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A 31P nuclear magnetic resonance in vivo study of cerebral ischaemia in the gerbil.
J Cereb Blood Flow Metab ; 2(3): 299-306, 1982 Sep.
Article en En | MEDLINE | ID: mdl-7096457
We have used the noninvasive method of 31phosphorus nuclear magnetic resonance (31P NMR) in vivo to follow changes in phosphorous metabolite concentrations and the intracellular pH in the right and left hemispheres and in the cerebellum of gerbil brains after the occlusion of the right carotid artery. Spatial resolution over the brain was possible using surface coils. Ligation, which is know to cause ischaemia in this species in the ipsilateral hemisphere, resulted in the diminution of phosphocreatine and adenine nucleotides and a decrease in tissue pH. Less acidification occurred in the contralateral hemisphere and in the cerebellum. The high-energy metabolite concentrations, phosphocreatine and adenosine triphosphate (ATP), declined in unison in the ischaemic region, in marked contrast to the sequence of events in skeletal muscle, in which phosphocreatine buffers against an immediate fall in ATP concentration. In a separate series of gerbils, 31P NMR spectra were followed for exactly 1 h after carotid ligation. The animals were then sacrificed and brain grey matter specific gravity was rapidly measured to assess the development of oedema. There was a clear correlation between abnormality of spectra and the presence of oedema. It cannot, however, be confidently asserted that a normal spectrum is never seen in oedematous gerbil brains. 31P NMR spectra specific gravity and histological changes shown by light microscopy have been correlated and show that useful signals are received from a depth of at least 4 mm or more from the 10-mm diameter coil.
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Bases de datos: MEDLINE Asunto principal: Isquemia Encefálica / Gerbillinae Idioma: En Revista: J Cereb Blood Flow Metab Año: 1982 Tipo del documento: Article
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Bases de datos: MEDLINE Asunto principal: Isquemia Encefálica / Gerbillinae Idioma: En Revista: J Cereb Blood Flow Metab Año: 1982 Tipo del documento: Article