慢性的な肺動脈の圧力上昇は,右心不全を説明するのに不十分です
Harm J Bogaard1, Ramesh Natarajan, Scott C Henderson
1Divisions of Pulmonary and Critical Care, Virginia Commonwealth University, Richmond, VA 23298-0281, USA. nvoelkel@mcvh-vcu.edu
Circulation
|November 4, 2009
まとめ
肺動脈高血圧の長寿は,右心室 (RV) の機能に依存する. ある研究では,肺高血圧におけるRV不全は,単なる負荷の増加以上のことを含んでおり,RV疾患の新たな治療目標を示唆しています.
科学分野:
- 心血管研究 循環器科の研究
- 肺高血圧の病理生理学 肺高血圧の病理生理学
- 右心室機能について
背景:
- 右心室 (RV) の機能は,肺動脈高血圧 (PAH) の長寿にとって重要です.
- 左心室不全と比較して,RV不全の細胞および分子メカニズムに関するデータは限られている.
研究 の 目的:
- 肺高血圧におけるRV不全のメカニズムを調査する.
- RVの圧力過負荷だけで RVが故障するかどうかを判断する.
- RV機能障害に対する潜在的な治療的介入を探求する.
主な方法:
- 慢性的な進行性RV圧力過負荷の機械的な動物モデルを開発しました.
- このモデルを血管増殖性肺高血圧モデルと比較した.
- Nrf2とHO-1経路を標的にする栄養補助食品 (Protandim) を投与しました.
主要な成果:
- 孤立したRVの圧力過負荷は高縮を引き起こしたが,故障は起こさなかった.
- 血管増殖性肺高血圧は,アポトーシス,線維症,および毛細血管密度の低下によるRV不全につながりました.
- Protandim治療は,線維症と毛細血管喪失を予防し,RVの機能を保ちました.
結論:
- 肺高血圧におけるRV不全は,RV後負荷の増加のみによるものではありません.
- 負荷後の特定の分子経路は,RVの故障に寄与します.
- Nrf2とヘム-オキシゲナーゼ1をターゲットにすることで,RV機能障害に対する保護効果がもたらされる可能性があります.
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