The role of the pneumotaxic mechanism in the tachypnea of pulmonary vagal origin.
The tachypnea due to stimulation of pulmonary vagal irritant and J.receptors with histamine (5%, aerosol) and phenyldiguanide (150 mu g, i.v.) was studied in 11 pentobarbitone anesthetized cats before and after uni (UL) and bilateral (BL) lesion of sites of the pneumotaxic mechanism. BL prolonged the timing parameters of spontaneous and occluded breaths (no phasic input from pulmonary stretch receptors) more under drug stimulation than in control: thus the shortening effect of drug stimulation increased going from intact to BL. Drug stimulation caused a decrease in volume threshold for inspiratory cut-off and this effect was reduced by about 50% by BL. Under hyperoxic iso-PCO2 conditions drug stimulation reduced the respiratory output (indexed by the rate of change of the pressure developed in the airways during occluded breaths) and this effect was left unaltered by BL. The results suggest that the pneumotaxic mechanism plays a role in the reflex respiratory excitatory frequency effect resulting from activation of irritant and J receptors while it seems to be excluded from a control on respiratory output.
D000818:Animals; D001645:Biguanides / Q000494:pharmacology; D002415:Cats; D006632:Histamine / Q000494:pharmacology; D008168:Lung / Q000294:innervation*; D012120:Respiration Disorders / Q000139:chemically induced / Q000209:etiology / Q000503:physiopathology*; D013990:Tidal Volume; D013997:Time Factors; D014630:Vagus Nerve / Q000503:physiopathology*
D001645:Biguanides; D006632:Histamine; C008846:phenyl biguanide