produced upon the lung of the guinea-pig during the anaphylactic shock. 

 They proved conclusively that the great distention of the lung found at 

 autopsy and the respiratory symptoms accompanying the shock during 

 life were dependent upon a constriction of the smooth muscles of the 

 bronchioles. The asphyxia which is caused by this extreme contraction is 

 immediately responsible for the death of the animal in acute shock. In 

 the guinea-pigs that survive for some time, after the onset of symptoms, 

 the marked distention of the lungs and the bronchiospasm are not obvious, 

 and may even be absent. In these animals hemorrhages are frequently 

 found over the pleura and in the lung itself. The extraordinary bronchial 

 spasm so characteristic of anaphylactic shock in guinea-pigs has not been 

 found in other animals that have been subjected to experimentation. In 

 the rabbit it seems probable that, though the bronchial musculature escapes, 

 the walls of the smaller arteries are constricted and so narrowed that they 

 greatly impede the pulmonary circulation and are directly responsible 

 for the death of the animal. Schulz(&) has offered some evidence to show 

 that this may also occur in the cat. 



The cardiovascular mechanism is profoundly affected during both acute 

 and subacuto shock. It was shown first by Biedl and Kraus(a) that, in the 

 dog, a profound drop in blood pressure takes place. This abrupt fall in 

 blood pressure which is so characteristic of shock in dogs occurs apparently 

 in one form or another in anaphylactic shock in all animals upon which 

 experiments have been done so far and has, too, been observed in man. 

 In the dog the fall is usually very abrupt, whereas in the rabbit and in 

 the guinea-pig the lowering of blood pressure may be slower and more 

 protracted and is generally preceded by a very temporary but distinct 

 rise. The changes in blood pressure, in the dog at least, are not dependent 

 upon primary cardiac failure, as has been definitely demonstrated by 

 Pearce and Eisenbrey(a) (6), but are probably dependent upon changes 

 in the peripheral circulation and are analogous to the low pressure which 

 occurs in surgical shock. 



Though there has not been any definite evidence forthcoming to show 

 that the capillaries themselves are disturbed during anaphylactic shock, 

 collateral observations have been made which suggest that this important 

 portion of the peripheral circulation may undergo changes which hitherto 

 have been unsuspected. The recent work of Dale and Laidlaw(a) (&) and 

 Dale and Richards has indicated first that in histamin poisoning in cats, 

 evidence is obtainable in favor of the view that there occurs a general loss 

 of tone by the capillaries throughout the body, and that the excessive 

 permeability of these vessels, which allows escape of plasma, may be 

 regarded as an important factor in the production of histamin shock. 

 They demonstrated further by appropriate experiments that, though 

 histamin contracts the fine arterioles, there is a fall of blood pressure in 

 histamin shock and show that this is due to a dilatation of the capillary 



