细胞形态呈现多样化，如圆形、梭形及椎形。缺氧复氧损伤后心肌细胞伪足缩短或消失，折光性下降，搏动减弱或消失。
ResultsBeing injured by hypoxia and reoxygenation, refracting power of the cells declined, pseudo-podium became shortened or disappeared, cell beat became weak or stopped.
目的：观察新生大鼠缺氧缺血性脑损伤(HIBD)后海马区细胞增殖的情况，探讨脑组织内源性修复的可能机制。
Objective to observe the expression of proliferation in hippocampus following hypoxic-ischemic brain damage (HIBD) in neonatal rats and to explore the possible endogenous neurogenesis of brain.
结论急性低压缺氧可引起老龄大鼠大脑皮质和丘脑中et、NO含量明显升高以及大脑皮质血管内皮细胞和神经细胞明显损伤，ET、NO可能参与了缺氧性脑损害的病理过程。
Conclusion It is suggested that, the increase of ET and NO contents of cerebral cortex and thalamus may participate in the pathogenesis of hypoxia brain injury in old rats.
方法制备心肌组织缺氧损伤模型，观察不同剂量的地高辛抗血清对缺氧损伤心肌组织内源性洋地黄样因子水平和心肌细胞膜atp酶活性的影响。
Methods it was observed that different concentration anti_digoxin antiserum effect on endogenous digitalis_like factor and cell membrane ATPase activity in hypoxic myocardium model.
该文主要阐述细胞凋亡与新生儿缺氧缺血性脑损伤的关系，提出细胞凋亡机制在缺氧缺血性脑损伤中的重要性。
In this review, we summarized relationship between apoptosis and neonatal hypoxic-ischemic brain damage (HIBD) and importance of apoptosis mechanism in HIBD.
目的观察新生鼠缺血缺氧性损伤后皮层及海马神经干细胞的变化。
Objective To investigate the influence of hypoxic- ischemic(H-I) injury on the endogenous Neural Stem Cells (NSCs) of the cerebral cortex and hippocampus in the neonatal rats.
目的观察新生鼠缺血缺氧性损伤后皮层及海马神经干细胞的变化。
Objective To investigate the influence of hypoxic- ischemic(H-I) injury on the endogenous Neural Stem Cells (NSCs) of the cerebral cortex and hippocampus in the neonatal rats.
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