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Tranexamic acid attenuates oleic-acid-induced pulmonary extravasation
H Moriuchi1, I Arai, T Yuizono
1Department of Pathopharmacology, Faculty of Pharmaceutical Sciences, Kumamoto University, Japan.
Intensive Care Medicine
|December 1, 1995
Summary
Oleic acid (OA) causes lung vascular injury by activating plasmin, not histamine. Inhibiting plasmin effectively reduces this extravasation, offering a potential treatment strategy for OA-induced lung damage.
Area of Science:
- Pulmonary Medicine
- Vascular Biology
- Fibrinolysis Research
Background:
- Activation of fibrinolysis is linked to vascular injury in lung conditions.
- The role of plasmin in oleic acid (OA)-induced pulmonary extravasation remains unclear.
Purpose of the Study:
- To investigate the involvement of plasmin in OA-induced pulmonary extravasation.
- To determine if histamine plays a role in this process.
Main Methods:
- Prospective laboratory study using guinea pigs.
- Oleic acid (OA) was administered at varying doses and times.
- Evans blue (EB) dye was used to quantify extravasation.
- Tranexamic acid (TA) or diphenhydramine hydrochloride was administered to assess the role of plasmin and histamine, respectively.
Main Results:
- OA induced dose- and time-dependent extravasation in the airways, particularly in peripheral tissues.
- Tranexamic acid (TA) significantly reduced OA-induced extravasation.
- Diphenhydramine hydrochloride did not affect OA-induced extravasation.
Conclusions:
- Plasmin, not histamine, is implicated in OA-induced pulmonary extravasation.
- Inhibition of plasmin presents a promising therapeutic strategy for OA-induced lung injury.