Longitudinal prostaglandin E2 generation in various organs during evolution of experimental portal hypertension

被引:5
作者
Ackerman, Z
Karmeli, F
Rachmilewitz, D
机构
[1] Hadassah Univ Hosp, Dept Med, IL-91240 Jerusalem, Israel
[2] Hebrew Univ Jerusalem, Hadassah Med Sch, Jerusalem, Israel
[3] Shaare Zedek Med Ctr, Dept Med, IL-91000 Jerusalem, Israel
来源
PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS | 2002年 / 67卷 / 04期
关键词
D O I
10.1054/plef.2002.0419
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
It has been suggested that the arteriolar vasodilatation and hyperdynamic circulation observed in rats with partial portal vein ligation (PPVL) is caused by increased splanchnic and systemic delivery of vasodilator substances. The aims of our study were to determine organ-specific generation of prostaglandin E-2 (PGE(2)) in rats with PPVL during the evolution of portal hypertension. Rats with PPVL and sham-operated (S) rats were studied in the first, third, fourth and 14th postoperative days. They were anesthetized and splenic pulp pressure and blood pressure were measured. Spleen, colon and lungs were removed and the splenic, pulmonary and mucosal colonic PGE(2) were determined. All PPVL rats developed sequential hemodynamic changes compatible with evolving portal hypertension. Splenic pulp pressure was higher in PPVL rats compared with S rats during all days of the study Within the group of PPVL the splenic pulp pressure was higher in the first postoperative day and decreased in the ensuing days. No changes in splenic and colonic PGE(2) generation were noted during the study period. Pulmonary PGE(2) generation increased significantly in the first postoperative day in PPVL rats compared with S rats. However, similar increase was observed on the third postoperative day in S rats. PGE(2) probably has no role in splanchnic hemodynamic changes during evolution of portal hypertension. Pulmonary PGE(2) generation may increase as a response to increased portal pressure, or to abdominal surgery. (C) 2002 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:197 / 201
页数:5
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