EXPERIMENTAL PRODUCTION OF GASTRIC ULCER. 133 



At first it seemed doubtful whether any change was demonstrable after admin- 

 istration of the latter substance, but Doctor Loeb has since succeeded in pro- 

 ducing lesions. It seems, therefore, certain that this reaction is in no wise spe- 

 cific for venom and that possibly all poisons, whether organic or inorganic, 

 which will keep the animal in a state of marked intoxication will produce some 

 change in the gastric mucosa. Whether this lesion is directly proportional to 

 the depression caused by the poison we are not prepared to state. Certainly 

 this is not invariably the case, inasmuch as magnesium-chloride animals, 

 although markedly affected, showed very few lesions; usually, however, the 

 severity of the lesion was in direct proportion to the degree of intoxication 

 manifested by the animal. 



SIGNIFICANCE OF THROMBOSIS IN GASTRIC ULCERATION. 



As has been previously stated, thrombi were found in the vessels in the 

 neighborhood of the ulcer, and as a decrease in the blood-supply had to be con- 

 sidered as a possible cause of the ulcers, and inasmuch as thrombi might be the 

 cause of such a diminution in the blood-supply, we had to determine whether 

 thrombosis was a primary or secondary factor in the formation of the ulcers. 

 For this purpose we caused experimentally an incoagulability of the blood by 

 injecting hirudin into the jugular vein, this being followed by the injection of 

 venom. If ulcers occurred under such conditions, it was certain that throm- 

 bosis could be ruled out as an etiological factor. After several failures due to 

 errors in technique, we succeeded in fulfilling all conditions in eight animals, 

 and in all of them hirudin, instead of preventing ulceration and hemorrhage, 

 actually augmented the latter. There were just as many ulcers present, and 

 the hemorrhage, which was formerly in direct proportion to the degree of ero- 

 sion of the vessels, assumed alarming proportions after the injection of this 

 substance. Immediately on the death of the animal we were accustomed to 

 -withdraw 5 to 10 c.c. of blood from the heart, to test its coagulability and to 

 control the action of the hirudin. In several instances the blood was not coag- 

 ulated in vitro two hours after death. In one interesting case the animal had 

 been in a very weak condition for some time before death. On opening its 

 heart we were unable to withdraw more than a few drops of blood; the stomach, 

 however, was distended with liquid blood and in the wall of the stomach were 

 found several well-defined ulcers. The animal had practically bled to death 

 into its stomach. In several animals a hemorrhagic mottling of the spleen was 

 also observed. 



From these observations we may conclude that thrombosis is not a pri- 

 mary factor in the production of the ulcers ; that it is a secondary process due to 

 changes in the circulation and to the liberation of tissue coagulins in the affected 

 .area; moreover, that it is beneficial, inasmuch as it prevents fatal hemorrhage. 



IS THE ULCERATION DEPENDENT UPON PEPTIC DIGESTION ? 



Beneke believed that in the cases reported by him the ulcers were primarily 

 caused by digestion, but no adequate experimental proof was offered for this 

 interpretation. Bolton concluded that inasmuch as alkali prevented the for- 



