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Quantitative Autonomic Testing
Published on: July 19, 2011
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自律機能不全における共感的に媒介された高血圧
J R Shannon1, J Jordan, A Diedrich
1Autonomic Dysfunction Center, Vanderbilt University, Nashville, TN 37232-2195, USA.
Circulation
|June 14, 2000
まとめ
残留シンパシー活動により,多発性システム縮 (MSA) の患者で横行高血圧が発生します. この活動は,純粋な自律機能不全 (PAF) 患者における仰向け高血圧に寄与するが,完全には説明できない.
科学分野:
- 自律神経系の生理学 自律神経系の生理学
- 心血管の規制についてです.
- 神経学 神経学とは
背景:
- 頂上高血圧は,主治体機能不全の患者の約50%に影響します.
- この仰向け高血圧を誘発する残留シンパシー活動の役割は,完全に理解されていません.
研究 の 目的:
- 主要な自律機能不全の患者において,残留シンパシー活動が仰向け高血圧の原因であるかどうかを調査する.
- マルチプルシステム縮 (MSA) と純粋自律性衰弱 (PAF) での仰向け高血圧のメカニズムを区別する.
主な方法:
- ヨーヒンビン (アルファ-2 抗剤),トリメタファン (ギャングリオンブロック),フェントラミン (アルファ-1 ブロック) がMSAおよびPAF患者における血圧に及ぼす影響を研究した.
- 測定されたシストリック血圧 (SBP),プラズマカテキオラミン濃度,心臓指数,および全周回路抵抗.
主要な成果:
- SBPに対するヨーヒンビンの効果は,PAF患者と比較して,MSA患者において有意に大きかった.
- トリメタファンによるギャングリオン阻害は,MSA患者において,横のSBPを著しく減少させましたが,PAF患者において,より変動的な効果を示しました.
- MSA患者のヨヒンビンに対するプレッサー反応とトリメタファンに対する抑うつ反応の間に強い相関が観察されました.
結論:
- 残留シンパシー活動は,多発性システム縮 (MSA) のレピイン高血圧の主な要因です.
- 残留シンパシー活動は,純粋な自律機能不全 (PAF) のレパイン高血圧に寄与しますが,完全に説明していません.
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