摘要
实验观察了在模拟海拔６０００ｍ缺氧冻伤对大鼠血清血管紧张素Ⅰ转换酶（ＡＣＥ）活性的影响。大鼠血清ＡＣＥ活性以Ｕ（ｎｍｏｌ·ｍｌ－１·ｍｉｎ１）表示。致冻前，缺氧习服缺氧冻伤（ＦＨＡＣ）组和急性缺氧冻伤（ＦＡＨ）组大鼠血清ＡＣＥ活性分别为５０．０±５．８和６０．０±６．７Ｕ（Ｐ＞０．０５）明显低于平原冻伤（ＦＮ）组的７８．１±４．０Ｕ（Ｐ＜０．０１和Ｐ＜０．０５）；冻后４ｈ，ＦＡＨ组和ＦＨＡＣ组大鼠血清ＡＣＥ活性均呈现较冻前增高趋势；冻后２４ｈ，ＦＡＨ组与冻前无差异，而ＦＨＡＣ组冻后７２ｈ仍呈增长趋势。结果表明：单纯缺氧暴露可使大鼠血清ＡＣＥ活性降低，而缺氧复合冷损伤则使大鼠血清ＡＣＥ活性呈现增高趋势，提示可能有内皮细胞损伤。
The effects of frostbite during hypoxia at 6 000 m simulated altitude on serum angiotensin Ⅰ converting enzyme (ACE) activity in rats were investigated. Before freezing, the serum ACE activity in rats of frostbite during hypoxia after high altitude acclimation (FHAC) group and frostbite during acute hypoxia (FAH) group was 50.0±5.8 U and 60.0±6.7 U respectively, and much lower than that of frostbite at normoxia (FN) group(78.1±4.0 U, P<0.05). At 4 hours after frostbite, ACE activities of FN and FAH groups all tended to increase. At 24 hours after frostbite, the ACE activity of FAH group recovered, but the activity of FHAC group detected at 72 hours after frostbite was still higher than that before freezing. The results showed that exposure to hypoxia alone could decrease the serum ACE activity in rats. Combination of exposure to hypoxia and cold could make the ACE activity tend to increase, suggesting that there might be damage of vascular endothelial cells, and that the damage in rats of FHAC group might be much severe.
出处
《解放军预防医学杂志》
CAS
北大核心
1998年第1期15-17,共3页
Journal of Preventive Medicine of Chinese People's Liberation Army
基金
总后勤部"八五"指令性课题
关键词
冻伤
急性缺氧
血管紧张素Ⅰ
转换酶
缺氧
forstbite, acute hypoxia, hypoxia acclimation, angiotensin Ⅰ converting enzyme
