肺毛細血管のストレス不全:肺や心臓病における役割
1Department of Medicine, University of California San Diego, La Jolla 92093-0623.
Lancet (London, England)
|September 26, 1992
まとめ
高圧または弱まったコラーゲンによって引き起こされる肺毛細血管のストレス不全は,肺腫と出血につながる. このメカニズムは,様々な肺や心臓の疾患に関与しています.
科学分野:
- 肺医学は肺を治療する薬です.
- 心血管研究に関する研究.
- 細胞生物学 細胞生物学
背景:
- 肺毛細血管は,その薄い壁のため,ガス交換に不可欠です.
- 高圧の毛細血管は,これらの壁に重大なストレスと超構造的損傷を引き起こす可能性があります.
- 細胞外マトリックスにあるIV型コラーゲンは,毛細血管の壁に強さを与えます.
研究 の 目的:
- 肺毛細血管ストレス不全の現象を調査する.
- 毛細血管壁の損傷のメカニズムと結果を特定するために.
- 様々な肺や心臓疾患におけるストレス不全の役割を調査する.
主な方法:
- 高圧にさらされた麻酔したウサギの研究.
- 毛細血管壁の超構造的損傷の分析.
- 毛細血管壁の整体性に関連した臨床状態のレビュー.
主要な成果:
- ウサギの40mmHg以上の圧力で観察された超構造的損傷.
- 損傷には,内皮と上皮の層,およびすべての壁の層の破裂が含まれます.
- ストレス不全は,高透性の腫れや出血につながる.
結論:
- 肺毛細血管のストレス不全は,神経原性および高空肺腫のような状態の重要な要因です.
- それはレースホースの運動誘発性肺出血とミトラル狭窄症の特徴を説明します.
- 弱体化したIV型コラーゲン (グッドパストゥース症候群,中性粒子のエラスタゼなど) は,ストレス不全を誘発し,エムフィゼマやその他の肺疾患に寄与します.
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