Corbett R J, Laptook A R
Mary Nell and Ralph Rogers Magnetic Resonance Center, Department of Radiology, Dallas, Texas.
J Neurochem. 1993 Jul;61(1):144-9. doi: 10.1111/j.1471-4159.1993.tb03549.x.
Ischemia-induced changes in 31P NMR relaxation were examined in 16 piglets. NMR spectra were acquired under control conditions and during complete cerebral ischemia induced via cardiac arrest. Changes in T1 were assessed directly in six animals during control conditions and after 30-45 min of complete ischemia when changes in brain Pi levels had reached a plateau. The T1 for Pi did not change, i.e., 2.3 +/- 0.5 s during control conditions versus 2.4 +/- 1.0 s during ischemia. To evaluate phosphocreatine and ATP, two types of spectra, with a long (25-s) or short (1-s) interpulse delay time, were collected during the first 10 min of ischemia (n = 10). Both types of spectra showed the same time course of changes in phosphocreatine and ATP levels, implying that the T1 relaxation times do not change during ischemia. There were no changes in the linewidths of phosphocreatine, ATP, or Pi during ischemia, implying that the T2* values remain constant. Our results suggest that the 31P T1 and T2* for phosphocreatine, Pi, and ATP do not change during ischemia, and therefore changes in 31P NMR peak intensity accurately reflect changes in metabolite concentrations.
在16只仔猪中研究了缺血诱导的31P NMR弛豫变化。在对照条件下以及通过心脏骤停诱导的完全脑缺血期间采集NMR光谱。在对照条件下以及在完全缺血30 - 45分钟后，当脑Pi水平变化达到平台期时，直接评估6只动物的T1变化。Pi的T1没有变化，即在对照条件下为2.3±0.5秒，缺血期间为2.4±1.0秒。为了评估磷酸肌酸和ATP，在缺血的前10分钟（n = 10）收集了两种类型的光谱，具有长（25秒）或短（1秒）的脉冲间隔时间。两种类型的光谱都显示出磷酸肌酸和ATP水平变化的相同时间进程，这意味着T1弛豫时间在缺血期间没有变化。缺血期间磷酸肌酸、ATP或Pi的线宽没有变化，这意味着T2值保持恒定。我们的结果表明，磷酸肌酸、Pi和ATP的31P T1和T2在缺血期间没有变化，因此31P NMR峰强度的变化准确反映了代谢物浓度的变化。
