The Journal of Trauma

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The Journal of Trauma: Injury, Infection, and Critical Care:
October 2006 - Volume 61 - Issue 4 - pp 873-878
doi: 10.1097/01.ta.0000195986.50315.4f
Original Articles

Endothelin-1, Inducible Nitric Oxide Synthase and Macrophage Inflammatory Protein-1[alpha] in the Pathogenesis of Stress Ulcer in Neurotraumatic Patients

Hsieh, Jan-Sing MD; Howng, Shen-Long MD; Huang, Tsung-Jen MD; Wang, Jaw-Yuan MD; Chen, Fang-Ming MD

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Abstract

Background: To prospectively identify histologically and endoscopically the effect of omeprazole on the expression of endothelin-1 (ET-1), inducible nitric oxide synthase (iNOS) and macrophage inflammatory protein-1α (MIP-1α) in the gastric mucosa of neurosurgical patients with stress ulcer.

Methods: Twenty-five patients with severe acute intracranial lesions caused by trauma were enrolled in this study. A 40 mg intravenous bolus of omeprazole (OME) was given daily for 7 days. The intragastric pH was continuously recorded for 24 hours on day 1 and 8. Endoscopic evaluation of the gastric corpus, antrum, and duodenal bulb was performed in the ICU, within 24 hours after brain injury, and at follow-up on the 7th day after admission. Paired biopsies were obtained for histologic examinations and immunohistochemical analysis was performed using a LSAB method for MIP-1α, ET-1, and iNOS.

Results: There were 72% and 70% of gastroduodenal mucosal lesions at the initial and follow-up endoscopies, respectively. However, the severity of mucosal lesions showed significant improvement in most patients at follow-up (p < 0.05). Mean percentages of time intragastric pH were greater than or equal to 4.0 were 20 ± 11% and 70 ± 17% on day 1 and 8, respectively (p < 0.05). The incidences of ET-1, iNOS and MIP-1α expression were not significantly different between the patients before and after OME prophylaxis.

Conclusions: Prophylactic OME is effective in reducing the severity of stress ulcerations in severe neurotraumatic patients. High incidence of tissue ET-1 expression combined with increased activity of iNOS and MIP-1α may be responsible for the gastric mucosal injury. We also show that OME fails to counter the enhancement in the mucosal expression of ET-1, iNOS, and MIP-1α caused by severe brain damage.

© 2006 Lippincott Williams & Wilkins, Inc.

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