Abstract
1. 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 CO2%, 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 CO2%. 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 and phenyl diguanide (Karczewski & Widdicombe, 1969b) it is concluded that anaphylaxis stimulates lung deflation and irritant receptors which mediate much of the reflex responses.
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