ROLE OF OXYGEN IN THE CELLULAR-DAMAGE INDUCED BY RE-OXYGENATION OF HYPOXIC HEART
ROLE OF OXYGEN IN THE CELLULAR-DAMAGE INDUCED BY RE-OXYGENATION OF HYPOXIC HEART
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DOI：
10.1016/0022-2828(80)90081-4
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发表时间：
1980-01-01
影响因子：
5
通讯作者：
CALDARERA, CM
中科院分区：
文献类型：
--
作者：
GUARNIERI, C;FLAMIGNI, F;CALDARERA, CM
在离体Langendorff灌流的大鼠心脏上研究了氧在缺氧心脏复氧过程中诱导细胞损伤的作用。缺氧80分钟的时间增加导致超氧化物歧化酶和谷胱甘肽过氧化物酶活性下降。这种下降继续时，心脏灌注在缺氧40和60分钟，再氧合20分钟。在这些条件下，再氧合引起的脂质过氧化反应的增加，这被评价为丙二醛的形成。与有氧心脏相比，缺氧后细胞内酸溶性巯基、不溶性巯基和还原型谷胱甘肽含量均降低，而氧化型谷胱甘肽含量无明显变化。重新接纳的O2缺氧的心脏产生了进一步减少巯基和还原型谷胱甘肽。与氧合良好的大鼠心脏相反，无底物的缺氧介质灌注导致还原型谷胱甘肽显着释放到冠状动脉流出物中，再氧合后继续。在缺氧中，氧化型谷胱甘肽的释放开始后30分钟的灌注，并在接下来的60分钟的缺氧略有增加。缺氧60分钟后再给氧并没有增强缺氧氧化型谷胱甘肽的释放。缺氧无底物灌注降低了细胞防御机制，能够中和O2代谢产物介导的毒性反应时，复氧可诱导大鼠心脏组织脂质过氧化损伤。
The role of O2 in the induction of cellular damages during re-oxygenation of hypoxic hearts was studied in isolated Langendorff perfused rat hearts. An increase in the period of hypoxia of up to 80 min resulted in a decrease in superoxide dismutase and glutathione peroxidase activity. This decrease continued when the hearts perfused in hypoxia 40 and 60 min were reoxygenated for an additional 20 min. Under these conditions, re-oxygenation caused an increase in lipid peroxidation which was evaluated as malondialdehyde formation. Compared to aerobic hearts, the cellular contents of acid soluble thiol groups, insoluble thiol groups and reduced glutathione were all decreased by hypoxia, while oxidized glutathione remained unchanged. The re-admission of O2 to hypoxic hearts produced a further reduction in thiol groups and reduced glutathione. In contrast to well-oxygenated rat hearts, perfusion with substrate-free hypoxic medium resulted in a marked release of reduced glutathione into coronary effluents, which continued after re-oxygenation. In hypoxia the release of oxidized glutathione began after 30 min of perfusion and slightly increased during the next 60 min of hypoxia. Re-oxygenation after 60 min of hypoxia did not enhance hypoxic oxidized glutathione release. Reoxygenation can induce lipid peroxidative damage in cardiac rat tissue when hypoxic substrate-free perfusions previously reduced the cellular defensive mechanisms capable of neutralizing the toxic reactions mediated by O2 metabolites.