Lefer A M, Tabas J, Smith E F
Pharmacology. 1980;21(3):206-12. doi: 10.1159/000137434.
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.
用大肠杆菌内毒素(5毫克/千克,静脉注射)在麻醉的猫身上诱导内毒素休克。这导致平均动脉血压严重下降,肠系膜上动脉血流量(SMAF)在1小时内显著降低。溶酶体蛋白酶组织蛋白酶D的血浆活性在2小时内增加了6倍。在5小时时,心肌抑制因子(MDF),一种0.75纳摩尔·千克-1·分钟-1的毒素,扩张了内脏循环并显著增加了SMAF。此外,前列环素(PGI2)几乎完全阻止了内毒素处理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可防止血小板聚集并抑制血栓素形成,这两种额外的作用在内毒素休克中可能具有积极的生存价值。