Kawabata A, Hata T
Department of Pharmacology, Faculty of Pharmacy, Kinki University, Higashi-Osaka, Japan.
Thromb Res. 1993 Nov 15;72(4):321-31. doi: 10.1016/0049-3848(93)90141-a.
Abnormal hemostatic profiles indicating hemorrhagic tendency have been reported in rodents exposed to prolonged fluctuation in ambient temperature, known as SART (specific alternation of rhythm in temperature)-stressed animals. In this study, investigation was made of possible involvement of oxygen-derived free radicals in the development of stress-induced hemostatic alteration. SART-stressed rats and mice exhibited marked decrease in platelet count, fibrinogen level and factor VIII:C activity. Superoxide dismutase, when administered s.c. twice a day to mice for 7 days of stress exposure, inhibited the above alterations. Catalase given in the same manner, had essentially the same effect, though to a lesser extent. Allopurinol administered orally once daily during stress reduced stress-induced thrombocytopenia, but caused considerable increase in fibrinogen and factor VIII:C activity in stressed and unstressed mice. Lipid peroxide significantly increased in the heart but not in the plasma following stress exposure in rats and mice. Active oxygens would thus appear to be, at least partially, involved in the development of abnormal hemostasis induced by SART stress.
据报道，暴露于环境温度长期波动的啮齿动物（即经受SART（温度节律特异性改变）应激的动物）会出现表明出血倾向的异常止血情况。在本研究中，我们调查了氧衍生自由基是否可能参与应激诱导的止血改变的发生过程。经受SART应激的大鼠和小鼠血小板计数、纤维蛋白原水平和因子VIII:C活性显著降低。在应激暴露7天期间，每天两次皮下注射超氧化物歧化酶给小鼠，可抑制上述改变。以同样方式给予的过氧化氢酶也有基本相同的效果，只是程度较小。在应激期间每天口服一次别嘌呤醇可减轻应激诱导的血小板减少，但会使应激和未应激小鼠的纤维蛋白原和因子VIII:C活性显著增加。在大鼠和小鼠应激暴露后，心脏中的脂质过氧化物显著增加，但血浆中未增加。因此，活性氧似乎至少部分参与了SART应激诱导的异常止血的发生。
