EXPERIMENTAL PRODUCTION OF GASTRIC ULCER. 135 



inasmuch as it is questionable whether such a variety of poisons should all cause 

 a constriction of the vessels, especially if we consider that several of these sub- 

 stances were vasodilators. That fatty degeneration of the glandular elements, 

 such as described by Gay and Southard, is not the cause of the ulceration is evi- 

 denced by our inability to demonstrate any such change in sections through 

 ulcerated areas stained by osmic acid. 



It remains for further experiments to determine whether or not it is pos- 

 sible to establish a chronic lesion. In one instance an animal which had been 

 injected with venom several months previously was killed and a somewhat 

 older ulcer found, which under the microscope revealed a base infiltrated with 

 round cells; no attempt at healing was observed. It is not unlikely that, if the 

 animal remains alive, such an acute toxic ulcer may become chronic, especially 

 if it be perpetuated by a bacterial infection, hyperchlorhydria, or anemia. 



Total number of guinea-pigs, excluding those used for testing the strength of the venom, 127. 



Of 41 injected with venom alone, 35 showed ulcer (85 per cent). 



Of 30 animals injected with venom and alkali (or with venom + atropine and alkali), 6 



showed ulcer (20 per cent). 

 Pilocarpine, 14 animals: 



Control (venom alone), 4 animals, 4 showed ulcer (100 per cent). 



Venom and pilocarpine, 8 animals, 8 showed ulcer (100 per cent). 



Pilocarpine alone, 2 animals, 2 showed ulcer (100 per cent). 

 Atropine, 34 animals: 



Control (venom alone), 9 animals, 8 showed ulcer. 



Venom and atropine, 6 animals, 6 showed ulcer. 



Venom, atropine, and alkali, 13 animals, 4 showed ulcer (1 of these cases was doubtful). 



Atropine alone, 6 animals, 2 showed ulcer (2 died too early). 

 MgCl 2 , 4 animals, 1 showed hemorrhagic erosion. 

 Paraldehyde, 2 animals, 2 showed ulcers. 

 Phenol, 2 animals, 2 showed ulcer. 

 Chloroform, 2 animals, 2 showed ulcer and hemorrhagic erosion. 



In addition several animals were injected with sodium fluoride, CuSo 4 , and MgCls with 

 positive results. 



Hirudin experiments, 14 animals: 



Hirudin + venom, 8 animals, 8 showed ulcer. 

 Controls (venom alone), 5 animals, 5 showed ulcer. 



CONCLUSIONS. 



After subcutaneous injections of the venom of Heloderma into guinea-pigs, 

 gastric ulcer and hemorrhagic erosions are found in approximately 85 per cent 

 of all the animals used. These ulcerations are aggravated by atropine as well 

 as by pilocarpine; it is, therefore, unlikely that ulceration is due to the excre- 

 tion of the venom through the intact mucosa. Various poisonous substances, 

 otherwise differing widely in their chemical character and pharmacological 

 actions, may all produce similar changes in the gastric mucosa. The effect of 

 these substances is not a specific, but is probably an indirect one, acting either 

 through a weakening influence on the circulation or through a direct injurious 

 effect on the cells of the mucosa. The degree of efficacy of these substances is, 

 on the whole, parallel to their general toxic effect or to the extent to which they 

 affect the general vitality of the animals. There exist, however, marked differ- 

 ences in the tendency of these substances to produce ulceration (cf. especially 

 magnesium chloride and paraldehyde) . 



