In vivo 31P NMR studies on experimental cerebral infarction.
Sequential metabolic changes in rat brain were monitored by in vivo measurements of 31P NMR spectra using a topical magnetic resonance (TMR) spectrometer, during the course of experimentally induced cerebral infarction and also during recovery produced by restoration of circulation. The experimental cerebral infarction was rendered by a slightly modified version of the method of Pulsinelli and Brierley (1979). The bilateral coagulation of the vertebral arteries at the level of alar foramina of the first cervical vertebra (preinfarction) did not show any change in NMR spectrum, but the subsequent bilateral ligation of internal carotid arteries produced a decrease in the peaks of ATP and phosphocreatine and a concomitant increase in the peak of inorganic phosphate within a few minutes. Intracellular pH, calculated from the chemical shift of inorganic phosphate, declined. These changes became maximal at approximately 30 min after the infarction. Reinstatement of blood flow to the cerebrum, produced by untying the ligature of internal carotid arteries, resulted in an immediate restoration of the peaks of ATP and phosphocreatine, which was followed by a reduction in the peak of inorganic phosphate within a few minutes. The spectrum recovered to its preinfarction pattern about 30 min after the restoration of the circulation. These experiments demonstrate that phosphorus compounds change very rapidly during infarction, and that these changes were reversible at least during a 30 min period.
D000255:Adenosine Triphosphate / Q000032:analysis; D000818:Animals; D001923:Brain Chemistry; D002544:Cerebral Infarction / Q000378:metabolism*; D009682:Magnetic Resonance Spectroscopy; D010710:Phosphates / Q000032:analysis; D010725:Phosphocreatine / Q000032:analysis; D010758:Phosphorus / Q000032:analysis*; D051381:Rats; D011919:Rats, Inbred Strains
D010710:Phosphates; D010725:Phosphocreatine; D010758:Phosphorus; D000255:Adenosine Triphosphate