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肝素辅因子II在受损血管壁抑制凝血酶中的意义。

Heparin cofactor II significance for the inhibition of thrombin at the injured vessel wall.

作者信息

Pasche B, Swedenborg J, Frebelius S, Olsson P

机构信息

Department of Experimental Surgery, Karolinska Institute, Stockholm, Sweden.

出版信息

Thromb Res. 1991 Jun 1;62(5):409-19. doi: 10.1016/0049-3848(91)90014-n.

Abstract

The thrombin inhibitory role of antithrombin III (ATIII) and heparin cofactor II (HCII) was studied in vitro using intact and injured rabbit aortae. When intact vessels were loaded with thrombin and then exposed to either heat defibrinogenated human plasma (HDHP) or ATIII the same degree of thrombin inhibition was achieved demonstrating that ATIII was the only plasma component involved in thrombin inhibition on the intact vessel wall. When the media of the vessel wall was loaded with thrombin and then exposed to ATIII or HCII a significantly higher thrombin activity remained on the surface than when it was exposed to defibrinogenated plasma. A mixture of ATIII and HCII resulted in a greater inhibition of thrombin than ATIII or HCII alone. It is concluded that, contrary to what happens on the endothelium, HCII and ATIII inhibit additively thrombin on the injured vessel wall. HCII thus plays an essential role for the inhibition of thrombin at the injured vessel wall. It is also concluded that an additional plasma component participates in thrombin inhibition on the media but its contribution is negligible as compared with ATIII or HCII.

摘要

使用完整和受损的兔主动脉在体外研究了抗凝血酶III(ATIII)和肝素辅因子II(HCII)的凝血酶抑制作用。当完整血管加载凝血酶后,再暴露于热去除纤维蛋白原的人血浆(HDHP)或ATIII时,凝血酶抑制程度相同,这表明ATIII是完整血管壁上参与凝血酶抑制的唯一血浆成分。当血管壁中层加载凝血酶后,再暴露于ATIII或HCII时,表面残留的凝血酶活性明显高于暴露于去除纤维蛋白原的血浆时。ATIII和HCII的混合物对凝血酶的抑制作用比单独使用ATIII或HCII更强。得出的结论是,与在内皮细胞上的情况相反,HCII和ATIII在受损血管壁上对凝血酶的抑制作用是相加的。因此,HCII在受损血管壁上对凝血酶的抑制起着至关重要的作用。还得出结论,另一种血浆成分参与中层的凝血酶抑制,但与ATIII或HCII相比,其贡献可忽略不计。

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