Pathogenesis. 401 



established; the lack of arterial blood and the proportionately 

 increased contents of the blood and tissues in carbon-dioxide act 

 for some time as a stimulus to peristalsis. Some of the more 

 active intestinal contractions become convulsive, the intestinal 

 tube becomes hard and unyielding-, and colicky pains are caused 

 by compression and pulling of terminal nerve filaments in the 

 intestinal wall and its mesentery. Since contractions appear at 

 variable intervals in the excluded portion of intestines, and since 

 their duration is variable, the attacks of pain last a shorter or 

 longer period and appear after variable intervals. If arteries 

 have become thrombosed which supply very large portions of 

 the intestines, we may see a continuous colicky attack, because 

 individual places in the affected long piece of intestinal tube are 

 necessarily convulsively contracted, so that tliere may not be 

 any interval free from pain. 



In cases with lasting anemia of the affected parts, the erst- 

 while increased intestinal peristalsis soon becomes sluggish and, 

 as shown by experiments, it ceases entirely after one to two 

 hours. The early cessation of peristalsis is due to the complete 

 stoppage of the arterial blood supply; as soon as the supply of 

 oxygen and nutritive material is used up this leads to a dis- 

 turbance of nutrition of the tissue elements, and the muscularis 

 then loses the power to contract. 



It is different when hemorrhagic infiltration of the intes- 

 tinal wall has occurred. The blood current through the capil- 

 laries does not cease entirely, and even after thrombosis the 

 tissue elements receive a certain amount of oxygen and nutri- 

 tive material. To this is due the fact that the muscularis retains 

 its contractility, and in the presence of accumulating carbon- 

 dioxide it will therefore undergo severe convulsive contractions. 

 Nevertheless, in some of these cases there occurs, sooner or 

 later, a cessation of peristalsis, due to several factors. If the 

 territory affected by thrombosis is very extensive there may be 

 a severe and long continued lowering of the blood pressure, 

 which will so damage the nutrition of the muscularis that its 

 contractility is lost. The damaging effect of the lowered blood 

 pressure upon the nutrition of the tissues is intensified by an 

 edematous-hemorrhagic infiltration which occurs. An infiltra- 

 tion of a higher degree may mechanically interfere with mus- 

 cular contraction. 



An important factor in the cessation of peristalsis is over- 

 distension of the intestinal wall by extravasated blood and still 

 more, by gases accumulating within a short time. This may 

 very easily occur in horses, since the intestinal contents are of 

 vegetable origin; the feed enters the intestinal tract compara- 

 tively rapidly, and abundant blood extravasation into the bowels 

 in the presence of bacteria leads to rapid fermentative and 

 putrefactive processes, as had already been shown by Bollinger 

 and Panum. In this manner gases are formed abundantly in the 

 infarcted intestine, and^ since they cannot be absorbed sufficient- 



