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Rapid Point-of-Care Assay of Enoxaparin Anticoagulant Efficacy in Whole Blood
Published on: October 12, 2012
プロタミンは,全身動脈からエンドセリウム由来のリラックスファクターを放出します. ヘパリン中和時の低血圧の可能性のあるメカニズム
P J Pearson1, P R Evora, K Ayrancioglu
1Cardiac Surgical Research, Mayo Clinic, Rochester, Minn 55905.
Circulation
|July 1, 1992
まとめ
ヘパリンを逆行するために使用されるプロタミン硫酸は,内皮由来リラックス因子 (EDRF) の放出によって低血圧を引き起こす可能性があります. この研究は,プロタミンが動脈からEDRFの放出を刺激し,血管拡張効果を説明することを確認しています.
科学分野:
- 心血管薬理学について
- 内皮機能の機能について
背景:
- プロタミン硫酸はヘパリンの抗凝固効果を逆転させるために使用されます.
- プロタミンの投与は低血圧を引き起こし,潜在的に血管拡張に関連している可能性があります.
- プロタミンは,酸化窒素 (NO) の前駆体であるアルギニンを含み,エンドセリウム由来リラックス因子 (EDRF) の活性成分である.
研究 の 目的:
- プロタミンがEDRFの放出を刺激し,血管拡張と低血圧を引き起こすかどうかを調査する.
- プロタミン誘発性低血圧の背後にあるメカニズムを解明する.
主な方法:
- エンドテリウムを含むおよび含まれない犬の動脈環 (冠動脈,股関節,腎臓) を研究した.
- リングは収縮し,プロタミン濃度の上昇に曝された.
- EDRF阻害剤であるNG-モノメチル-L-アルギニン (L-NMMA) とL-アルギニンの効果が評価されました.
主要な成果:
- プロタミンは,エンドテリウムを持つ動脈のセグメントにおける濃度依存のリラックスを引き起こした.
- このリラクゼーションは,内皮のないセグメントよりも有意に大きかった.
- EDRF媒介のリラクゼーションはL-NMMAによって抑制され,L-アルギニンによって逆転した.
結論:
- プロタミンは,動脈内皮からEDRFの放出を刺激します.
- 内皮に依存する血管拡張は,プロタミン誘発性全身性低血圧の重要な要因である.
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