Premium
In vivo measurement of cytosolic free calcium during cerebral ischemia and reperfusion
Author(s) -
Uematsu Daisuke,
Greenberg Joel H.,
Reivich Marchtin,
Karp Andrea
Publication year - 1988
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410240311
Subject(s) - ischemia , nicotinamide adenine dinucleotide , in vivo , calcium , anesthesia , nad+ kinase , chemistry , calcium metabolism , cerebral cortex , endocrinology , medicine , biochemistry , biology , enzyme , microbiology and biotechnology
An increase in cytosolic free calcium concentration ([Ca 2 + ] i ) may trigger irreversible cell injury following cerebral ischemia. We have measured changes in [Ca 2 + ] i in cat cortex in vivo during ischemia produced by 1 hour of middle cerebral artery occlusion and during 30 minutes of reperfusion. Indo‐1, a fluorescent Ca 2+ indicator, was loaded into the exposed cortex by superfusion, and changes in the [Ca 2+ ] i signal (400/506 nm ratio)were measured microfluorometrically during ultraviolet excitation (340 nm). The nicotinamide adenine dinucleotide/reduced nicotinamide adenine dinucleotide (NAD/NADH) redox state and hemodynamic changes were measured simultaneously. The animals showing severe deterioration in their electroencephalograms (EEG) showed a progressive increase in the [Ca 2+ ] i signal during ischemia (baseline: 1.46 0.05; 60 minutes after occlusion: 2.99 0.37; n = 7). At 30 minutes following reperfusion, the animals showing little recovery in their EEG exhibited a further increase in [Ca 2+ } i (4.71 0.87,n = 3), whereas animals showing significant recovery in their EEG also showed recovery of {Ca 2+ ] i (1.55 0.09, n = 4). By contrast, the moderate or mild stroke animals with less deterioration in their EEGs showed no increase in [Ca 2+ ] i during either ischemia or reperfusion. These data suggest that the increase in [Ca 2+ ] i might be closely related not only to deterioration of brain function during ischemia but also to poor recovery during the reperfusion period.