31P NMR relaxation does not affect the quantitation of changes in phosphocreatine, inorganic phosphate, and ATP measured in vivo during complete ischemia in swine brain.
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.
Mary Nell and Ralph Rogers Magnetic Resonance Center, Department of Radiology, Dallas, Texas.
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Laptook
D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism*; D009682:Magnetic Resonance Spectroscopy; D009994:Osmolar Concentration; D010710:Phosphates / Q000378:metabolism*; D010725:Phosphocreatine / Q000378:metabolism*; D010758:Phosphorus; D013552:Swine
D010710:Phosphates; D010725:Phosphocreatine; D010758:Phosphorus; D000255:Adenosine Triphosphate