Relation between complement and the febrile response of guinea pigs to systemic endotoxin.

Relation between complement and the febrile response of guinea pigs to systemic endotoxin.
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补体与豚鼠全身内毒素发热反应的关系。

DOI:
10.1152/ajpregu.1999.277.6.r1635
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发表时间:
1999
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Blatteis,CM
Blatteis,CM
中科院分区:
--
文献类型:
--
作者:
Li,S;Sehic,E;Wang,Y;Ungar,AL;Blatteis,CM

文献摘要

被引文献

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我们最近报道,补体(C)系统可能在豚鼠静脉注射脂多糖(LPS)引起的发热反应中起作用,因为C耗竭消除了LPS引起的核心温度(Tc)升高。本研究旨在进一步研究C减少[由眼镜蛇毒因子(CVF)诱导; 20,50,100和200 U/动物iv]与CVF后18 h静脉注射(2 μg/kg)或腹腔注射(8,16,32 μg/kg)LPS引起的成年清醒豚鼠发热之间的关系;对照动物接受无热原盐水。在注射CVF前和注射CVF后18 h测定血清C水平,以总溶血C活性表示,并以CH 100单位表示。在其他实验中,在静脉内和腹膜内注射不同剂量的单独LPS后,在不同的时间间隔测定血清C水平。LPS产生的发热一般高度相似,但不同的发病时间和持续时间,这取决于剂量和给药途径。CVF引起血清C的剂量相关性降低,从0.1136 U降至低于检测值。这些减少成比例地减轻了腹腔内LPS引起的发热,但不是静脉内LPS。静脉内和腹腔内LPS本身引起血清C分别减少25%和40%,表明C级联的激活。然而,这些降低是短暂的,发生在LPS注射后30分钟内发热上升的早期。因此,这些数据支持的概念,C系统可能是至关重要的参与豚鼠全身,特别是腹腔内,LPS的发热反应。
We reported recently that the complement (C) system may play a role in the febrile response of guinea pigs to intravenous lipopolysaccharide (LPS) administration because C depletion abolished the LPS-induced rise in core temperature (Tc). The present study was designed to investigate further the relation between C reduction [induced by cobra venom factor (CVF); 20, 50, 100, and 200 U/animal iv] and the fever of adult, conscious guinea pigs produced by LPS injected intravenously (2 μg/kg) or intraperitoneally (8, 16, 32 μg/kg) 18 h after CVF; control animals received pyrogen-free saline. Serum C levels were measured as total hemolytic C activity before and 18 h after CVF injection and expressed as CH100units. In other experiments, serum C levels were determined at various intervals after the intravenous and intraperitoneal injections at different doses of LPS alone. LPS produced fevers generally of similar heights but of different onset latencies and durations, depending on the dose and route of administration. CVF caused dose-related reductions in serum C, from ∼1,136 U to below detection. These reductions proportionately attenuated the fevers induced by intraperitoneal LPS, but not by intravenous LPS. Intravenous and intraperitoneal LPS per se caused reductions in serum C of 25 and 40%, respectively, indicating activation of the C cascade. These decreases were transient, however, occurring early during the febrile rise ∼30 min after LPS injection. These data thus support the notion that the C system may be critically involved in the febrile response of guinea pigs to systemic, particularly intraperitoneal, LPS.