[abstract] INFLAMMATORY RESPONSE TO DECOMPRESSION STRESS: PHARMACOLOGICAL INTERVENTION.

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[abstract] INFLAMMATORY RESPONSE TO DECOMPRESSION STRESS: PHARMACOLOGICAL INTERVENTION.

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Title: [abstract] INFLAMMATORY RESPONSE TO DECOMPRESSION STRESS: PHARMACOLOGICAL INTERVENTION.
Author: Little, T; Butler, BD
Abstract: INTRODUCTION: Experimental decompression sickness (DCS) reportedly causes an inflammatory-like reaction with activation of granulocytes and release of metabolites of arachidonic acid. The release of cyclooxygenase and lipoxygenase mediated eicosanoids, namely thromboxane B2 (TXB2), 11-dehydro thromboxane B2 (11 dh TXB2) and leukotriene E4 (LKE4) may contribute to the DCS response. In this study we examined the effect of several inhibitors of both pathways on DCS outcome. METHODS: The cyclooxygenase inhibitors, indomethacin [Indo] and aspirin [ASA]; the 5-lipoxygenase inhibitor, zilueton [Zil]; the leukotriene receptor antagonist zafirlukast (Accolate) [Acc] and isoproterenol [ISP], a beta-agonist, were administered individually, either subcutaneously or by gavage to randomly selected Sprague-Dawley rats (470 +/- 30gm) prior to compression to 683 kPa for 60 min. Saline or water controls were used for comparison. Following 60 min recovery post decompression, DCS evaluation included: gross symptoms, pulmonary edema (EVLW), bronchoalveolar lavage (BAL) and pleural fluid protein, WBC and differential cell counts, and urine, BAL and plasma eicosanoid analysis using ELISA techniques. Statistical evaluation used ANOVA with Fisher's Test for post hoc analysis (p less than 0.05). RESULTS: Significant changes (+), treated versus controls: A, Zil, Indo, ASA, ISP; c; c; EVLW, +, +, , , ; Art WBC/neutrophils, +/+, , +/, +/, ; Pleural WBC/neutrophils +/+, +/+, /+, , /+; Pleural Protein, +, +, , , ; BAL WBC/neutrophils, +/+, +/, , /+, ; BAL Protein, +, +, , , ; Art TxB2/11dhTxB2/LKE4, /+/, / /+, +/ /, +/ /, / /+; BAL TxB2/11dhTxB2/LKE4, / /+, / /+, +/+/, +/+/+, +/ /; Urine TxB2/11dhTxB2/LKE4, / /, / /, +/+/+, +/+/, +/+/. CONCLUSIONS: The effect of inflammatory-like responses to DCS can be reduced with pharmacological inhibition, however, the mechanical aspects of intavascular bubbles on DCS outcome may remain if no hemodynamic intervention is implemented.
Description: Undersea and Hyperbaric Medical Society, Inc. (http://www.uhms.org)
URI: http://archive.rubicon-foundation.org/5534
Date: 2000

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  • UHMS Meeting Abstracts
    This is a collection of the published abstracts from the Undersea and Hyperbaric Medical Society (UHMS) annual meetings.

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