CARDIOVASCULAR CHANGES DURING CEREBRAL ANEMIA 37 



(temporary or permanent) is recorded under both conditions within 

 half the time normally occupied by the blood vascular response. When 

 the animal is intact, this drop of pressure occurs in the seventh or 

 eighth occlusion and in all subsequent curves of a given series. When 

 the adrenals are ligated, it may be established immediately, although 

 this is not necessarily the case. Under these conditions the halving 

 of the response is recorded before four successive occlusions have been 

 inflicted and is found in all occlusions which follow in these animals. 

 This precocious loss of level in blood pressure can therefore be obtained 

 either when the animal has been exposed to rapidly repeated cerebral 

 anemia, or when the activity of the adrenal glands is completely abol- 

 ished. Accordingly, the main factor in the production of this early 

 failure of pressure seems concerned in all cases with the availability 

 in the blood stream of some product of adrenal activity. 



Restoration of level of blood pressure. An examination of the supple- 

 mentary rise of blood pressure in the repeatedly occluded but intact 

 cats in comparison with the permanent failure of pressure at half the 

 normal occlusion time when the adrenals are ligated, leads to a consid- 

 eration of the theories of emergency function of the adrenals. This 

 secondary rise is most probably related to the presence of functional 

 adrenals. 



The secondary rise was interpreted in a preliminary report of these 

 experiments as an indication of an increased liberation of adrenalin 

 from the glands, and the constant interval prior to its appearance, as a 

 latent period, relatively long, of adrenal secretion. The argument was 

 advanced that these experiments offered evidence confirming Cannon's 

 position on the increased secretion of adrenalin under emergency condi- 

 tions. However, in view of the presumable consumption of the pro- 

 ducts of adrenal activity during cerebral anemia already discussed, the 

 conception of the emergency liberation of adrenalin must be somewhat 

 modified. The further discussion of any of the current hypotheses of 

 the liberation of adrenalin must be deferred until further experimental 

 evidence has been accumulated. Two definite statements, however, 

 appear justified by the facts. In the first place, since curves of per- 

 fectly normal contour were obtainable in two animals after ligation of 

 the adrenals, an increased liberation or secretion of adrenalin, one or 

 both, is not necessary for the carrying out of the typical blood vascular 

 response to anemia in the fresh animal. 



That these results were due to experimental error can hardly be pos- 

 sible since there was seen in these animals a gradual and relatively slow 



