エンドセリンA受容体阻害は左心室の不良改造を引き起こしますが,ネズミの心臓発作後の肺動脈の圧力を改善します
Q T Nguyen1, P Cernacek, A Calderoni
1Department of Medicine, Montreal Heart Institute, Montreal, Quebec, H1T 1C8, Canada.
Circulation
|November 24, 1998
まとめ
ネズミの心筋梗塞 (MI) の後のエンドセリンA (ETA) 受容体アンタゴニストの早期使用は,傷痕の治癒を阻害し,左心室 (LV) 機能不全を引き起こしました. これらの発見は,早期のETAアンタゴニスト治療の潜在的有害な影響をMI後の示唆しています.
科学分野:
- 心血管科学の研究について
- 薬理学 薬理学とは
- 実験医学は,実験医学である.
背景:
- エンドセリンA (ETA) 受容体抗生物質は,以前,心筋梗塞 (MI) の10日後にラットで開始された場合,アウトカムを改善しました.
- MI後の早期にETA受容体アンタゴニストを投与した後の影響は不明である.
研究 の 目的:
- ネズミのモデルで心筋梗塞後の心室リモデリングと機能に対するETA受容体アンタゴニストの早期投与の影響を調査する.
- 心筋梗塞直後に開始されたLU 127043とその活性エナチオメールLU 135252の使用の結果を比較するために.
主な方法:
- 急性心筋梗塞から24時間 (n=403) 生き延びたマウスを4週間,塩水,LU 127043またはLU 135252で治療した.
- 評価された生存率,心室改造,心圧,ET-1レベル.
主要な成果:
- 慢性的なLU治療は全生存率に影響を与えませんでした.
- LU治療は,傷痕の薄め,左心房 (LV) の膨張の増加,LVの末期透析圧の上昇,および肺の重量の増加をもたらしました.
- LV機能の低下にもかかわらず,LU治療は右心室 (RV) のシストリックおよび右心房圧を下げ,肺ET-1増加を予防しました.
結論:
- ネズミのMI後のETA受容体抗体 (LU 127043/LU 135252) の早期使用は,傷痕の治癒が低下し,LVの拡張,機能不全を引き起こしました.
- これらの効果は,RVのシストリックおよび右心房圧の低下,およびET-1レベルの変化に伴いました.
- 発作後の早期のETA受容体アンタゴニスト投与は有害である可能性があります.
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