Argov Z, Maris J, Damico L
Department of Biochemistry and Biophysics, University of Pennsylvania School of Medicine, Philadelphia 19104.
J Neurol Sci. 1988 Sep;86(2-3):185-93. doi: 10.1016/0022-510x(88)90097-4.
Skeletal muscle bioenergetics of dystrophic hamsters (DH) were studied by in vivo 31P-NMR in order to evaluate possible metabolic impairment. 31P-NMR data were obtained during rest, during muscle work that was induced by nerve stimulation at 3 frequencies (0.2, 0.4 and 1.0 Hz) and during postexercise recovery. At rest, phosphocreatine-to-inorganic phosphate ratio (PCr/Pi) was significantly (P less than 0.02) lower in adult DH (5.3 +/- 1.1; +/- 2 SD) compared with control hamsters (6.55 +/- 0.5). An increased PCr depletion was found in DH muscle during nerve stimulation and the steady-state PCr/Pi was significantly (P less than 0.05) lower at 0.4 and 1.0 Hz. Slow PCr/Pi recovery was observed in DH (0.5 +/- 0.2 units per min compared with 1.42 +/- 0.28 for control, +/- 2 SD, P less than 0.02). These findings suggest a significant in vivo mitochondrial malfunction in DH muscle that may result from either mitochondrial abnormalities or cardiac insufficiency or a combination of both.
为了评估可能存在的代谢损伤,通过活体31P-NMR研究了营养不良仓鼠(DH)的骨骼肌生物能量学。在休息期间、由3种频率(0.2、0.4和1.0Hz)的神经刺激诱导的肌肉工作期间以及运动后恢复期间获取了31P-NMR数据。休息时,成年DH的磷酸肌酸与无机磷酸的比率(PCr/Pi)(5.3±1.1;±2SD)显著低于对照仓鼠(6.55±0.5)(P<0.02)。在神经刺激期间,发现DH肌肉中磷酸肌酸的消耗增加,并且在0.4和1.0Hz时,稳态PCr/Pi显著降低(P<0.05)。观察到DH的PCr/Pi恢复缓慢(每分钟0.5±0.2单位,而对照为1.42±0.28,±2SD,P<0.02)。这些发现表明,DH肌肉中存在明显的活体线粒体功能障碍,这可能是由线粒体异常或心脏功能不全或两者共同作用引起的。