230 K. G. HOSKOTS 



in dogs the vagi were cooled by the application of glass tubes through 

 which ice water was circulating. The nerves were then allowed to return 

 to room temperature. The pulse rate, arterial pressure, respiratory rate 

 and amplitude were all affected, but little change in venous pressure 

 occurred. The data as a whole were regarded as indicating that in the 

 anesthetized dogs the venopressor mechanism played very little part. 

 The rise in venous pressure was ascribed predominantly to decreased 

 capacity of the arterial system and slowed heart rate. 



In experiments on decerebrated cats, however, clear evidence was 

 obtained of the operation of the venopressor mechanism. With the vagi 

 intact, there was a rise of arterial pressure and slowing of the heart 

 accompanying the rise in venous pressure. With the vagi cut, the cardiac 

 factor being thereby eliminated, the rise in venous pressure was still 

 produced. Since the respiratory movements were decreased in height and 

 frequency, a condition which would tend to lower rather than raise venous 

 pressure, the venomotor mechanism would seem necessarily to have to be 

 invoked to explain the venous rise. 



One gathers from the somewhat involved presentation that Connet's 

 data as a whole indicate that epmephrin, administered in doses to cause 

 a clean-cut rise in arterial pressure, results almost uniformly in aug- 

 mented venous pressure. This augmentation is due in varying propor- 

 tions to contraction of the arterial bed, interference with the cardiac 

 output, changes in the respiratory rate, and stimulation of sympathetic 

 fibers causing contraction of the veins themselves. 



From the foregoing evidence it would appear that epmephrin, at least 

 in such quantities as those with which the body normally has to deal, 

 exercises little influence upon venous blood-pressure. Venous pressure 

 changes, therefore, apparently play at most a minor role in the general 

 circulatory reactions to this substance. 



Factors Modifying the Pressor Response to Epinephrin 



In connection with the discussion of the vasodilator effects of epineph- 

 rin, and in subsequent paragraphs the action of certain factors in converting 

 depressor reactions to pressor is discussed. Obviously, a reversal of any 

 of the conditions mentioned would result in the conversion of pressor 

 to depressor reactions. The first effect in this latter case would be a 

 decrease in the pressor response. Other conditions modifying the reaction 

 to epinephrin have been reported. 



In any condition in which the sympathetic system becomes abnor- 

 mally irritable the response to epinephrin is of course increased. This 

 fact forms the basis of the well-known Goetsch test for thyroid disorders. 

 The data on this point are discussed in the chapter on "Tests for Thyroid 



