Neutrophil lipoxygenase activation and leukosequestration in postischemic myocutaneous flaps: role of LTB4.
Reperfusion of ischemic tissues leads to eicosanoid- and polymorphonuclear leukocyte (PMN)-dependent injury. The present experiments were undertaken to examine the effect of myocutaneous flap ischemia-reperfusion on neutrophil 5-lipoxygenase activity and to define the role of leukotriene B4 (LTB4) in postischemic PMN infiltration into such composite tissue grafts. Anesthetized Yorkshire pigs underwent 6 h of rectus abdominis myocutaneous flap ischemia or sham ischemia, and LTB4 generation was measured in calcium ionophore-stimulated neutrophils isolated from the circulation. At 30 min of reperfusion, neutrophil generation of LTB4 increased from a baseline value of 31.0 +/- 6.8 to 98.5 +/- 5.1 ng/5 x 10(6) PMN (P < 0.01) and was significantly greater than those neutrophils isolated from animals subjected to sham ischemia and reperfusion (54.3 +/- 4.1 ng/5 x 10(6) PMN; P < 0.01). Pretreatment of animals with the LTB4-receptor antagonist, SC-41930 (n = 5), significantly attenuated reperfusion-associated 5-lipoxygenase activation (60.3 +/- 11.6 ng LTB4/5 x 10(6) PMN; P < 0.01), suggesting the presence of a positive feedback mechanism for eicosanoid biosynthesis.(ABSTRACT TRUNCATED AT 250 WORDS)[1]References
- Neutrophil lipoxygenase activation and leukosequestration in postischemic myocutaneous flaps: role of LTB4. Kirschner, R.E., Chiao, J.J., Fyfe, B.S., Hoffman, L.A., Davis, J.M., Fantini, G.A. Am. J. Physiol. (1995) [Pubmed]
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