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氨甲环酸可减轻油酸诱导的肺血管外渗。

Tranexamic acid attenuates oleic-acid-induced pulmonary extravasation.

作者信息

Moriuchi H, Arai I, Yuizono T

机构信息

Department of Pathopharmacology, Faculty of Pharmaceutical Sciences, Kumamoto University, Japan.

出版信息

Intensive Care Med. 1995 Dec;21(12):1003-8. doi: 10.1007/BF01700662.

Abstract

OBJECTIVE

Activation of fibrinolysis is implicated in the development of vascular injury in certain lung injuries. It has yet to be reported that activation of plasmin is involved in extravasation caused by oleic acid (OA). We examined whether or not plasmin is involved in pulmonary extravasation by OA.

DESIGN

Prospective trial.

SETTING

University laboratory.

SUBJECTS

A total of 78 guinea pigs (498.9 +/- 10.6 g).

INTERVENTIONS

Evans blue (EB) was administered to anesthetized guinea pigs. Subsequently four protocols were followed: (1) After 1 min, 60 micro l/kg of OA was injected. Perfusion was performed 30, 60 or 90 min after OA injection to wash out intravascular EB. (2) After 1 min, 15, 30 or 60 micro l/kg of OA was injected. (3) Tranexamic acid (TA) (2 g/kg) or saline was administered 30 min before OA (15 micro l/kg) injection. (4) Diphenhydramine hydrochloride (2.9 mg/kg) or saline was administered 7 min before OA (15 micro l/kg) injection.

MEASUREMENT AND RESULTS

Except in protocol 1, the chest cavity was opened 90 min after OA injection. Perfusion was then performed. Airway was separated into four parts from trachea to distal bronchus. EB was extracted from the tissues and measured. OA caused an extravasation throughout airways in a time- and dose-dependent manner. Extravasation was more conspicuous in peripheral tissues. TA significantly attenuated extravasation, while diphenhydramine hydrochloride did not.

CONCLUSIONS

It is suggested that plasmin, but not histamine, is involved in extravasation by OA. Inhibition of plasmin can be an effective strategy for treatment of this kind of lung injury.

摘要

目的

纤溶激活与某些肺损伤中血管损伤的发生有关。目前尚未有报道称纤溶酶的激活参与油酸(OA)所致的血管外渗。我们研究了纤溶酶是否参与OA所致的肺血管外渗。

设计

前瞻性试验。

地点

大学实验室。

对象

总共78只豚鼠(498.9±10.6克)。

干预措施

将伊文思蓝(EB)给予麻醉的豚鼠。随后遵循四个方案:(1)1分钟后,注射60微升/千克的OA。在OA注射后30、60或90分钟进行灌注以冲洗血管内的EB。(2)1分钟后,注射15、30或60微升/千克的OA。(3)在注射OA(15微升/千克)前30分钟给予氨甲环酸(TA)(2克/千克)或生理盐水。(4)在注射OA(15微升/千克)前7分钟给予盐酸苯海拉明(2.9毫克/千克)或生理盐水。

测量与结果

除方案1外,在OA注射后90分钟打开胸腔。然后进行灌注。气道从气管到远端支气管分为四个部分。从组织中提取EB并进行测量。OA以时间和剂量依赖的方式导致整个气道的血管外渗。外周组织中的血管外渗更明显。TA显著减轻血管外渗,而盐酸苯海拉明则没有。

结论

提示纤溶酶而非组胺参与OA所致的血管外渗。抑制纤溶酶可能是治疗这类肺损伤的有效策略。

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