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用高营养法对缺血/再灌注进行复苏可增加肠道前列环素合成酶(PS)含量及前列环素释放。

Resuscitation of ischemia/reperfusion with hyperalimentation increases intestinal PGI2 synthase (PS) content and PGI2 release.

作者信息

Myers S I, Hernandez R, Turnage R H, Bartula L, Taylor-Kalley B

机构信息

Department of Surgery, University of Texas Southwestern Medical School, Dallas 75235, USA.

出版信息

Shock. 1995 Jun;3(6):422-9.

PMID:7656066
Abstract

Normal rat splanchnic blood flow and eicosanoid synthesis were compared to sham (Sham) and hemorrhage/reperfusion (SK + R) animals treated with 5 days of total parenteral nutrition (TPN). After in vivo measurement of superior mesenteric artery (SMA) blood flow, the splanchnic bed was perfused in vitro and venous effluent assayed for eicosanoid release by EIA. Aortic, SMA, ileal muscularis/serosa, and mucosa homogenates were analyzed for cyclooxygenase (COX) and prostacyclin synthase (PS) content by Western blot and for COX activity by radiochromatography. SK + R + TPN decreased SMA blood flow 33% and increased splanchnic PGI2 release twofold (p < .05) compared with the Sham +TPN and normal groups. groups SK + R + TPN did not alter COX activity in any of the tissues but Western blot analysis showed a twofold increase in COX and PS content in ileum muscularis/serosa (p < .05). These data show that SK + R + TPN induced a decrease in SMA blood flow and a compensatory increase in release of splanchnic PGI2. The mechanism for increased splanchnic PGI2 release after SK + R + TPN was an increase in PS and COX content (not activity) in the ileal muscularis/serosa.

摘要

将正常大鼠的内脏血流和类花生酸合成与接受5天全胃肠外营养(TPN)治疗的假手术(Sham)和出血/再灌注(SK + R)动物进行比较。在体内测量肠系膜上动脉(SMA)血流后,对内脏床进行体外灌注,并通过酶免疫分析(EIA)测定静脉流出液中类花生酸的释放。通过蛋白质免疫印迹法分析主动脉、SMA、回肠肌层/浆膜和黏膜匀浆中环氧合酶(COX)和前列环素合酶(PS)的含量,并通过放射色谱法分析COX活性。与假手术+ TPN组和正常组相比,SK + R + TPN组使SMA血流减少33%,内脏前列环素I2(PGI2)释放增加两倍(p < 0.05)。SK + R + TPN组未改变任何组织中的COX活性,但蛋白质免疫印迹分析显示回肠肌层/浆膜中COX和PS含量增加两倍(p < 0.05)。这些数据表明,SK + R + TPN导致SMA血流减少和内脏PGI2释放代偿性增加。SK + R + TPN后内脏PGI2释放增加的机制是回肠肌层/浆膜中PS和COX含量(而非活性)增加。

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