Histamine and phenyldiguanide induced tachypnea in hypercapnia and hypoxia.

The rapid shallow breathing of pulmonary vagal origin following administration of histamine (H) and phenyldiguanide (PDG) was studied at different levels of hypercapnic and hypoxic stimulation. At all levels of chemical drive H and PDG caused an excitatory effect on timing of breathing and an inhibitory effect on the respiratory output. The latter was evaluated from the mean inspiratory flow rate and the mean rate of change of pressure developed in the lungs during an inspiratory effort against closed airways. The timing effect was greater at low than at high PaCO2 while the opposite was true for the output effect. At all PaCO2, H and PDG decreased the volume-threshold for termination of inspiration (leftward displacement of the VT vs TI relationship) of the VT Vs TI relationship). Hypoxia increased the respiratory output in control as much as with drug stimulation. Moreover, hypoxia did not affect the volume-threshold curve both in control and with H and PDG. We concluded that vagal afferents stimulated by H and PDG (irritant and/or J receptors) interfere with the timing and output response to central chemoreceptors stimulation (CO2 sensitivity) without affecting the response to peripheral chemoreceptors stimulation (mainly hypoxic chemosensitivity).