Salutary effects of prostacyclin in endotoxic shock.

Salutary effects of prostacyclin in endotoxic shock.
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前列环素在内毒素休克中的有益作用。

DOI:
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发表时间:
1980
期刊:
影响因子:
3.1
通讯作者:
E. F. Smith
E. F. Smith
中科院分区:
医学4区
文献类型:
--
作者:
A. M. Lefer;J. Tabas;E. F. Smith

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用大肠杆菌内毒素(5 mg/kg,静脉注射)对麻醉猫进行内毒素休克,导致平均动脉血压严重下降,1 小时内肠系膜上动脉血流 (SMAF) 显着下降。组织蛋白酶 D(一种溶酶体蛋白酶)的血浆活性在 2 小时内增加了 6 倍。 5小时时,心肌抑制因子(MDF)(0.75 nmol.kg-1.min-1的有毒物质)扩张内脏循环并显着增加SMAF。此外,PGI2几乎完全阻止了给予内毒素的猫循环血液中组织蛋白酶D和MDF的积累。这些发现表明,PGI2 在内毒素休克中发挥多种有益作用,包括血管舒张和溶酶体膜的稳定。此外,已知 PGI2 可以防止血小板聚集并抑制血栓素形成,这两种额外作用可能在内毒素休克中具有积极的生存价值。
Endotoxin shock was induced in anesthetized cats with E. coli endotoxin (5 mg/kg, i.v.) This produced a severe decline in mean arterial blood pressure and a marked decrease in superior mesenteric artery flow (SMAF) within 1 h. The plasma activity of cathepsin D, a lysosomal protease, increased 6-fold by 2 h. At 5 h, myocardial depressant factor (MDF), a toxic of 0.75 nmol.kg-1.min-1 dilated the splanchnic circulation and significantly increased SMAF. In addition, PGI2 almost completely prevented the accumulation of cathepsin D and MDF in the circulating blood of cats given endotoxin. These findings suggest that PGI2 exerts a variety of beneficial actions in endotoxin shock including vasodilation and stabilization of lysosomal membranes. In addition, PGI2 is known to prevent platelet aggregation and suppress thromboxane formation, two additional effects that may be of positive survival value in endotoxin shock.