内皮素-1通过释放前列环素减少毛细血管后液体外渗。

Endothelin-1 decreases postcapillary fluid efflux via prostacyclin release.

作者信息

Victorino Gregory P, Chong Terry J, Curran Brian

机构信息

Department of Surgery, University of California San Francisco-East Bay, Alameda County Medical Center, Oakland, CA 94602, USA.

出版信息

Surgery. 2004 Aug;136(2):473-7. doi: 10.1016/j.surg.2004.05.027.

DOI:10.1016/j.surg.2004.05.027

PMID:15300217

Abstract

BACKGROUND

Endothelin-1 (ET-1) decreases water efflux across the endothelial barrier (Lp). ET-1 may exert this permeability-decreasing effect by stimulating prostacyclin (PGI2) release. The purposes of this study were to (1) examine the effect of PGI2 on Lp, (2) measure Lp after inhibition of PGI(2) synthesis, and (3) determine the effect of ET-1 on Lp during inhibition of PGI2 production.

METHODS

After microscopic cannulation of mesenteric venules, Lp was measured during PGI2 infusion (0.1 micromol/L, 1 micromol/L, and 10 micromol/L; n = 6 in each group). Lp was also measured after 100 micromol/L of the PGI2 synthase inhibitor, tranylcypromine (TCPN) (n = 6). Finally, the influence of ET-1 on Lp during PGI2 synthase inhibition was assessed (n = 6).

RESULTS

Compared to baseline Lp of 1.05 +/- 0.06, PGI2 decreased Lp at 1 micromol/L (Lp = 0.63 +/- 0.03, P < .003) and 10 micromol/L (Lp = 0.52 +/- 0.04, P < .0001). TCPN increased Lp compared to baseline (P < .0001). Compared to ET-1 alone, venules perfused with TCPN + ET-1 increased Lp (P < .005). Units for Lp ) are 10(-7) cm x sec(-1) x cmH2O(-1).

CONCLUSIONS

We found that (1) PGI2 decreases Lp, (2) inhibition of PGI2 synthesis increases Lp, and (3) permeability-decreasing effects of ET-1 can be blocked by inhibiting PGI2 synthesis. These data suggest that constitutive production of PGI2 modulates basal microvessel permeability and that ET-1 may exert its permeability-decreasing effect via the stimulation of PGI2 release.

摘要

背景

内皮素 -1（ET -1）可降低水通过内皮屏障的流出率（Lp）。ET -1可能通过刺激前列环素（PGI2）释放来发挥这种降低通透性的作用。本研究的目的是：（1）检测PGI2对Lp的影响；（2）在抑制PGI2合成后测量Lp；（3）确定在抑制PGI2产生过程中ET -1对Lp的影响。

方法

在肠系膜小静脉进行显微插管后，于PGI2输注期间（0.1 μmol/L、1 μmol/L和10 μmol/L；每组n = 6）测量Lp。在给予100 μmol/L的PGI2合酶抑制剂反苯环丙胺（TCPN）后也测量Lp（n = 6）。最后，评估在PGI2合酶抑制期间ET -1对Lp的影响（n = 6）。

结果

与基线Lp 1.05±0.06相比，PGI2在1 μmol/L时降低Lp（Lp = 0.63±0.03，P <.003），在10 μmol/L时降低Lp（Lp = 0.52±0.04，P <.0001）。与基线相比，TCPN增加了Lp（P <.0001）。与单独使用ET -1相比，用TCPN + ET -1灌注的小静脉Lp增加（P <.005）。Lp的单位为10^(-7) cm×sec^(-1)×cmH2O^(-1)。