Mozet Christian, Martin Rosemarie, Welt Klaus, Fitzl Günther
Institute of Anatomy, Department of Medicine, University of Leipzig, Leipzig, Germany.
Aging Clin Exp Res. 2009 Feb;21(1):14-21. doi: 10.1007/BF03324893.
Acute hypoxia is a threatening clinical case of emergency and may result in ultrastructural damage, with complete loss of cellular and organ functions. However, little is known about the differences in hypoxia tolerance between young and old myocardia and the protective effects of radical scavenging agents in acute hypoxic stress situations.
We investigated the age-dependent differences of the myocardial ultrastructure and antioxidative status (superoxide-dismutase (SOD) activity and malondialdehyde (MDA) content) of young (6 months) and old (22-24 months) Wistar rats (Crl (Wi)Br) after acute respiratory hypoxia of 20 min at 5% v/v O2 in N2O mixture, and the protective effect of Ginkgo biloba extract (EGb 761).
Ultrastructural-morphometric and biochemical age analysis only revealed a decrease in the sarcoplasma volume fraction, an increase in homogeneous intramitochondrial areas, significant higher SOD activity and lower MDA levels in the group of old rats. Pretreatment with EGb 761 led to a significant decrease in MDA content in both control groups. Acute hypoxic stress increased the volume fractions of sarcoplasmatic reticulum, t-tubules, vacuoles, and lipid droplets, and caused mitochondrial swelling, with a more significant increase in degenerated and homogeneous intramitochondrial areas in the old group. SOD activity decreased only in the old hypoxic group; MDA content fell in both. Pretreatment with EGb 761 reduced ultrastructural-morphometric hypoxic damage in both groups, significantly below the levels of control. Young rat myocardium showed significantly higher SOD activity after hypoxia than untreated or older specimens.
Better hypoxia tolerance is demonstrated by the young myocardium, and an obvious hypoxia-protective effect of EGb 761 in both age groups.
急性缺氧是一种威胁生命的临床急症,可能导致超微结构损伤,使细胞和器官功能完全丧失。然而,关于年轻和老年心肌在缺氧耐受性方面的差异以及自由基清除剂在急性缺氧应激情况下的保护作用,人们了解甚少。
我们研究了6个月大(年轻)和22 - 24个月大(老年)的Wistar大鼠(Crl (Wi)Br)在含5% v/v氧气的一氧化二氮混合气体中急性呼吸性缺氧20分钟后,心肌超微结构和抗氧化状态(超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量)的年龄依赖性差异,以及银杏叶提取物(EGb 761)的保护作用。
超微结构形态计量学和生化年龄分析仅显示老年大鼠组肌浆体积分数降低、线粒体内均匀区域增加、SOD活性显著升高以及MDA水平降低。用EGb 761预处理导致两个对照组的MDA含量均显著降低。急性缺氧应激增加了肌浆网、横小管、液泡和脂滴的体积分数,并导致线粒体肿胀,老年组线粒体退化和均匀区域的增加更为显著。SOD活性仅在老年缺氧组降低;两组的MDA含量均下降。用EGb 761预处理可减轻两组超微结构形态计量学上的缺氧损伤,显著低于对照组水平。缺氧后,年轻大鼠心肌的SOD活性显著高于未处理或老年标本。
年轻心肌表现出更好的缺氧耐受性,EGb 761在两个年龄组中均具有明显的缺氧保护作用。