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前列环素I2可在体内降低人动脉平滑肌细胞的活性。

Prostaglandin I2 reduces activation of human arterial smooth muscle cells in-vivo.

作者信息

Sinzinger H, Zidek T, Fitscha P, O'Grady J, Wagner O, Kaliman J

机构信息

Atherosclerosis Research Group (ASF) Vienna, Austria.

出版信息

Prostaglandins. 1987 Jun;33(6):915-8. doi: 10.1016/0090-6980(87)90118-3.

Abstract

Patients suffering from peripheral vascular disease have been "ultima ratio"-treated with PGI2 at a rate of 5 ng/kg/min for 6 hours a day and 5 consecutive days i.v. 20 of them underwent surgery thereafter as therapy was not sufficient. A histological examination and quantification of vascular tissue revealed that the number of activated smooth muscle cells was significantly lower in treated patients vascular segments than in untreated ones in all the different age groups. A comparable suppression was found in the intima and the media as well. It is thus concluded, that PGI2 inhibits smooth muscle cell proliferation most probably by inhibiting PDGF-release from the platelets and stimulation of smooth muscle cell cAMP. To achieve a more beneficial PGI2-effect at the vascular level, a prolonged PGI2-therapy looks rather promising.

摘要

患有外周血管疾病的患者已接受“终极治疗”,即以5纳克/千克/分钟的速率静脉注射前列环素(PGI2),每天6小时,连续5天。其中20名患者因治疗效果不佳,随后接受了手术。对血管组织进行组织学检查和定量分析后发现,在所有不同年龄组中,接受治疗患者的血管段中活化平滑肌细胞的数量明显低于未治疗患者。在内膜和中膜也发现了类似的抑制作用。因此得出结论,前列环素(PGI2)很可能通过抑制血小板释放血小板衍生生长因子(PDGF)和刺激平滑肌细胞环磷酸腺苷(cAMP)来抑制平滑肌细胞增殖。为了在血管水平上获得更有益的前列环素(PGI2)效果,延长前列环素(PGI2)治疗似乎很有前景。

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