Nandiwada P, Hyman A L, Feigen L P, Kadowitz P J
Arch Int Pharmacodyn Ther. 1980 May;245(1):118-28.
The cardiopulmonary actions of prostaglandin (PG) 6-keto-E1, a newly discovered metabolite of PGI2, were investigated in the intact chest dog. Injections of 6-keto-PGE1 into the superior vena cava in doses of 1-30 microgram caused dose-dependent decreases in pulmonary arterial and systemic arterial pressures. Inasmuch as cardiac output increased and left or right atrial pressure was unchanged, the decreases in pulmonary and systemic vascular resistances. Reductions in systemic arterial pressure and systemic vascular resistance were similar when 6-keto-PGE1 was injected into the superior vena cava or into the left atrium suggesting that this newly discovered substance is not inactivated in transit through the pulmonary vascular bed in the dog. Decreases in pulmonary arterial pressure and pulmonary vascular resistance were enhanced when pulmonary vascular tone was elevated by infusion of a stable prostaglandin endoperoxide analog or 15-methyl-PGF2 alpha. The present results demonstrate that 6-keto-PGE1 has significant vasodilator activity in pulmonary and systemic vascular beds in the dog and since this substance is not inactivated in the lung, it would serve as a circulating hormone in this species.
在开胸犬身上研究了前列腺素(PG)6-酮-E1(一种新发现的前列环素代谢产物)的心肺作用。向上腔静脉注射剂量为1 - 30微克的6-酮-PGE1可引起肺动脉压和体动脉压呈剂量依赖性下降。由于心输出量增加且左心房或右心房压力未变,肺血管阻力和体循环血管阻力下降。当将6-酮-PGE1注入上腔静脉或左心房时,体动脉压和体循环血管阻力的降低相似,这表明这种新发现的物质在通过犬的肺血管床时未被灭活。当通过输注稳定的前列腺素内过氧化物类似物或15-甲基-PGF2α使肺血管张力升高时,肺动脉压和肺血管阻力的下降会增强。目前的结果表明,6-酮-PGE1在犬的肺血管床和体循环血管床中具有显著的血管舒张活性,并且由于这种物质在肺中未被灭活,它将作为该物种中的一种循环激素发挥作用。