No abstract

Mesenteric venous thrombosis (MVT), an uncommon but important clinical entity, is one possible cause of ischemia or infarction of the small intestine. Diagnosis of this condition is sometimes difficult and treatment is often delayed because patients usually present with nonspecific abdominal symptoms. The hallmark is pain that is out of proportion to the physical findings. We report two cases of MVT, where the patients initially presented with vague abdominal symptoms. Diagnosis was made on the basis of computed tomography of the abdomen showing thrombus within the superior mesenteric vein. A search for a precipitating condition revealed no evidence of a hypercoagulable state, myeloproliferative disorder, or malignancy. These cases illustrate well the nonspecific clinical presentation of MVT. A high index of suspicion, recognition of known risk factors, or a previous history of venous thrombosis coupled with a history of nonspecific abdominal symptoms should alert clinicians to the possibility of MVT. Early diagnosis and prompt anticoagulation are the mainstay of therapy unless there are signs of peritonitis that necessitate surgical resection of the infarcted bowel.

SUMMARY Since intestinal fluid production in experimental cholera can be limited by cycloheximide, an inhibitor of protein synthesis, the same agent was used to determine whether there are similar mechanisms for fluid production in response to an osmotic gradient. Intestinal fluid production was measured by perfusion of paired rabbit jejunal loops (10 cm) in vivo, in controls, and in animals receiving 20 nig/kg intravenous cycloheximide one hour before perfusion. In each animal one loop was perfused with isotonic Ringer's lactate and the other with a hypertonic glucose-Ringer's lactate solution, 563 mOsm/litre. In control animals mean fluid production in the hypertonic loop was seven times that in the isotonic loop. Cycloheximide decreased the fluid response to the hypertonic stimulus by one half (p < 0'001). In a separate measurement of bidirectional sodium fluxes, using sodium22, it was shown that the decreased net sodium movement into the lumen observed after cycloheximide was the result of decreased flux from blood to lumen. The major histological alteration after cycloheximide was on the crypt epithelial cells with sparing of villus crests. Glucose absorption was unaffected. These data parallel the observed effect of cycloheximide on cholera exotoxin induced secretion, suggesting that a process requiring continued protein synthesis is also necessary for the intestinal fluid response to an osmotic gradient.Intravenous cycloheximide prevents the cholera exotoxin induced movement of fluid into loops of rabbit jejunum. Glucose absorption is unaffected by the combination of intravenous cycloheximide and intraluminal cholera exotoxin (Serebro, Iber, Yardley, and Hendrix, 1969). Studiesof bidirectional sodium fluxes indicate that the major effect of cycloheximide is in diminishing the cholera exotoxin stimulated movement of sodium into the lumen (Grayer, Serebro, Iber, and Hendrix, 1970

No abstract