[Physiopathology of paralytic ileus secondary to chemical peritonitis. Experimental study in dogs]

The intestinal paralysis that follows peritonitis has been classically explained as the result of local inflammation of the overlying serosa (Stokes's law). The main object of this study is to determine if these motor alterations, the most relevant of them being intestinal paralysis, are really due to local factors or to general factors in view of the intense affectation that peritonitis induces in the organism. For this purpose we used animals with an isolated and exteriorized intestinal loop to study loop motility during peritonitis in the absence of direct local contact with the process. To test the operation of the smooth intestinal muscle and intrinsic plexus we used two types of motor stimuli: hormonal (insulin) and pure (prostigmine). We found that the isolated loop presented the normal motor characteristics of the small intestine. When peritonitis was achieved, all motor activity ceased in the intracavitary loops and in the isolated loops exposed to acid, so all the intestinal segments were completely paralyzed. The administration of insulin under these circumstances only had effect on the exteriorized loop, where we recorded motor activity similar to that of normal conditions. The administration of prostigmine caused the appearance of a sharp, synchronic contraction of the three intestinal segments studied. Based on these findings, we conclude that the smooth fiber of the small intestine is not paralyzed during peritonitis and can exhibit intense contraction when the motor plate is stimulated with prostigmine.(ABSTRACT TRUNCATED AT 250 WORDS)