With recent technologic developments, the role of computed tomography (CT) in the diagnosis of bowel obstruction has expanded. CT is recommended when clinical and initial radiographic findings remain indeterminate or strangulation is suspected. This modality clearly demonstrates pathologic processes involving the bowel wall as well as the mesentery, mesenteric vessels, and peritoneal cavity. CT should be performed with intravenous injection of contrast material, and use of thin sections is recommended to evaluate a particular region of interest. CT is reported to have a sensitivity of 78%-100% for the detection of complete or high-grade small bowel obstruction but may not allow accurate diagnosis in cases involving incomplete obstruction. In such cases, the use of adjunct enteroclysis is indicated. Furthermore, multiplanar reformatted imaging may help identify the site, level, and cause of obstruction when axial CT findings are indeterminate. CT can also demonstrate findings that indicate the presence of closed-loop obstruction or strangulation, both of which necessitate emergency exploratory laparotomy. Unfortunately, these pathologic conditions may be missed, and patients with suspected severe obstruction or bowel ischemia in whom CT and clinical findings are widely disparate must also undergo laparotomy. In general, however, CT allows appropriate and timely management of these emergency cases.

Madin-Darby canine kidney cells behave like the renal medulla and accumulate small organic solutes (osmolytes) in a hypertonic environment. The accumulation of osmolytes is primarily dependent on changes in gene expression of enzymes that synthesize osmolytes (sorbitol) or transporters that uptake them (myo-inositol, betaine, and taurine). The mechanism by which hypertonicity increases the transcription of these genes, however, remains unclear. Recently, it has been reported that yeast mitogen-activated protein (MAP) kinase and its activator, MAP kinase-kinase, are involved in osmosensing signal transduction and that mutants in these kinases fail to accumulate glycerol, a yeast osmolyte. No information is available in mammals regarding the role of MAP kinase in the cellular response to hypertonicity. We have examined whether MAP kinase and MAP kinase-kinase are regulated by extracellular osmolarity in Madin-Darby canine kidney cells. Both kinases were activated by hypertonic stress in a time-and osmolarity-dependent manner and reached their maximal activity within 10 min. Additionally, it was suggested that MAP kinase was activated in a protein kinase C-dependent manner. These results indicate that MAP kinase and MAP kinase-kinase(s) are regulated by extracellular osmolarity. (J. Clin. Invest. 1994. 93:2387-2392

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