No abstract

The role of intracerebral adenosine levels in the control of ventilatory response to hypoxia was explored in 15 spontaneously breathing intubated piglets, 1-5 days old, sedated with chloral hydrate. Respiration was recorded via by a pneumotachograph. In all animals exposed to hypoxia (12% O2) for 10 minutes. There was an initial increase in ventilation followed by a late decrease (the biphasic ventilatory response). Both intravenous caffeine citrate (20 mg/kg) and an FiCO2 of 0.05 separately abolished or attenuated the late ventilatory depression associated with hypoxia. In the same piglets, the administration of 10 micrograms dipyridamole, a competitive inhibitor of adenosine receptors, directly into the cerebral ventricles abolished the hyperventilatory response to hypoxia. Conversely, the use of 20 micrograms intraventricular 8-phenyltheophylline abolished the late ventilatory depression associated with hypoxia. Neither drug had a direct effect on ventilation at the time of injection. These results suggest that adenosine is a part of the diphasic ventilatory response to hypoxia.