Mechanisms of hyperpnea induced by isoproterenol.

We injected boluses of isoproterenol (2 to 3 micrograms) into the inferior vena cava to determine the effects on phrenic activity, end-tidal PCO2, arterial pressure and aortic flow in anesthetized cerebrate and unanesthetized decerebrate cats. We studied both spontaneously breathing animals and those paralyzed and servo-ventilated to keep end-tidal PCO2 constant. Isoproterenol caused an increase of respiratory output within a few seconds if carotid bodies were intact; recordings of the carotid sinus nerves showed that the response was due to activation of carotid body chemoreceptors. After denervation of both carotid bodies isoproterenol still caused a late (approximately 16 sec) but smaller increase of respiratory output, which persisted after section of vagi and thoracic (T1-5) dorsal roots. We concluded that the major effect of isoproterenol on respiration is through its excitatory action on the carotid bodies. There is another small, late facilitatory effect, of uncertain mechanism but not caused by peripheral chemoreceptors, by other receptors in the heart and lungs or by a change in PaCO2 acting on the central chemoreceptors.