J Reconstr Microsurg 2001; 17(2): 139-144
DOI: 10.1055/s-2001-12703
Copyright © 2001 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel.: +1(212) 584-4662

Thromboxane A2 Release in Ischemia and Reperfusion of Free Flaps in Rats, Studied by Microdialysis

Mihai Ionac1 , Dirk Schaefer2 , Max Geishauser3
  • 1Second Surgical Clinic, University of Medicine and Pharmacy, Timisoara, Romania
  • 2Verfuegungsgebaeude fuer Forshchung and Entwicklung, Universitaet Mainz, Germany
  • 3Department of Plastic and Reconstructive Surgery, Klinikum Rechts der Isar, Technical University of Munich, Germany
Further Information

Publication History

Publication Date:
31 December 2001 (online)

ABSTRACT

Several studies have implicated enhanced eicosanoid production in reperfusion injury. The reported study investigated the use of microdialysis in the in vivo measurement of thromboxane levels during reperfusion in ischemic and reperfused experimental free muscle flaps. Microdialysis probes were inserted, via a guide, into the gracilis and semitendinosus free flap in the rat. The probe was perfused at a flow of 5 μl/min, with samples collected at intervals of 20 min, and analyzed by the ELISA technique. Animals were randomly distributed into three groups. After ischemic periods of 2, 4, and 6 hr, respectively, the free muscle flaps were revascularized on the contralateral femoral vessels. The mean thromboxane level during ischemia was 1785.34 ± 124.81 pg/ml. The mean levels of thromboxane rose significantly (p < 0.05), compared to base level, with 151.65 percent in the 2-hr ischemia group, 192.33 percent in the 4-hr ischemia group, and 294.69 percent in the 6-hr ischemia group, and correlated well with histologic observations.

The results suggest that a microdialysis technique, combined with a sensitive assay for measuring thromboxane, is a useful method for in vivo monitoring of inflammatory processes during ischemia and reperfusion. The evolution of thromboxane release following 6 hr of ischemia indicates that this mediator may be involved in facilitation of cell death, following ischemia and reperfusion, since its tissue level correlates with histologic tissue damage.

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