Inhibitors of prostaglandin synthesis or cathepsin B prevent muscle wasting due to sepsis in the rat.
Inhibitors of prostaglandin synthesis or cathepsin B prevent muscle wasting due to sepsis in the rat.
复制标题
前列腺素合成抑制剂或组织蛋白酶 B 可防止大鼠因败血症而导致肌肉萎缩。
DOI：
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发表时间：
1984
影响因子：
15.9
通讯作者：
D. Secrist
中科院分区：
文献类型：
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作者：
R. Ruff;D. Secrist
肺炎链球菌全身感染引起大鼠骨骼肌萎缩，抽搐和强直张力降低，并改变细胞内电解质组成。组织蛋白酶B活性在病程早期选择性升高。组织蛋白酶B抑制剂Luepepeptin和前列腺素合成抑制剂吲哚美辛可预防肌肉萎缩和收缩力受损。吲哚美辛，但不是亮抑酶肽，防止细胞内电解质的变化。对乙酰氨基酚可减少发热，但不能防止肌肉萎缩、收缩力受损或细胞内电解质改变。与脓毒症相关的肌肉萎缩和收缩力受损可能涉及组织蛋白酶B活性的选择性前列腺素刺激。细胞内电解质变化可能涉及前列腺素合成，但不需要组织蛋白酶B激活。
Systemic infection with Streptococcus pneumoniae produced atrophy, decreased twitch and tetanic tension, and altered intracellular electrolyte composition in rat skeletal muscle. Cathepsin B activity was selectively elevated early in the course of illness. Luepeptin, a cathepsin B inhibitor, and indomethacin, a prostaglandin synthesis inhibitor, prevented muscle atrophy and impaired contractility. Indomethacin, but not leupeptin, prevented the intracellular electrolyte changes. Acetaminophen reduced fever but did not prevent muscle atrophy, impaired contractility, or altered intracellular electrolytes. Muscle wasting and impaired contractility associated with sepsis may involve selective prostaglandin stimulation of cathepsin B activity. Intracellular electrolyte changes may involve prostaglandin synthesis but do not require cathepsin B activation.