心筋再注射中のトロンビンの不律性作用は,イノシトール1,4,5-トリフォスファートの放出による
A N Jacobsen1, X J Du, K A Lambert
1Cellular Biochemistry Laboratory, Baker Medical Research Institute, Melbourne, Australia.
Circulation
|January 1, 1996
まとめ
リパーフュージョン不律症は,イノシトール1,4,5-トリフォスファート (Ins(1,4,5) P3) の放出に依存する. トロンビンとノレピネフリンはIns(1,4,5) P3の放出を刺激し,再注射中に心律不整を引き起こします.
科学分野:
- 心臓病学 心臓病学
- バイオケミストリー バイオケミストリー
- 薬理学 薬理学とは
背景:
- 心臓の再注入は,部分的にアルファ1-アドレネルゲン受容体のノルエピネフリン刺激を通じて,不律を誘発する可能性があります.
- イノシトール1,4,5-トリフォスファート (Ins(1,4,5) P3) の放出がこのプロセスに関与しています.
研究 の 目的:
- トロンビン刺激によるIns(1,4,5) P3の放出によるリズム障害を引き起こす効果を調査する.
- リパーフュージョン誘発性心律不整症におけるIns(1,4,5) P3の役割を理解する.
主な方法:
- 高性能液体クロマトグラフィを使用して,孤立したネズミの心臓でIns(1,4,5) P3の放出を測定しました.
- バッファに浸透したネズミの心臓における心律異常の評価.
- カテコアミン欠乏した心臓と特定の阻害剤 (ゲンタミシン,U-73122) を使用して信号伝達経路を解明する.
主要な成果:
- 再輸血は,無傷の心臓ではIns{1,4,5) P3のレベルを有意に上昇させたが,カテキオラミンが欠乏した心臓ではそうではなかった.
- トロンビンまたはそのアゴニストペプチドは,カテコアミン不足の心臓でIns(1,4,5) P3の放出を回復し,不律を誘発した.
- ジェンタミシンとフォスフォリファーゼC阻害剤U-73122は,トロンビン誘発のIns(1,4,5) P3放出と不律を抑制したが,U-73122はノレピネフリン誘発の反応に影響しなかった.
結論:
- リパーフュージョン不律症は,Ins{1,4,5) P3の放出に極めて依存しています.
- トロンビンは,ノレピネフリン経路とは異なるIns{1,4,5) P3シグナル伝達経由でリパーフュージョン不律に寄与する.
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