Ischemia/reperfusion injury of skeletal muscle: plasma taurine as a measure of tissue damage.
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.


CONCLUSIONS
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.
Nanobashvili
Joseph
J
Department of Vascular Surgery, Ludwig Boltzmann Research Institute for Interdisciplinary Vascular Medicine, University of Vienna Medical School, Vienna, Austria.
Neumayer
Christoph
C
Fügl
Alexander
A
Punz
Andreas
A
Blumer
Roland
R
Prager
Manfred
M
Mittlböck
Martina
M
Gruber
Helmut
H
Polterauer
Peter
P
Roth
Erich
E
Malinski
Tadeusz
T
Huk
Ihor
I
D000818:Animals; D015415:Biomarkers; D002462:Cell Membrane / Q000473:pathology; D003402:Creatine Kinase / Q000097:blood; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008297:Male; D008315:Malondialdehyde / Q000032:analysis; D008854:Microscopy, Electron; D009119:Muscle Contraction; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000473:pathology* / Q000648:ultrastructure; D011817:Rabbits; D020127:Recovery of Function; D015427:Reperfusion Injury / Q000097:blood* / Q000473:pathology*; D013654:Taurine / Q000032:analysis / Q000097:blood*
D015415:Biomarkers; D013654:Taurine; D008315:Malondialdehyde; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase