Biosynthesis of Intestinal Mucin in Shock

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Abstract
Little is known concerning the specificity of the so-called mucus barrier and the exact mechanism of its protective role against intra-cellular penetration of potentially toxic materials, whether normally present In the intestinal lumen or unnatural poisons. Our studies indicate that such a barrier against unnatural poisons exists and that during normovolemic shock it is markedly reduced. The enzymatic digestion of the intestinal mucosa seen late in shock in the dog is another example of the fall of the mucosal defense barrier throughout the whole intestinal surface. The etiologic agent of this "tryptic" hemorrhagic necrosis was demonstrated in a previous study. In the present study the cessation of mucus production by the intestinal mucosa has been demonstrated early in shock. In vivo biopsies have shown that the normal mucosa is always covered by a continuous coat of mucin. The rate of production of mucin is such that a 2 to 3 hr. period of decreased production is reflected by the disappearance of the mucus coat from the tips of the villi. The time and the site of appearance of the initial tryptic hemorrhagic necrosis seem to coincide with the. loss of the shield of mucin. It is thus postulated that the loss of mucus production is a possible pathogenetlc factor in rendering the intestinal mucosa accessible to proteolytlc digestive enzymes. Should the observed fall in the mucus barrier to both unphysiologic and physiologic poisons involve other toxins normally present In the intestinal lumen, passage into the blood stream of these noxious substances might play an important role In determining the pattern of the later stages of shock.