Büsing C M, Kreinsen U, Bühler F, Bleyl U
Virchows Arch A Pathol Anat Histol. 1975;366(2):137-47. doi: 10.1007/BF00433587.
Heart muscle necroses following normobaric hyperoxia as examined under a light microscope occur after 40 hours exposure in the rabbit and increase in intensity with prolongation of the exposition time. Simultaneous arterial blood gas analysis excludes a hypoxemis as the cause, In addition electron microscopic examination of the necroses demonstrate the primary changes in the myofibrils but not in the mitochondria. The ultramorphological picture is however, quite similar to the myocardial necroses after epinephrine application in the rabbit. A pathogenetic relationship between heart muscle necroses after normobaric hyperoxia and after epinephrine should be considered.
在光学显微镜下观察发现，常压高氧暴露后兔心肌坏死在暴露40小时后出现，并随着暴露时间的延长而加重。同时进行的动脉血气分析排除了低氧血症作为病因。此外，对坏死区域的电子显微镜检查显示，肌原纤维出现了原发性变化，而线粒体未出现变化。然而，超微形态学表现与兔应用肾上腺素后的心肌坏死非常相似。应考虑常压高氧后与肾上腺素后心肌坏死之间的发病机制关系。
