Ost'ádal Bohuslav, Ost'ádalová Ivana, Skárka L, Kolár F, Kopecký Jan
Institute of Physiology, Academy of Sciences, Centre for Experimental Cardiovascular Research, and.
Exp Clin Cardiol. 2002 Fall;7(2-3):93-8.
the immature heart appears to be more resistant to ischemic injury than the adult myocardium. The mechanisms of the higher tolerance of the developing heart have not yet been satisfactorily clarified; age-dependent changes in energy metabolism have to be taken into consideration. Marked ontogenetic changes are displayed by the mitochondrial membrane potential (MMP): in newborn rats a single population of mitochondria with a relatively high MMP was observed but, with increasing age, the second population with a lower MMP appeared. Adaptation to chronic hypoxia and ischemic preconditioning failed to improve ischemic tolerance of the rat heart on the first postnatal day; the cardioprotective effect only developed at the end of the first postnatal week. Decreasing tolerance of the neonatal heart to ischemia is thus counteracted by the development of endogenous protection. It seems likely that both mitochondrial K(ATP) channels and nitric oxide may be involved in the protective mechanisms of adaptation to chronic hypoxia but not to that of ischemic preconditioning, at least in neonatal rats. Basic knowledge of the possible improvements of immature heart tolerance to ischemia may contribute to the design of therapeutic strategies for both pediatric cardiology and cardiac surgery.
未成熟心脏似乎比成年心肌对缺血损伤更具抵抗力。发育中心脏更高耐受性的机制尚未得到令人满意的阐明；必须考虑能量代谢的年龄依赖性变化。线粒体膜电位（MMP）显示出明显的个体发育变化：在新生大鼠中观察到单一群体的线粒体具有相对较高的MMP，但随着年龄的增长，出现了第二群体具有较低MMP的线粒体。对慢性缺氧和缺血预处理的适应未能改善出生后第一天大鼠心脏的缺血耐受性；心脏保护作用仅在出生后第一周结束时才出现。因此，新生心脏对缺血耐受性的降低被内源性保护的发展所抵消。线粒体K（ATP）通道和一氧化氮似乎都可能参与适应慢性缺氧的保护机制，但至少在新生大鼠中不参与缺血预处理的保护机制。关于改善未成熟心脏对缺血耐受性的可能性的基础知识可能有助于儿科心脏病学和心脏外科治疗策略的设计。
