SUMMARY1. 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 CO2 %, 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°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 bradyeardia. W. KARCZEWSKI AND J. C. WIDDICOMBE 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 CO2 % and increased right atrial pressure by direct (non-vagal) actions on lung tissues. Histamine also caused a non-vagal hypertension.

SUMMARY1. Rabbits, previously sensitized to egg albumen, were anaesthetized and then rendered anaphylactic by a further injection of egg albumen; total lung conductance of flow, lung compliance, breathing rate, tidal volume, end-tidal C02 %, systemic arterial and right atrial blood pressures and heart rate were measured. Before induction of anaphylaxis, some rabbits were vagotomized, some had their vagi cooled to block differential conduction, and others were paralysed and artificially ventilated to minimize secondary changes in afferent activity from the lungs and in blood gas tensions.2. Lung conductance was reduced by anaphylaxis in spontaneously breathing and in artificially ventilated rabbits, and the effect was lessened by vagal cooling and greatly reduced by vagotomy; the hyperventilation of anaphylaxis took the form of an increase in tidal volume rather than in respiratory frequency during vagal cooling, and all changes in ventilation were abolished by vagotomy. These effects are therefore dependent on the integrity of vagal nervous pathways.3. Lung compliance was reduced by anaphylaxis to a similar degree in all groups of rabbits; all groups showed similar falls in end-tidal C02%. These effects are therefore not dependent on the integrity of vagal conduction.4. Anaphylaxis reduced systemic arterial blood pressure, the response being smaller when the vagi were cooled or cut.5. It is concluded that anaphylaxis has direct actions on the pulmonary vascular bed, the distal airways or the alveoli. However, the changes in breathing, blood pressure and large airway calibre are mainly dependent on vagal reflex activity. By analogy with responses to injections of histamine

SUMMARY1. The effects of bilateral cervical vagotomy, of bilateral vagal cooling and of efferent vagal stimulation were studied on rabbits anaesthetized with pentobarbitone sodium. Total lung conductance, lung compliance, breathing frequency, tidal volume, end-tidal CO2 %, systemic arterial and right atrial blood pressures and heart rate were measured. Some of the rabbits were first paralysed and artificially ventilated.2. The changes in lung conductance were consistent with the presence of a tonic efferent vagal discharge in bronchoconstrictor fibres, reflexly damped down by a tonic afferent vagal discharge dilator to the airways, probably the Hering-Breuer inflation reflex.3. Neither vagotomy nor efferent vagal stimulation significantly influenced lung compliance, right atrial pressure or end-tidal C02 %; vagal cooling lowered end-tidal CO2 % in spontaneously breathing rabbits, but did not affect the other variables.4. Efferent vagal stimulation in the rabbit decreased lung conductance with no significant change in lung compliance.5. In the rabbit, vagal efferent activity affects primarily the larger (resistance) air passages with little action on the distal (complianceinfluencing) airways.

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