ミルリノンは,心停止後の蘇生を促進し,蘇生後の心筋機能不全を緩和します
James T Niemann1, Daniel Garner, Emad Khaleeli
1Harbor-UCLA Medical Center, Department of Emergency Medicine and the David Geffen UCLA School of Medicine, Los Angeles, Calif, USA. jniemann@emedharbor.edu
Circulation
|November 26, 2003
まとめ
ミルリノンの治療は,蘇生後の左心室機能不全を軽減することによって,心停止後の結果を改善しました. このフォスフォディエステラーゼIII阻害剤は,豚の回復を促進し,蘇生後の合併症を予防しました.
科学分野:
- 心臓病学 心臓病学
- クリティカルケア・メディシン
- 薬理学 薬理学とは
背景:
- 左心室 (LV) 機能障害と心肺蘇生後 (CPR) の低心指数は,多臓器不全による早期死亡率と関連しています.
- 再蘇生後のLV機能不全の効果的な治療法は,未だに難解である.
研究 の 目的:
- 選択性フォスフォディエステラーゼIII阻害剤であるミルリノンの有効性を調査し,心停止からの成功した蘇生後のLV機能不全の治療に.
主な方法:
- 32匹の豚に5分間の電気誘発性心房細動 (VF) を施しました.
- 動物はCPR中に塩分液 (対照) またはミルリノンを投与された.
- 血動力学的パラメータは,脳卒中容量およびLV dp/dtを含む,蘇生後評価されました.
主要な成果:
- ミルリノンの治療は,デフィブリレーション後の耐火性無パルス電気活動を有意に低下させた (0/16対6/16対照動物).
- 脳卒中の体積とLV dp/dtは,蘇生後30分と60分にミルリノンを投与したグループで有意に高かった.
- 心拍の有意な差は認められず,外周血管抵抗はミルリノーン群で低かった.
結論:
- ミルリノンは,長期にわたる心房細動から成功した蘇生を促進します.
- ミルリノンは,蘇生後の左心房機能不全を弱める.
- ミルリノンの治療は,心筋の酸素需要の重要な決定因子を悪化させない.
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