Kobayashi H, Kobayashi K, Hirohata Y, Aihara K, Ohtsuka T
Central Institute for Electron Microscopic Researches, Nippon Medical School, Tokyo, Japan.
Adv Prostaglandin Thromboxane Leukot Res. 1987;17A:388-91.
Thus, ONO-3144 treatment affords great protection against reoxygenation injury in the anoxic myocardium through the scavenging mechanism that includes .OH or closely related species of free radicals and also may inhibit thromboxane synthetase in the anoxic myocardium. We would hypothesize that free radical formation generated through the conversion of PGG2 to PGH2 should play an important role in the reoxygenation injury of the anoxic myocardium.
因此,ONO - 3144治疗通过清除机制为缺氧心肌的复氧损伤提供了强大的保护作用,该清除机制包括·OH或与之密切相关的自由基种类,并且还可能抑制缺氧心肌中的血栓素合成酶。我们推测,通过PGG2转化为PGH2产生的自由基形成在缺氧心肌的复氧损伤中应起重要作用。