Stancheva S, Georgiev V, Alova L, Getova D
Institute of Physiology, Bulgarian Academy of Sciences, Bulgaria.
Acta Physiol Pharmacol Bulg. 1996;22(1):27-30.
The effects of angiotensin II (ATII) administered intracerebroventricularly (i.c.v.) at a dose of 0.5 microgram per mouse on the activity of monoamine oxidase A (MAO-A) and monoamine oxidase B (MAO-B) in the forebrain of normoxic and hypoxic mice were studied. The influence of hypoxia (asphyctic and haemic) on MAO-A and MAO-B activity was also investigated. MAO-A activity was increased in haemic hypoxia; MAO-B activity increased in both asphyctic and haemic hypoxia. ATII increased MAO-A activity without affecting MAO-B activity under normoxic conditions. ATII increased MAO-A activity but decreased MAO-B in hypoxic (asphyctic) mice as compared to normoxic controls. The results suggest the role of MAO-A and MAO-B in the ATII-induced increase of susceptibility to acute hypoxia.
研究了以每只小鼠0.5微克的剂量脑室内注射血管紧张素II(ATII)对常氧和低氧小鼠前脑单胺氧化酶A(MAO-A)和单胺氧化酶B(MAO-B)活性的影响。还研究了低氧(窒息性和血液性)对MAO-A和MAO-B活性的影响。血液性低氧时MAO-A活性增加;窒息性和血液性低氧时MAO-B活性均增加。在常氧条件下,ATII增加MAO-A活性而不影响MAO-B活性。与常氧对照组相比,低氧(窒息性)小鼠中ATII增加MAO-A活性但降低MAO-B活性。结果提示MAO-A和MAO-B在ATII诱导的急性低氧易感性增加中起作用。