The role of the vagus nerves in the respiratory and circulatory responses to intravenous histamine and phenyl diguanide in rabbits.

Abstract

1. The responses of rabbits, anaesthetized with pentobarbitone sodium, to intravenous injections of histamine and phenyl diguanide have been studied. Total lung conductance, lung compliance, breathing frequency, tidal volume, end-tidal CO(2)%, systemic arterial and right atrial blood pressures and heart rate were measured. Some of the rabbits were first paralysed and artificially ventilated.2. The role of vagal afferent nerves was determined by observing the responses before and after bilateral vagotomy, and before and during cooling the vagus nerves to 8-10 degrees C; such cooling selectively blocks some vagal afferent pathways.3. Histamine decreased conductance (bronchoconstriction), in spontaneously breathing and in paralysed, artificially ventilated animals, and caused rapid shallow breathing. The responses were considerably reduced or abolished by vagal cooling and vagotomy and are thought to be mainly vagal reflexes due to stimulation by histamine of irritant receptors in the lungs.4. Phenyl diguanide also decreased conductance, in spontaneously breathing and in paralysed, artificially ventilated animals, and caused rapid shallow breathing. Vagotomy abolished the respiratory changes and considerably reduced the bronchoconstriction. Vagal cooling caused an equal reduction of the bronchoconstriction but an increase in minute volume persisted. This respiratory response to phenyl diguanide which persists during vagal cooling is thought to be due to stimulation of deflation receptors in the lungs; it was associated with vagal reflex hypotension and bradycardia.5. Both histamine and phenyl diguanide decreased lung compliance when vagal conduction was unimpaired. The effects were largely secondary to changes in the pattern of breathing, although histamine also had a weak direct action on lung tissue leading to a fall in compliance.6. Both histamine and phenyl diguanide decreased end-tidal CO(2)% and increased right atrial pressure by direct (non-vagal) actions on lung tissues. Histamine also caused a non-vagal hypertension.