Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using ten normal dogs, the right upper lobe of the lung was isolated in vivo by a balloon catheter and was artificially ventilated with nitrogen, air, 60% oxygen in nitrogen, and 60% oxygen and 20% carbon dioxide in nitrogen, while the rest of the lungs maintained a spontaneous breathing of ambient air. Aminophylline did not show a vasodilating action under severe alveolar hypoxia (PAO2: ca. 40 mmHg); on the contrary, it seemed to potentiate hypoxic pulmonary vasoconstriction. When the regional alveolar oxygen tension became less hypoxic (PAO2: ca. 70 mmHg) or higher than that in the rest of the lungs which spontaneously breathed ambient air, aminophylline showed a definite vasodilating action. Aminophylline also showed a vasodilating action in alveolar hypercapnia in the presence of alveolar hyperoxia.
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PMID:Effect of aminophylline on regional perfusion distribution in the lungs. 48 2

In 10 normal young adults, ventilation was evaluated with and without pretreatment with aminophylline, an adenosine blocker, while they breathed pure O2 1) after breathing room air and 2) after 25 min of isocapnic hypoxia (arterial O2 saturation 80%). With and without aminophylline, 5 min of hyperoxia significantly increased inspiratory minute ventilation (VI) from the normoxic base line. In control experiments, with hypoxia, VI initially increased and then declined to levels that were slightly above the normoxic base line. Pretreatment with aminophylline significantly attenuated the hypoxic ventilatory decline. During transitions to pure O2 (cessation of carotid bodies' output), VI and breathing patterns were analyzed breath by breath with a moving-average technique, searching for nadirs before and after hyperoxia. On placebo days, at the end of hypoxia, hyperoxia produced nadirs that were significantly lower than those observed with room-air breathing and also significantly lower than when hyperoxia followed normoxia, averaging, respectively, 6.41 +/- 0.52, 8.07 +/- 0.32, and 8.04 +/- 0.39 (SE) l/min. This hypoxic depression was due to significant decrease in tidal volume and prolongation of expiratory time. Aminophylline partly prevented these alterations in breathing pattern; significant posthypoxic ventilatory depression was not observed. We conclude that aminophylline attenuated hypoxic central depression of ventilation, although it does not affect hyperoxic steady-state hyperventilation. Adenosine may play a modulatory role in hypoxic but not in hyperoxic ventilation.
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PMID:Aminophylline effects on ventilatory response to hypoxia and hyperoxia in normal adults. 279 6