Midorikawa Y, Ogata H
First Department of Anesthesiology, School of Medicine, Dokkyo University, Tochigi.
Masui. 1994 Sep;43(9):1297-303.
It is generally known that ischemic reperfusion injury is caused by cell membrane injuries due to superoxide. The present study was carried out to clarify an increase of superoxide production in human neutrophils in state of hypoxia and hyperoxia in vitro. Superoxide of neutrophils was studied at various PO2 values (air, 100% O2, 50% O2, and 100% N2 gas) by chemiluminescence method. The superoxide production (O2-) rates were 84% (air), 84% (100% N2), 87% (100% O2) and 84% (50% O2), respectively. At these stages, PO2 values were 178, 36, 764 and 370 mmHg, respectively. Since superoxide is generated in mitochondria under PO2 of 1 mmHg, it was considered that these different values of PO2 (100% N2, 100% O2 and 50% O2) do not influence the superoxide production. Other factors, such as PAF or cytokine, were speculated to increase superoxide production.
众所周知，缺血再灌注损伤是由超氧化物导致的细胞膜损伤引起的。本研究旨在阐明体外缺氧和高氧状态下人中性粒细胞中超氧化物生成的增加情况。通过化学发光法在不同的PO2值（空气、100%氧气、50%氧气和100%氮气）下研究中性粒细胞的超氧化物。超氧化物生成（O2-）率分别为84%（空气）、84%（100%氮气）、87%（100%氧气）和84%（50%氧气）。在这些阶段，PO2值分别为178、36、764和370 mmHg。由于在PO2为1 mmHg时线粒体中会产生超氧化物，因此认为这些不同的PO2值（100%氮气、100%氧气和50%氧气）不会影响超氧化物的生成。推测其他因素，如血小板活化因子或细胞因子，会增加超氧化物的生成。
