吸入された酸化窒素は,高血圧なしで人工輸血を可能にします
Binglan Yu1, Michael J Raher, Gian Paolo Volpato
1Anesthesia Center for Critical Care Research of the Department of Anesthesia and Critical Care, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
Circulation
|April 9, 2008
まとめ
ヘモグロビンベースの酸素媒介体 (HBOCs) によって引き起こされる全身血管収縮を予防することができます. HBOC輸注前に投与された吸入された酸化窒素 (NO) は,メトヘモグロビン血症を引き起こすことなく,この副作用を軽減します.
科学分野:
- バイオメディカルエンジニアリング
- 薬理学 薬理学とは
- 生理学 生理学とは
背景:
- ヘモグロビンベースの酸素媒介体 (HBOCs) の臨床開発は,全身血管収縮によって制限されています.
- HBOC誘発性血管収縮のメカニズムを理解することは,治療の進歩にとって極めて重要です.
研究 の 目的:
- HBOCsが全身血管収縮を引き起こすメカニズムを調査する.
- 窒素酸化物 (NO) のHBOC誘発性血管収縮の予防における有効性を評価する.
主な方法:
- 実験は野生型および内皮酸化窒素合成酵素 (NOS3) 欠乏症のマウス,および子羊で行われました.
- 動物は,ネズミのテトラメリックヘモグロビンまたはHBOC-201.の注入を受けた.
- 介入には,HBOC輸注の前にNOの吸入またはナトリウム窒素酸塩の投与が含まれていました.
主要な成果:
- 静脈注入のHBOCは,野生型のマウスでは全身血管収縮を誘導したが,NOS3欠乏したマウスではそうではなかった.
- NOまたはナトリウム・ニートリートの吸入投与は,メトヘモグロビネミアを引き起こすことなく,マウスのHBC誘発性高血圧を予防しました.
- 吸入されたNOは,また,子羊のHBOC誘発性高血圧を予防しました.
結論:
- HBOCは,NOS3.3によって生成される内皮酸化窒素 (NO) を取り除き,全身血管収縮を引き起こす.
- 吸入NOによる予備治療は,複数の種において,HBOC誘発の血管収縮を効果的に防ぐことができます.
- この戦略は,HBOCに関連する副作用を軽減するための有望なアプローチを提供します.
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