Role of leukocytes in reperfusion injury of skeletal muscle after partial ischemia.

Role of leukocytes in reperfusion injury of skeletal muscle after partial ischemia.
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白细胞在部分缺血后骨骼肌再灌注损伤中的作用。

DOI:
10.1152/ajpheart.1989.257.4.h1068
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发表时间:
1989
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Shires,GT
Shires,GT
中科院分区:
--
文献类型:
--
作者:
Yokota,J;Minei,JP;Fantini,GA;Shires,GT

文献摘要

被引文献

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这些实验评估了白细胞作为缺血后骨骼肌再灌注损伤期间氧自由基(OFR)产生的潜在来源。将肝素化Sprague-Dawley大鼠肾下主动脉钳夹90 min,松开钳夹,再灌注60 min。在基线、缺血期间和再灌注时测定后肢肌肉静息跨膜电位差(Em)和高能磷酸盐含量。研究了四组:对照组,第二组在松开夹钳时接受超氧化物歧化酶和过氧化氢酶(SOD + CAT),第三组在实验前7天接受二甲双胍(DMM)以获得选择性白细胞减少症(白色血细胞= 1,210 +/-144/mm3,中性粒细胞= 1.2%),第四组用别嘌呤醇(ALLO)预处理。在缺血期间,对照组的静息Em显著去极化(从-90.3 +/- 0.3-78.6 +/- 0.5 mV; P <0.05),而磷酸肌酸(CP)耗尽,ATP维持。其他三组在缺血期收集的数据与对照组相似(P = NS)。在再灌注时,尽管对照组和ALLO组的肌肉CP含量恢复(分别为-75.4和-77.0 mV),但观察到静息Em的持续去极化。相比之下,SOD + CAT和DMM组在再灌注后观察到静息Em明显复极(分别为-86.5和-88.6 mV)。这些数据暗示白细胞产生的氧自由基介导缺血后骨骼肌再灌注相关的细胞膜损伤。
These experiments evaluated the leukocyte as a potential source of oxygen free radical (OFR) generation during reperfusion injury in post-ischemic skeletal muscle. The infrarenal aorta of heparinized Sprague-Dawley rats was clamped for 90 min, declamped, and reperfused for 60 min. Hindlimb muscle resting transmembrane potential difference (Em) and high-energy phosphate content were determined at base line, during ischemia, and on reperfusion. Four groups were studied: a control group, a second group receiving superoxide dismutase and catalase (SOD + CAT) on declamping, a third group receiving dimethylmyleran (DMM) 7 days before the experiment to obtain a selective leukopenia (white blood cells = 1,210 +/- 144/mm3, neutrophils = 1.2%), and a fourth group pretreated with allopurinol (ALLO). During the ischemic period, resting Em was significantly depolarized (-78.6 +/- 0.5 mV from -90.3 +/- 0.3; P less than 0.05) in the control group, whereas creatine phosphate (CP) was depleted and ATP maintained. Data collected during the ischemic phase of the three other groups were similar to the control group (P = NS). On reperfusion, persistent depolarization of resting Em was observed despite restoration of muscle CP content in the control and ALLO groups (-75.4 and -77.0 mV, respectively). In contrast, significant repolarization of resting Em was noted after reperfusion in the SOD + CAT and DMM groups (-86.5 and -88.6 mV, respectively). These data implicate leukocyte-generated OFR as mediators of reperfusion-associated cellular membrane injury in postischemic skeletal muscle.