Balestrino M, Lensman M, Parodi M, Perasso L, Rebaudo R, Melani R, Polenov S, Cupello A
Department of Neurological and Vision Sciences, University of Genova, Italy.
Amino Acids. 2002;23(1-3):221-9. doi: 10.1007/s00726-001-0133-3.
Phosphocreatine can to some extent compensate for the lack of ATP synthesis that is caused in the brain by deprivation of oxygen or glucose. Treatment of in vitro rat hippocampal slices with creatine increases the neuronal store of phosphocreatine. In this way it increases the resistance of the tissue to anoxic or ischemic damage. In in vitro brain slices pretreatment with creatine delays anoxic depolarization (AD) and prevents the irreversible loss of evoked potentials that is caused by transient anoxia, although it seems so far not to be active against milder, not AD-mediated, damage. Although creatine crosses poorly the blood-brain barrier, its administration in vivo at high doses through the intracerebroventricular or the intraperitoneal way causes an increase of cerebral phosphocreatine that has been shown to be of therapeutic value in vitro. Accordingly, preliminary data show that creatine pretreatment decreases ischemic damage in vivo.
磷酸肌酸在一定程度上可以补偿因缺氧或葡萄糖剥夺导致的大脑中三磷酸腺苷（ATP）合成不足的情况。用肌酸处理体外培养的大鼠海马切片可增加神经元中的磷酸肌酸储备。通过这种方式，它可增强组织对缺氧或缺血性损伤的抵抗力。在体外脑切片中，肌酸预处理可延迟缺氧去极化（AD），并防止由短暂缺氧引起的诱发电位的不可逆丧失，尽管到目前为止它似乎对较轻的、非AD介导的损伤没有作用。虽然肌酸很难穿过血脑屏障，但通过脑室内或腹腔内途径在体内高剂量给药会导致脑内磷酸肌酸增加，这在体外已显示具有治疗价值。因此，初步数据表明，肌酸预处理可减少体内的缺血性损伤。
