【摘要】 小鼠经锻炼和药物复合处理后进行低压舱模拟海拔５０００ｍ高度的低氧实验，同时设正常与５０００ｍ低氧对照，用图象分析法计量分析各组心肌线粒体长轴（Ｌ）、短轴（Ｓ）、截面积（Ａ）、比表面积（Ｓ／Ｖ）的变化。结果显示，５０００ｍ高度缺氧小鼠线粒体Ｌ、Ｓ、Ａ分别较正常组增高１２．９％、１８．９％（Ｐ＜０．０５）、２４．２％，Ｓ／Ｖ减少１２．０％（Ｐ＜０．０５）。经复合方案处理后再模拟５０００ｍ缺氧的小鼠，上述各项指标均可恢复至正常水平。结果表明，高原急性缺氧可致线粒体肿胀，脊减少，伴有空泡化，这是高原低氧下能量代谢障碍、劳动能力降低的病理学基础。复合处理对缺氧造成的心肌线粒体的结构改变有纠正作用，能良好地保护心肌，进而有助于提高高原劳动能力。更多还原

【Abstract】 mice pretreated with training and drugs were exposed to hypoxia at simulated altitude of 5000m in hypobaric chamber.Changes of long(L)and short(S)axis,cross section area(A),and specific surface area(S/V)of myocardial mitochondria were quantitatively analyzed by an image analysis system and com-pared with those in control groups.It was found that hypoxia at simulated altitude of 5000m resulted in the increases of L,S and A by 12.9%,18.9%(P<0.05)and 24.2%respectively while S/V de-creased by 12.0%(P<0.05)compared with mormal control.The combination use of training and drug intervention could reverse the aforementioned effects of the hypobaric hypoxia.The results suggested that acute hypoxia at simulated altitude of 5000m can cause mitochondrial swelling and vacuoliztion.The mitochondrial damage may be responsible for the decrement of labour capacity and is the pathological ba-sis for energy failure induced by hypoxia.The combination use of training and drug intervention can pro-tect myocardial mitochondria from structural changes and thus protect cardiac function.These beneficial effects,therefore,improve the labour capacity at high altitude.更多还原