ニトログリセリンによる継続的および中断的な治療に対する反調節反応
J D Parker1, B Farrell, T Fenton
1Cardiovacular Division, Brigham and Women's Hospital, Boston, MA 02115.
Circulation
|December 1, 1991
まとめ
継続的なニトログリセリン (GTN) 治療は,中断的なGTNとは異なり,ナトリウム保持と耐性を引き起こします. 断続的な治療は,これらの反調節反応を回避し,持続的な血管拡張に対してより有効である可能性を示唆します.
科学分野:
- 心血管薬理学について
- エンドクリノロジー エンドクリノロジー
背景:
- ニトログリセリン (GTN) を含む血管拡張剤療法は,反射反調節反応を引き起こす可能性があります.
- これらの反応は,GTNの効果に対する耐性の発達に寄与する可能性があります.
研究 の 目的:
- 継続的対間隔的経皮ニトログリセリン (GTN) 投与に対する対規制反応を比較する.
- ニトログリセリン耐性におけるこれらの反応の役割を調査する.
主な方法:
- 正常なボランティアは,継続的または中断的な経皮GTNを投与された.
- 測定対象は,血圧,体重,尿中のナトリウム,血圧,血ホルモンレベル (ノレアピネフリン,心房内ナトリウレチンペプチド,アルギニンバソプレシン,レニン活性) でした.
主要な成果:
- 継続的なGTNは,低血圧反応の急速な衰弱,体重増加,ナトリウム保持,およびプラズマ容量の膨張をもたらしました.
- 断続的なGTNは,重要な体重増加やナトリウム保持を示さなかったが,ホルモン反応はベースラインに戻った.
- 継続的な治療は,血のノルエピネフリン,心房内ナトリウレチンペプチド,アルギニンバソプレシン,および血のレニン活性を増大させた.
結論:
- 継続的なトランスダーマルのGTN治療は,ナトリウム保持とプラズマ容量の膨張の可能性を含む,逆調節反応を誘発する.
- 断続的な経皮GTN治療は,ナトリウム保持や血量の膨張なしに異なるホルモンパターンをもたらします.
- これらの反調節メカニズムは,窒素効果を弱めるための鍵となる可能性があり,中断的な治療が耐性を軽減することを示唆しています.
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