Surgery
Volume 133, Issue 1 , Pages 91-100, January 2003

Ischemia/reperfusion injury of skeletal muscle: Plasma taurine as a measure of tissue damage☆☆

Departments of Vascular Surgery, Anatomy, Surgical Research Laboratories, Ludwig Boltzmann Research Institute for Interdisciplinary Vascular Medicine, Department of Medical Computer Sciences, University of Vienna Medical School, Vienna, Austria; and Department of Chemistry and Biochemistry, Ohio University, Athens, Ohio

Accepted 26 June 2002.

Abstract 

Background. Cell membrane rupture by oxygen-derived free radicals is a systematic feature of ischemia/reperfusion (I/R) injury. High taurine concentration gradients in skeletal muscle prompted us to evaluate whether plasma taurine levels (pTau) are a useful marker of I/R injury after different periods of ischemia. Methods. Rabbits were randomly assigned to either 1 or 2.5 hours of hind-limb ischemia followed by 2 hours of reperfusion (groups IR1 [n = 12] and IR2.5 [n = 13], respectively). Corresponding sham groups (SHAM1 [n = 8] and SHAM2.5 [n = 9]) were used as controls. Analyzed parameters included histomorphometry and electron microscopy of skeletal muscle biopsies, pTau, and plasma level of malondialdehyde. Skeletal muscle function was assessed 3 weeks after I/R injury. Results. No significant morphologic changes were detectable at the end of ischemia. After reperfusion, mild interstitial edema with intact muscle cell membranes developed in IR1 group; pTau was not increased. IR2.5 group, by contrast, showed severe interstitial edema formation (interfiber area increased by 112%, P < .005), microvascular constriction (microvessel area decreased by 33%, P < .0005), and damage to the muscle cell membranes that was confirmed by the increased plasma malondialdehyde. pTau was higher than in the SHAM2.5 group (P < .0005). Pronounced cell damage in IR2.5 group resulted in impaired muscle function (maximal tetanic tension was reduced 2 times, P < .005) but not in IR1 group. Conclusion. Skeletal muscle tolerates 1 h/2 h but not 2.5 h/2 h of I/R, the latter resulting in interstitial edema formation, microvascular constriction, and a late muscle dysfunction. Cell membrane rupture through stimulated lipid peroxidation promotes leakage of intracellular taurine, leading to increased pTau after reperfusion and may be considered as prognostically unfavorable in terms of organ function reversibility. In the rabbit model, pTau seems to be a sensitive marker of I/R injury to skeletal muscle. (Surgery 2003;133:91-100.)

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 Supported in part by a grant from Public Health Service (HL 55397).

☆☆ Reprint requests: Joseph Nanobashvili, MD, Department of Vascular Surgery, University of Vienna Medical School, Waehringer Guertel 18-20, A-1090, Vienna, Austria.

 0039-6060/2003/$30.00 + 0

PII: S0039-6060(02)21671-2

doi:10.1067/msy.2003.65

Surgery
Volume 133, Issue 1 , Pages 91-100, January 2003