圧力過負荷性多動性におけるグルコーストランスポーター活性障害は,失敗への進行の早期指標である
1Department of Cardiac Surgery, The Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Circulation
|November 24, 1999
まとめ
血糖吸収の障害は重度の心筋縮の初期に発生し,心室の膨張に先行する. このグルコース利用の減少は,心筋縮の心臓における心不全の進行に寄与する可能性があります.
科学分野:
- 心血管生理学 心血管の生理学
- メタボリック・レギュレーション
- 心臓高縮症 (ハート・ハイパートロフィー) とは
背景:
- 重度の心筋縮と心不全は,心臓外科手術における重大なリスクである.
- 早期の縮症は,心室質量対腔体積比 (M/V比) の増加とグルコース代謝依存を伴う.
- 遅い段階の高縮症は,心房の膨張と衰えとともに,グルコースの吸収が低下することを示します.
研究 の 目的:
- 血糖の吸収が低下していることが,縮症の進行の早期徴候であるかどうかを調査する.
- 減少したグルコースの吸収が心房の膨張の発生と相関するかどうかを判断する.
主な方法:
- ウサギは,多動脈を誘発するために大動脈帯を帯びました.
- トランストラシックエコーカルディオグラフィーは,左心室のM/V比を測定しました.
- (31) P-核磁気共鳴スペクトロスコーピーは,異なるM/V比率の上昇で,隔離された浸透した心臓のグルコース吸収率を評価した.
主要な成果:
- 補償性多動症では,グルコースの摂取量は正常であった (15%のM/V比増加).
- 早期デコンペンスされた高血圧症では,グルコースの吸収が著しく低下することが観察されました (M/V比率が30%増加).
- グルコーストランスポータータンパク質の発現は,すべてのグループで変化しませんでした.
結論:
- 補償性心筋縮では,グルコースの吸収が維持されます.
- 静脈の膨張に先立つ重度の高縮症は,グルコースの吸収が著しく低下することを示します.
- このグルコース利用の障害は,心不全への進行に寄与する可能性があります.
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