Stroke, Vol 19, 608-614, Copyright © 1988 by American Heart Association
NM Bolas, B Rajagopalan, F Mitsumori and GK Radda
Progressive cerebral ischemia was induced in seven anesthetized
hyperglycemic rats by carotid artery ligation and hemorrhagic hypotension.
Phosphorus metabolites, intracellular pH, and lactate in the brain were
monitored by 31P and 1H magnetic resonance spectroscopy. Under conditions
in which blood flow was low, phosphocreatine (PCr) concentration and
intracellular pH decreased and the concentration of lactate increased. The
decrease in ATP was approximately one-third that of PCr until only 25% PCr
remained, after which ATP was lost more rapidly than PCr. These changes
were interpreted in terms of three regions observed by the magnetic
resonance coil, one of complete ischemia, one of partial ischemia, and one
of perfusion sufficient to maintain normal metabolite levels. The extent of
the three regions was estimated quantitatively. Broadening and splitting of
the inorganic phosphorus (Pi) peak into two components provided further
evidence of distinct populations of cells, one very acidic and another less
so. Apparent intracellular buffering capacity was calculated as 23.6 +/-
1.3 mumol lactate/g wet wt/pH.
ARTICLES
Metabolic changes during experimental cerebral ischemia in hyperglycemic rats, observed by 31P and 1H magnetic resonance spectroscopy
MRC Biomedical NMR Group, John Radcliffe Hospital, Headington, Oxford, United Kingdom.
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