心筋麻痺性停止時の筋細胞の予備条件化の有益な効果に寄与するメカニズム
1Department of Anesthesiology, Medical University of South Carolina, Charleston 29425, USA.
Circulation
|November 1, 1996
まとめ
プリコンディショニングは,シミュレートされた心筋梗塞停止と再温の際に心筋細胞を保護します. これらの保護効果はアデノシン経路またはATPに敏感なカリウム経路によって媒介され,心筋の保護に新しいアプローチを提供します.
科学分野:
- 心臓病学 心臓病学
- 細胞生物学 細胞生物学
- 生理学 生理学とは
背景:
- 肌動脈の予備条件付けは,イシュケミア,心臓麻痺停止,再温の際に内生的な心臓保護を提供します.
- これらの心臓手術の際に予備条件付けの利点の背後にある正確なメカニズムは,まだ完全に理解されていません.
- この研究は,シミュレートされた心臓麻痺停止および再温条件下での前条件付けが,筋細胞の収縮機能をどのように保護するのかを明らかにすることを目的とした.
研究 の 目的:
- プリコンディショニングが,シミュレートされた心筋麻痺停止と再加熱の間に肌細胞の収縮機能を保護するメカニズムを調査する.
- 非肌細胞細胞集団が,予備条件付けの保護効果に寄与するかどうかを判断する.
- プリコンディショニング媒介の心臓保護に関与する特定の分子経路を特定する.
主な方法:
- 隔離された豚の心臓筋細胞は,ノルモサーミア,シミュレートされた心臓麻痺の停止と再温,または心臓麻痺の停止と再温に続く予備条件付けを受けた.
- ビデオ顕微鏡では,肌細胞の縮小速度を評価した.
- また,実験では,先行条件付けされた内皮細胞および滑らかな筋肉細胞からのエリューエントを,ナイヴなミオサイトに適用した.
- 分子メカニズムは,アデノシンまたはアプリカリムで心筋梗塞の溶液を増強することによって調査されました.
主要な成果:
- シミュレートされた心臓麻痺停止と再加熱は,ノルモテルミアと比較して,筋細胞の縮小速度を著しく低下させた.
- 予備条件付けにより,心臓麻痺の停止と再加熱後に筋細胞の収縮機能が著しく改善されました.
- 前もって条件づけられた内皮細胞から抽出されるが,滑らかな筋肉細胞からは抽出されない,筋細胞の機能が改善される.
- アデノシンまたはアプリカリムによる増強は,アデノシン経路とATPに敏感なカリウムチャネルの活性化を示し,ミオサイト機能を著しく強化しました.
結論:
- 予備条件付けは,ミオサイト細胞集団以外のミオサイト細胞集団とは無関係に,ミオサイトの収縮機能に保護効果を与える.
- これらの保護効果は,アデノシン経路とATPに敏感なカリウムチャネルの活性化によって部分的に媒介されます.
- プリコンディショニングは,心筋麻痺と併用して使用され,心筋麻痺の停止と再加熱後の心筋筋膜の保護のための新しい戦略を提示します.
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