In rabbits with intact vagus nerves, HFOV applied for 10-20 s caused apnea (i.e., respiratory arrest for as long as HFOV lasted) accompanied by tonic discharges of the diaphragm. To identify the vagal mechanisms involved in this type of apnea, the vagus nerves of anaesthetized rabbits were gradually cooled from 37 degrees C to 0 degree C, i.e., the vagal fibres were, corresponding to their diameter, successively blocked. At each temperature, the effects of HFOV on spontaneous breathing were compared with those of static lung inflation and deflation: Between 20 degrees C and 14 degrees C, the lung inflation reflex (mediated by pulmonary slowly adapting stretch receptors = PSR) was weakened or abolished, whereas the lung deflation reflex (mediated by rapidly adapting stretch receptors = RAR) was reinforced; the HFOV-induced apnea occurred less frequently, however, the accompanying diaphragmatic activity was enhanced. Between 14 degrees C and 5 degrees C, both HFOV and large static inflation caused a slight increase of breathing frequency in the majority of animals. Some animals, however, responded even below 14 degrees C by apnea to both HFOV and inflation, and, under these conditions, both HFOV- and inflation-induced apnea were accompanied by a pronounced tonic diaphragmatic activity. At 5 degrees C, the effects of HFOV as well as of inflation (except in two animals) and deflation were abolished. From the results we conclude that in rabbits the apnea during HFOV is mainly mediated by stimulation of PSR, and the concomitant tonic activity of the diaphragm is mainly due to stimulation of RAR, as it is reinforced with gradual blockade of PSR fibres and abolished when only non-myelinated fibres are intact.