Welt K, Schaffranietz L, Lukas H, Wassilev G, Fitzl G
Institute of Anatomy, University Leipzig, Germany.
Exp Toxicol Pathol. 1998 Jun;50(3):229-37. doi: 10.1016/S0940-2993(98)80088-2.
A model system consisting of a hypoxia chamber combined with a commercial narcosis apparatus adapted to small animals was used to perform a controlled acute isobaric hypoxia on rats with N2O/O2. Ultrathin sections from the left ventricular wall were analysed qualitatively and quantitatively using a computer-aided morphometric program. Compared with the control the cardiomyocytes exhibited a significant increase of volume densities of cytoplasmic vacuoles, lipid drops, sarcoplasmic reticulum, mitochondria, and degenerated intramitochondrial areas. Hypoxic alterations of microvessels consisted mainly in localized endothelial swelling and perivascular edema, protrusions of the luminal surface and moderate mitochondrial alterations similar to those of cardiomyocytes. Further, the number of plasmalemmal vesicles decreased, and the number of vacuoles increased significantly. The results were confirmed by quantitative histochemistry performed by our group in a parallel study. The model can be recommended for studies concerning protective interventions in hypoxia experiments.
使用一个由缺氧舱与适用于小动物的商用麻醉设备相结合组成的模型系统,以N2O/O2对大鼠进行控制性急性等压缺氧。使用计算机辅助形态测量程序对左心室壁的超薄切片进行定性和定量分析。与对照组相比,心肌细胞的细胞质空泡、脂滴、肌浆网、线粒体以及线粒体退化区域的体积密度显著增加。微血管的缺氧改变主要表现为局部内皮肿胀和血管周围水肿、管腔表面突出以及与心肌细胞类似的中度线粒体改变。此外,质膜小泡数量减少,空泡数量显著增加。我们小组在一项平行研究中进行的定量组织化学证实了这些结果。该模型可推荐用于缺氧实验中有关保护性干预措施的研究。