Nanobashvili Joseph, Neumayer Christoph, Fügl Alexander, Punz Andreas, Blumer Roland, Prager Manfred, Mittlböck Martina, Gruber Helmut, Polterauer Peter, Roth Erich, Malinski Tadeusz, Huk Ihor
Department of Vascular Surgery, Ludwig Boltzmann Research Institute for Interdisciplinary Vascular Medicine, University of Vienna Medical School, Vienna, Austria.
Surgery. 2003 Jan;133(1):91-100. doi: 10.1067/msy.2003.65.
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.
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.
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.
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.
氧衍生自由基导致的细胞膜破裂是缺血/再灌注（I/R）损伤的一个系统性特征。骨骼肌中高浓度的牛磺酸梯度促使我们评估血浆牛磺酸水平（pTau）是否是不同缺血时间后I/R损伤的有用标志物。
将兔子随机分为后肢缺血1小时或2.5小时，随后再灌注2小时的两组（分别为IR1组[n = 12]和IR2.5组[n = 13]）。相应的假手术组（SHAM1组[n = 8]和SHAM2.5组[n = 9]）用作对照。分析的参数包括骨骼肌活检的组织形态计量学和电子显微镜检查、pTau以及血浆丙二醛水平。在I/R损伤3周后评估骨骼肌功能。
在缺血结束时未检测到明显的形态学变化。再灌注后，IR1组出现轻度间质水肿且肌细胞膜完整；pTau未升高。相比之下，IR2.5组出现严重的间质水肿形成（肌纤维间面积增加112%，P <.005）、微血管收缩（微血管面积减少33%，P <.0005），并且血浆丙二醛升高证实了肌细胞膜受损。pTau高于SHAM2.5组（P <.0005）。IR2.5组明显的细胞损伤导致肌肉功能受损（最大强直张力降低2倍，P <.005），但IR1组未出现这种情况。
骨骼肌能够耐受1小时/2小时的I/R，但不能耐受2.5小时/2小时的I/R，后者会导致间质水肿形成、微血管收缩和后期肌肉功能障碍。通过刺激脂质过氧化导致的细胞膜破裂促进细胞内牛磺酸泄漏，导致再灌注后pTau升高，就器官功能可逆性而言，这可能被认为是预后不良的。在兔模型中，pTau似乎是骨骼肌I/R损伤的敏感标志物。
