|The effect of dipyridamole and theophylline on hypercapnic ventilatory responses: the role of adenosine.|
|PMID: 9032509 Owner: NLM Status: MEDLINE|
|The purine nucleoside, adenosine, has been implicated as a neuromodulator in central respiratory depression during prolonged exposure to hypoxia. It may also be a mediator of hypoxic hyperpnoea, acting on the carotid bodies. As there may be adenosine-sensitive mechanisms of hypoxic respiratory control, we sought to determine whether adenosine might be involved as a respiratory modulator in another central but non-oxygen-related control mechanism, the ventilatory response to hyperoxic hypercapnia. Twelve normal subjects were studied following 3 days of oral treatment with placebo, dipyridamole (which potentiates adenosine effects by inhibiting cellular uptake), and theophylline (a specific adenosine antagonist of cell surface receptors). The drugs were given in a random order, double-blind fashion. Resting end-tidal carbon dioxide tension (PET,CO2) and the maximum rate of isometric inspiratory pressure change at the mouth ((dP/dt) max), an index of respiratory drive, were determined in all subjects on each treatment. Hyperoxic, hypercapnic ventilatory responses were determined in seven of these subjects using a rebreathing technique. For each hypercapnic response, minute ventilation (V1E) and (dP/dt) max were plotted against PET,CO2 breath-by-breath. Resting PET,CO2 breathing room air was lower with theophylline (5.47 (SD 0.21) kPa) than with placebo (5.74 (0.26) kPa) or dipyridamole (5.86 (0.34) kPa), with no significant drug differences in resting (dP/dt)max. However, neither the slope nor the PET, CO2 intercept of the relationship between ventilation or respiratory drive and PET, CO2 were altered by the study drugs under hyperoxic conditions. We conclude that endogenous adenosine-related mechanisms are unlikely to be involved in determining either the sensitivity or the threshold of the ventilatory response to carbon dioxide under hyperoxic conditions. However, in normoxia, a centrally-acting, tonic, adenosine-mediated, respiratory modulation is not ruled out.|
|T L Griffiths; J M Christie; S T Parsons; S T Holgate|
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|Type: Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't|
|Title: The European respiratory journal Volume: 10 ISSN: 0903-1936 ISO Abbreviation: Eur. Respir. J. Publication Date: 1997 Jan|
|Created Date: 1997-04-29 Completed Date: 1997-04-29 Revised Date: 2013-05-23|
Medline Journal Info:
|Nlm Unique ID: 8803460 Medline TA: Eur Respir J Country: DENMARK|
|Languages: eng Pagination: 156-60 Citation Subset: IM; S|
|Dept of Medicine, University of Southampton, Southampton, UK.|
|APA/MLA Format Download EndNote Download BibTex|
antagonists & inhibitors,
Analysis of Variance
Anoxia / physiopathology
Bronchodilator Agents / administration & dosage, pharmacology*
Carbon Dioxide / metabolism
Carotid Body / drug effects, physiology
Dipyridamole / administration & dosage, pharmacology*
Hypercapnia / physiopathology*
Hyperoxia / physiopathology
Inhalation / drug effects, physiology
Neurotransmitter Agents / antagonists & inhibitors, physiology
Respiration / drug effects*, physiology
Theophylline / administration & dosage, pharmacology*
Tidal Volume / drug effects
Vasodilator Agents / administration & dosage, pharmacology*
|0/Bronchodilator Agents; 0/Neurotransmitter Agents; 0/Placebos; 0/Vasodilator Agents; 124-38-9/Carbon Dioxide; 58-32-2/Dipyridamole; 58-55-9/Theophylline; 58-61-7/Adenosine|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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