Effects of histamine on slowly adapting pulmonary stretch receptor activities in vagotomized rabbits.

Thirty-two SAR fibers located below the carina were used in 32 anesthetized, bilaterally vagotomized, and artificially ventilated rabbits. After intravenous administration of histamine (20, 40, and 80 micrograms/kg, n = 13) or ACh (10, 20, and 40 micrograms/kg, n = 13), SARs became active during expiration but decreased their inspiratory activity. The effects of both drugs were dose-dependent. The injection of histamine or ACh at all doses examined had no effect on tracheal pressure (PT). Atropine (3 mg/kg) and isoprenaline (100 micrograms/kg) blocked the responses of SAR activity to low doses of histamine (20 and 40 micrograms/kg) and to all doses of ACh. The response of SARs to 80 micrograms/kg of histamine was not altered by atropine (n = 10) nor by isoprenaline (n = 10). These results suggest that low-dose effects of histamine on SARs occur as the result of ACh release whereas with high doses the effect of histamine on the receptors is mainly independent of ACh released from the nerve endings. In another series of experiments (n = 6) where animals were treated with isoprenaline (100 micrograms/kg) and, subsequently, physostigmine (200 micrograms/kg), histamine (20 and 40 micrograms/kg) or ACh (10 and 20 micrograms/kg) increased the inspiratory discharge in SARs and the level of PT. From these results, it is assumed that the changes of SAR activity following histamine injection in vagotomized animals reflect a local bronchomotor effect which takes place in a peripheral bronchial tree that does not affect the level of PT. Histamine seems to release ACh and to elicit bronchoconstriction that can be manifested by physostigmine treatment.