218 K. G. HOSKINS 



jection of such extracts. The generalization was offered that vasoconstric- 

 tion is caused* throughout the splanchnic area. Elliott has reported a single 

 instance in which he applied epinephrin directly to the wall of the in- 

 testine of the fowl, and also gave an intravenous injection. The result, as 

 determined hy inspection, was an intense vasoconstriction. 



Apparently the first to make a more accurate study of the problem was 

 Froehlich(fr) (1911). He enclosed a segment of intestine in a plethysmo- 

 graph and noted the effects of both d- and Z-suprarenin, as well as "ad- 

 renalin." In both cats and dogs a long-lasting contraction of the gut was 

 observed. Few details regarding the experiments were reported. Vincent 

 in his monograph states that sometimes the intestine expands under the 

 influence of epinephrin ; and he publishes a plethysmographic curve, which 

 shows a slight degree of expansion that might be interpreted as passive. 



Perfusion studies were made upon vessels of the isolated intestine by 

 Brodie and Dixon (1904). The addition of epinephrin to the perfusion 

 fluid materially decreased the venous outflow. They found that dosages 

 as small as 0.0001 mg. were effective. Ogawa (1912) has reported the 

 results of similar studies. He worked upon rabbits, cats, and dogs. HSs 

 findings were that the levorotatory form of epinephrin in greater con- 

 centration than 1:5,000,000 caused a clean-cut constriction in the in- 

 testinal vessels, as was shown by a decreased venous outflow. With higher 

 concentrations of this general magnitude, occasionally a secondary dilata- 

 tion was observed. In higher dilutions, e.g., 1:50,000,000, the effect was 

 primary dilatation. It was found that the dextrorotatory form had a 

 similar effect but larger doses were required. 



Hartman and McPhedran (1917) reported further plethysmograph 

 studies, using dogs and cats as the experimental animals. A loop of 

 small intestine, about a third of its total length, was isolated with care to 

 protect the circulation and placed in an oncometer. In most cases the 

 effect of epinephrin in both large and small doses was primarily to cause 

 constriction of the intestine. With the smaller doses this was almost in- 

 variably the effect. As the quantity was increased, however, a prolonged 

 and marked dilatation succeeded the preliminary constriction (Fig. 10). 

 In two exceptional cases studied by these investigators the least effective 

 dose caused at least apparent dilatation ; in these, there was some 

 probability of experimental error. The threshold for the constrictor 

 effects was found to vary within fairly wide limits, from 0.014 to 

 0.07 c.c. of 1:100,000 solution per kilogram of body weight. These 

 dosages were slightly depressor. That the contraction of the intestinal 

 segment was not merely a passive effect due to the lower arterial pressure, 

 however, appeared from the fact that the. intestinal decrease preceded that 

 of arterial pressure, that the lowest points of the plethysmographic and 

 blood-pressure curves did not correspond, and that the duration of the 

 effect in the intestine was quite different from that on systemic pressure. 



