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Research Article Free access | 10.1172/JCI115233

Leukotrienes as mediators in ischemia-reperfusion injury in a microcirculation model in the hamster.

H A Lehr, A Guhlmann, D Nolte, D Keppler, and K Messmer

Department of Experimental Surgery, University of Heidelberg, Germany.

Find articles by Lehr, H. in: PubMed | Google Scholar

Department of Experimental Surgery, University of Heidelberg, Germany.

Find articles by Guhlmann, A. in: PubMed | Google Scholar

Department of Experimental Surgery, University of Heidelberg, Germany.

Find articles by Nolte, D. in: PubMed | Google Scholar

Department of Experimental Surgery, University of Heidelberg, Germany.

Find articles by Keppler, D. in: PubMed | Google Scholar

Department of Experimental Surgery, University of Heidelberg, Germany.

Find articles by Messmer, K. in: PubMed | Google Scholar

Published June 1, 1991 - More info

Published in Volume 87, Issue 6 on June 1, 1991
J Clin Invest. 1991;87(6):2036–2041. https://doi.org/10.1172/JCI115233.
© 1991 The American Society for Clinical Investigation
Published June 1, 1991 - Version history
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Abstract

Leukotriene (LT)B4 promotes leukocyte chemotaxis and adhesion to the endothelium of postcapillary venules. The cysteinyl leukotrienes, LTC4, LTD4, and LTE4, elicit macromolecular leakage from this vessel segment. Both leukocyte adhesion to the endothelium and macromolecular leakage from postcapillary venules hallmark the microcirculatory failure after ischemia-reperfusion, suggesting a role of leukotrienes as mediators of ischemia-reperfusion injury. Using the dorsal skinfold chamber model for intravital fluorescence microscopy of the microcirculation in striated muscle in awake hamsters and sequential RP-HPLC and RIA for leukotrienes, we demonstrate in this study that (a) the leukotrienes (LT)B4 and LTD4 elicit leukocyte/endothelium interaction and macromolecular leakage from postcapillary venules, respectively, that (b) leukotrienes accumulate in the tissue after ischemia and reperfusion, and that (c) selective inhibition of leukotriene biosynthesis (by MK-886) prevents both postischemic leukotriene accumulation and the microcirculatory changes after ischemia-reperfusion, while blocking of LTD4/E4 receptors (by MK-571) inhibits postischemic macromolecular leakage. These results demonstrate a key role of leukotrienes in ischemia-reperfusion injury in striated muscle in vivo.

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