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血栓素作为一种可能的肝毒性因子,在梗阻性黄疸中因内毒素血症而增加。

Thromboxane as a possible hepatotoxic factor increased by endotoxemia in obstructive jaundice.

作者信息

Hanai T, Yura J, Ogino K, Hori K, Suzuki T

机构信息

First Department of Surgery, Nagoya City University Medical School, Japan.

出版信息

Jpn J Surg. 1989 Sep;19(5):556-62. doi: 10.1007/BF02471663.

DOI:10.1007/BF02471663
PMID:2687528
Abstract

In a study using rats, we investigated whether liver damage induced by endotoxemia in obstructive jaundice is associated with thromboxane (TX) in order to acertain whether its vasoconstrictive and platelet aggregating properties play a role in reducing liver blood flow. The rats were divided into the following 5 groups; a control group, an endotoxin (Et) group, a bile duct ligation (BDL) group, a bile duct ligation and endotoxin (BDL + Et) group and an OKY046 (Thromboxane synthetase inhibitor) treated bile duct ligation + endotoxin (OKY-BDL + Et) group. The blood TXB2 levels in the Et, BDL and BDL + Et groups were higher than those in the control group. The liver TXB2 levels in the Et and BDL + Et groups were also higher than those in the control group. Liver phospholipids and liver blood flow decreased in the BDL + Et group, whereas in the OKY-BDL + Et group they returned close to the control group levels by decreasing the TXB2 levels in both the liver and blood to normal. These results suggest that the high level of TX in the blood and liver tissue may further aggrevate the liver during endotoxemia in obstructive jaundice by inhibiting liver blood flow.

摘要

在一项以大鼠为对象的研究中,我们探究了阻塞性黄疸内毒素血症所致肝损伤是否与血栓素(TX)有关,以确定其血管收缩和血小板聚集特性是否在减少肝血流量中发挥作用。大鼠被分为以下5组:对照组、内毒素(Et)组、胆管结扎(BDL)组、胆管结扎加内毒素(BDL + Et)组以及用OKY046(血栓素合成酶抑制剂)处理的胆管结扎加内毒素(OKY - BDL + Et)组。Et组、BDL组和BDL + Et组的血液TXB2水平高于对照组。Et组和BDL + Et组的肝脏TXB2水平也高于对照组。BDL + Et组肝脏磷脂和肝血流量降低,而在OKY - BDL + Et组中,通过将肝脏和血液中的TXB2水平降至正常,它们恢复到接近对照组的水平。这些结果表明,血液和肝组织中高水平的TX可能通过抑制肝血流量在阻塞性黄疸内毒素血症期间进一步加重肝脏损伤。

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1
Thromboxane as a possible hepatotoxic factor increased by endotoxemia in obstructive jaundice.血栓素作为一种可能的肝毒性因子,在梗阻性黄疸中因内毒素血症而增加。
Jpn J Surg. 1989 Sep;19(5):556-62. doi: 10.1007/BF02471663.
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Administration of protegrin peptide IB-367 to prevent endotoxin induced mortality in bile duct ligated rats.给予防御素肽IB-367以预防胆管结扎大鼠内毒素诱导的死亡。
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本文引用的文献

1
Elevated thromboxane levels in the rat during endotoxic shock: protective effects of imidazole, 13-azaprostanoic acid, or essential fatty acid deficiency.内毒素休克期间大鼠血栓素水平升高:咪唑、13-氮杂前列腺酸或必需脂肪酸缺乏的保护作用。
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2
Endotoxemia, disturbance of coagulation, and obstructive jaundice.内毒素血症、凝血功能紊乱和梗阻性黄疸。
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3
Biliary obstruction and host defense failure.胆道梗阻与宿主防御功能衰竭。
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Role of lipid peroxidation in tissue injury after hepatic ischemia.脂质过氧化在肝脏缺血后组织损伤中的作用。
Exp Mol Pathol. 1983 Feb;38(1):69-76. doi: 10.1016/0014-4800(83)90099-0.
5
Endotoxin, prostaglandins and renal fibrin deposition in obstructive jaundice.阻塞性黄疸中的内毒素、前列腺素与肾脏纤维蛋白沉积
Br J Surg. 1982 Oct;69(10):625-9. doi: 10.1002/bjs.1800691022.
6
Changes in the levels of endogenous coenzyme Q homologs, alpha-tocopherol, and glutathione in rat liver after hepatic ischemia and reperfusion, and the effect of pretreatment with coenzyme Q10.肝脏缺血再灌注后大鼠肝脏内源性辅酶Q同系物、α-生育酚和谷胱甘肽水平的变化以及辅酶Q10预处理的影响
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Protective effects of thromboxane A2 synthetase inhibitors on endotoxin shock.
Prostaglandins Leukot Med. 1983 Jun;11(2):179-88. doi: 10.1016/0262-1746(83)90018-5.
8
Impaired bacterial clearance and trapping in obstructive jaundice.梗阻性黄疸时细菌清除和捕获功能受损。
Ann Surg. 1984 Jan;199(1):14-20. doi: 10.1097/00000658-198401000-00003.
9
Plasma thromboxane concentrations are raised in patients dying with septic shock.死于感染性休克的患者血浆血栓素浓度会升高。
Lancet. 1982 Jul 24;2(8291):174-5. doi: 10.1016/s0140-6736(82)91027-3.
10
Synthesis of prostanoids and cyclic nucleotides by phagocytosing rat Kupffer cells.吞噬作用的大鼠库普弗细胞合成前列腺素和环核苷酸。
Eur J Biochem. 1984 Jul 16;142(2):219-25. doi: 10.1111/j.1432-1033.1984.tb08274.x.