary These experiments examined the exercise-induced changes in pulmonary gas exchange in elite endurance athletes and tested the hypothesis that an inadequate hyperventilatory response might explain the large intersubject variability in arterial partial pressure of oxygen (P a02) during heavy exercise in this population. Twelve highly trained endurance cyclists [maximum oxygen consumption (VO2max) range = 65-77 ml·kg−1·min−1] performed a normoxic graded exercise test on a cycle ergometer toVO2max at sea level. During incremental exercise atVO2max 5 of the 12 subjects had ideal alveolar to arterial P02 gradients (P A-aO2) of above 5 kPa (range 5-5.7) and a decline from restingP aO2 (ΔP aO2) 2.4 kPa or above (range 2.4-2.7). In contrast, 4 subjects had a maximal exercise (P A-aO2) of 4.0-4.3 kPa with ΔP aO2 of 0.4-1.3 kPa while the remaining 3 subjects hadP A-aO2 of 4.3-5 kPa with ΔP aO2 between 1.7 and 2.0 kPa. The correlation between PAO2 andP aO2 atVO2max was 0.17. Further, the correlation between the ratio of ventilation to oxygen consumption VSP aO2 and arterial partial pressure of carbon dioxide VSP aO2 atVO2max was 0.17 and 0.34, respectively. These experiments demonstrate that heavy exercise results in significantly compromised pulmonary gas exchange in approximately 40% of the elite endurance athletes studied. These data do not support the hypothesis that the principal mechanism to explain this gas exchange failure is an inadequate hyperventilatory response.
    Type of Medium: Electronic Resource
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