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The Journal of Experimental Medicine logoLink to The Journal of Experimental Medicine
. 1910 Mar 14;12(2):151–175. doi: 10.1084/jem.12.2.151

THE PHYSIOLOGY OF THE IMMEDIATE REACTION OF ANAPHYLAXIS IN THE GUINEA-PIG

John Auer 1, Paul A Lewis 1
PMCID: PMC2124781  PMID: 19867320

Abstract

1. By an immediate anaphylactic reaction we mean the chain of symptoms which occur in highly sensitized guinea-pigs shortly after an intravenous or intracardiac injection of the toxic dose and usually end in death. 2. Immediate anaphylactic death occurs three to five minutes after the toxic injection in highly sensitized guinea-pigs. 3. Immediate anaphylactic death in guinea-pigs is caused by asphyxia; cessation of respiration is secondary to this asphyxia. 4. This asphyxia is apparently produced by a tetanic contraction of the smooth muscles of the bronchioles, which occludes their lumen gradually, so that finally no air enters or leaves the lung, in spite of violent respiratory efforts; the animal is strangulated. 5. The stage of complete broncho-constriction is preceded by a short broncho-dilatation, if the bronchioles have been in a state of tonus previous to the injection of the toxic dose. 6. Anatomically, the lungs of these guinea-pigs are typical and may be used as an indicator of the immediate anaphylactic state when the animal has been immobilized by curarin or by pithing. 7. The lungs of a guinea-pig killed by immediate anaphylaxis are distended and in an inspiratory position so that the diaphragm is pushed down; no marked collapse occurs when the chest is opened and when the lungs are excised in toto; their color is a pale bluish-pink ; the surfaces and borders are smooth; no foam is in the trachea or large bronchi; pieces of lung cut off do not collapse, float lightly on water, and contain a good amount of air and little fluid which escapes on pressure. The blood in the lungs and heart is black when the autopsy is made at once after the cessation of respiration. 8. Section of the vagi in the neck, or curarin (artificial respiration) exerts no appreciable effect on the development of immediate anaphylaxis. 9. This immobilization of the lungs, which is due to a broncho-constriction, is of peripheral origin, for destruction of the spinal cord and medulla affects in no appreciable way the promptness and extent of the typical lung response to the injection of the toxic dose. Artificial respiration is, of course, necessary. At the present time we do not care to state whether the toxic dose exerts its effects upon the bronchial muscles alone or upon the vagus motor endings or upon both structures. 10. The blood pressure in immediate anaphylaxis first shows a rise, which may be considerable; a short maintenance of this high level and then a gradual drop to IO to 20 millimeters of mercury and even less, within ten minutes after injection of the toxic dose. 11. Shortly after injection of the toxic dose a heart block develops, so that auricles and ventricles may beat in a 3:I rhythm; the block is probably due to asphyxia. 12. The cardiac vagus gradually loses its irritability after injection of the toxic dose. 13. Cooling of the guinea-pig delays the reaction to the toxic injection.

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