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失血性休克和饥饿期间的血浆纤连蛋白代谢

Plasma fibronectin metabolism during hemorrhagic shock and starvation.

作者信息

Bowersox J C, Scott R L

出版信息

J Surg Res. 1985 Nov;39(5):445-53. doi: 10.1016/0022-4804(85)90099-x.

Abstract

In this report we characterize the response of the plasma protein fibronectin to hemorrhagic shock and starvation, conditions associated with decreased function of mononuclear phagocyte system (MPS). Rats were starved for 3 days, then half of the animals were subjected to fixed-volume hemorrhagic shock by removing an estimated 35% of their blood volumes for 20 min. After volume replacement, animals were injected iv with [14C]valine. At time points up to 10 hr after hemorrhage, plasma fibronectin concentrations and fibronectin synthesis were quantitated. In additional rats treated identically, fibronectin clearance was assessed by measuring the disappearance of 125I-fibronectin from the plasma. When compared to control animals, either starvation or hemorrhagic shock produced similar perturbations in plasma fibronectin metabolism; fibronectin concentrations were reduced from 241.3 +/- 34.6 micrograms/ml (mean +/- SEM) (controls) to 123 +/- 32.6 micrograms/ml (starvation) or 150.0 +/- 13.0 micrograms/ml (hemorrhage). Plasma [14C]fibronectin specific radioactivities, indicative of fibronectin synthesis, were also significantly reduced. Hemorrhagic shock in rats that previously had been starved did not depress fibronectin concentrations or synthesis to a greater extent than starvation alone. The rates of 125I-fibronectin clearance were increased in starvation and hemorrhagic shock (t1/2 = 233.0 +/- 13.0 min, controls; 174.6 +/- 10.7 min, starvation; 167.4 +/- 13.6 min, hemorrhage). In contrast to changes observed in fibronectin metabolism, total plasma protein concentrations were not significantly altered in any experimental groups. Furthermore, total plasma protein synthesis increased in rats subjected to either starvation or hemorrhagic shock, but decreased in starved rats that were subsequently shocked.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在本报告中,我们描述了血浆蛋白纤连蛋白对失血性休克和饥饿的反应,这两种情况与单核吞噬细胞系统(MPS)功能下降有关。大鼠饥饿3天,然后将一半动物通过移除约35%血容量进行20分钟的固定容量失血性休克。补充血容量后,给动物静脉注射[14C]缬氨酸。在出血后长达10小时的时间点,对血浆纤连蛋白浓度和纤连蛋白合成进行定量。在另外一组同样处理的大鼠中,通过测量血浆中125I-纤连蛋白的消失来评估纤连蛋白清除率。与对照动物相比,饥饿或失血性休克在血浆纤连蛋白代谢方面产生了相似的扰动;纤连蛋白浓度从241.3±34.6微克/毫升(平均值±标准误)(对照组)降至123±32.6微克/毫升(饥饿组)或150.0±13.0微克/毫升(出血组)。指示纤连蛋白合成的血浆[14C]纤连蛋白比放射性也显著降低。先前饥饿的大鼠发生失血性休克时,纤连蛋白浓度或合成的降低程度并不比单独饥饿时更大。饥饿和失血性休克时125I-纤连蛋白清除率增加(半衰期:对照组为233.0±13.0分钟;饥饿组为174.6±10.7分钟;出血组为167.4±13.6分钟)。与纤连蛋白代谢的变化相反,任何实验组的总血浆蛋白浓度均无显著改变。此外,饥饿或失血性休克大鼠的总血浆蛋白合成增加,但在随后发生休克的饥饿大鼠中则降低。(摘要截短于250字)

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