Gastric prostacyclin (PGI2) prevents stress-induced gastric mucosal injury in rats primarily by inhibiting leukocyte activation
Gastric prostacyclin (PGI2) prevents stress-induced gastric mucosal injury in rats primarily by inhibiting leukocyte activation
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DOI：
10.1016/s0090-6980(98)00077-x
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发表时间：
1999-07-01
影响因子：
2.9
通讯作者：
Liu, WG
中科院分区：
文献类型：
--
作者：
Harada, N;Okajima, K;Liu, WG
我们在大鼠中研究了胃前列环素（PGI（2））是否通过抑制白细胞活化来预防水浸束缚应激引起的胃粘膜损伤。胃内6-keto-PGF（1）α（PGI（2）的稳定代谢物）水平在应激后30分钟短暂升高，随后在应激后6-8小时降至基线以下。应激后8 h胃粘膜血流量下降至基线水平的40%。髓过氧化物酶活性在胁迫后8h显著升高。应激前用吲哚美辛治疗可抑制6-keto-PGF（1）α水平的升高，并显著减少粘膜血流量。它还显著增加白细胞积聚和粘膜损伤形成。伊洛前列素是一种稳定的PGI（2）类似物，可抑制吲哚美辛诱导的粘膜血流量减少、粘膜病变恶化和白细胞蓄积增加。氮芥诱导的白细胞减少可抑制吲哚美辛相关病变恶化和白细胞蓄积增加，但对粘膜血流量减少无影响。这些观察结果表明，胃PGI（2）主要通过抑制白细胞积聚来减少胃粘膜病变的形成。(C)1999 Elsevier Science Inc. All rights reserved.
We investigated whether, in rats, gastric prostacyclin (PGI(2)) prevented gastric mucosal injury that was induced by water-immersion restraint stress by inhibiting leukocyte activation. Gastric levels of 6-keto-PGF(1)alpha, a stable metabolite of PGI(2), increased transiently 30 min after stress, followed by a decrease to below the baseline 6-8 h after stress. Gastric mucosal blood flow decreased to similar to 40% of the baseline level 8 h after stress. Myeloperoxidase activity was significantly increased 8 h after stress. Treatment with indomethacin before stress inhibited the increase in 6-keto-PGF(1)alpha levels and markedly reduced mucosal blood flow. It also markedly increased leukocyte accumulation and mucosal lesion formation. Iloprost, a stable PGI(2) analog, inhibited the indomethacin-induced decrease in mucosal blood flow, mucosal lesion exacerbation, and increase in leukocyte accumulation Nitrogen mustard-induced leukocytopenia inhibited the indomethacin-associated lesion exacerbation and the increase in leukocyte accumulation, but not the decreases in mucosal blood how. These observations indicate that gastric PGI(2) decreases gastric mucosal lesion formation primarily by inhibiting leukocyte accumulation. (C) 1999 Elsevier Science Inc. All rights reserved.