トニック・ケミオレフレクスの活性化は,心不全における筋肉交感神経の活性度の上昇に寄与しない
P van de Borne1, R Oren, E A Anderson
1Cardiovascular Center, University of Iowa, Iowa City 52242, USA.
Circulation
|September 15, 1996
まとめ
心不全の患者では,交感神経の活性が増加することは,過度に活動的な化学受容体によって引き起こされません. 純粋な酸素を吸い込むことは,交感神経の活動を変化させず,化学反射仮説を否定した.
科学分野:
- 心血管生理学 心血管の生理学
- 神経科学は神経科学である.
- 心不全に関する研究
背景:
- 心不全は,交感神経系の活動の増加と関連しています.
- この交感的活性化は,脳幹の信号伝達が変化したり,化学受容体の感受性が高まったりから生じる可能性があります.
- 心不全のシンパティック・ドライブにおける刺激性化学受容体アファレンスの役割は不明である.
研究 の 目的:
- 刺激性化学受容体アフェレンツのトニック活性化が,心不全における同情性の活性化に寄与するという仮説を検証する.
- 100%の酸素を吸い込むことでケモレセプターを無効化する事が,心不全患者の交感神経の活動に影響するかどうかを判断する.
主な方法:
- 12人の慢性心不全患者 (NYHAクラスIII,LVEF 24±2%) の経神経から交感神経の活性が測定されました.
- 患者は室内の空気と100%の酸素を呼吸しながら,化学受容体を非活性化させるために測定を行った.
- 休息中の交感神経の活動も,9人の健康な対照群で記録された.
主要な成果:
- 心不全の患者は,対照群 (36±4発/分) と比べて,静止シンパシー神経の活性 (59±5発/分) が著しく高かった.
- 100%酸素を呼吸すると,酸素飽和度 (94%から99%) が増加したが,筋肉の交感神経の活動 (798±122 U/min 室内の空気で vs. 824±35 U/min 100% O2で) が有意に変化しなかった.
- 血圧は酸素投与の影響を受けなかった.
結論:
- この研究では,心不全患者の筋肉循環に対するエフェルント交感活性の増加は,刺激性化学反射アフェルントのトニック活性化によって説明されないと結論づけています.
- これらの発見は,心不全で観察される同情的駆動の増大に他のメカニズムが責任を負うことを示唆しています.
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