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Intravenous infusion of adenosine but not inosine stimulates respiration in man.
Author(s) -
Reid PG,
Watt AH,
Routledge PA,
Smith AP
Publication year - 1987
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/j.1365-2125.1987.tb03053.x
Subject(s) - inosine , adenosine , respiration , anesthesia , heart rate , metabolite , nucleoside , respiratory minute volume , medicine , tidal volume , ventilation (architecture) , chemistry , respiratory system , pharmacology , blood pressure , biochemistry , mechanical engineering , anatomy , engineering
The effects on respiration of intravenous infusions of the endogenous nucleoside adenosine and its deaminated metabolite, inosine, administered in random order, single‐blind, were compared in six healthy volunteers. The infusion rate of each nucleoside was initially 3.1 mg min‐1 and was increased stepwise every 2 min, as tolerated, up to a possible maximum of 23.4 mg ml‐1. The maximum dose rates received by all subjects were 8.5 mg min‐1 for adenosine and 16.8 mg min‐1 for inosine. Adenosine infusion at rates of 6.1 mg min‐1 and above caused a significant increase in minute ventilation, principally due to an increase in tidal volume, with an associated significant fall in end‐ tidal Pco2. Mean inspiratory flow rate increased and expiratory duration decreased during adenosine infusion, but there was no change in inspiratory duration. Adenosine infusion also caused a significant increase in heart rate and a slight, but significant increase in systolic blood pressure. Infusion of inosine at dose rates up to 16.8 mg min‐1 produced no pharmacological effects. This study shows that adenosine by infusion produces sustained respiratory stimulation in man and demonstrates that it does not depend on prior conversion of adenosine to inosine or related metabolites and that it is not secondary to systemic hypotension.