EFFECT OF SUPEROXIDE-DISMUTASE PLUS CATALASE ON CA-2+ TRANSPORT IN ISCHEMIC AND REPERFUSED SKELETAL-MUSCLE
EFFECT OF SUPEROXIDE-DISMUTASE PLUS CATALASE ON CA-2+ TRANSPORT IN ISCHEMIC AND REPERFUSED SKELETAL-MUSCLE
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DOI：
10.1016/0022-4804(87)90060-6
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发表时间：
1987-01-01
影响因子：
2.2
通讯作者：
ZELENOCK, GB
中科院分区：
文献类型：
--
作者：
LEE, KR;CRONENWETT, JL;ZELENOCK, GB
细胞毒性氧代谢物可能导致与缺血和再灌注相关的骨骼肌损伤。本研究采用大鼠后肢缺血模型，研究氧自由基清除剂超氧化物歧化酶（SOD）和过氧化氢酶（CAT）预处理对缺血再灌注期肢体骨骼肌肌浆网（SR）对Ca2+摄取的影响。将SOD和CAT与聚乙二醇偶联以延长其半衰期。麻醉大鼠（约350 g）在单侧后肢止血带缺血3小时前5分钟静脉注射偶联SOD (2 mg/kg) + CAT (3.5 mg/kg) （n= 6，治疗组）或0.9生理盐水（4 ml/kg） （n= 6，对照组）。再灌注19小时后，从每条小腿切除肌肉并均质。差速离心分离骨骼肌SR。然后用双波长分光光度法测量SR对atp依赖性Ca2+的摄取，并将其用作肌肉功能的指标。SOD和CAT预处理维持了缺血再灌注肢体骨骼肌SR对Ca2+的较高摄取率(治疗组（2.29±0.21）vs对照组（1.61±0.06 μmol Ca2+/mg蛋白/min）。这些结果提示细胞毒性氧代谢物与缺血性再灌注骨骼肌损伤的发病机制有关。
Cytotoxic oxygen metabolites may contribute to skeletal muscle damage associated with ischemia and reperfusion. This study utilized a rat hindlimb ischemia model to investigate the effect of pretreatment with oxygen free radical scavengers superoxide dismutase (SOD) and catalase (CAT) on skeletal muscle Ca2+uptake by sarcoplasmic reticulum (SR) in limbs subjected to periods of ischemia and reperfusion. SOD and CAT were conjugated to polyethylene glycol to prolong their half lives. Anesthetized rats (ca. 350 g) received an iv injection of either conjugated SOD (2 mg/kg) plus CAT (3.5 mg/kg) (n= 6, Treated Group) or 0.9 saline (4 ml/kg) (n= 6, Control Group) 5 min before unilateral hindlimb tourniquet ischemia of 3 hr duration. After 19 hr of reperfusion, muscle from each lower leg was excised and homogenized. Skeletal muscle SR was isolated by differential centrifugation. ATP-dependent Ca2+uptake by the SR was then measured with dual wavelength spectrophotometry and used as an index of muscle function. Pretreatment with SOD and CAT maintained higher rates of Ca2+uptake by SR of skeletal muscle from postischemic reperfused limbs (Treated Group 2.29 ± 0.21 vs Control Group, 1.61 ± 0.06 μmole Ca2+/mg protein/min). These results implicate cytotoxic oxygen metabolites in the pathogenesis of ischemic reperfusion skeletal muscle injury.