Dynamic changes in glucose metabolism of living rat brain slices induced by hypoxia and neurotoxic chemical-loading revealed by positron autoradiography

1999 ◽  
Vol 106 (11-12) ◽  
pp. 1075-1087 ◽  
Author(s):  
T. Murata ◽  
N. Omata ◽  
Y. Fujibayashi ◽  
A. Waki ◽  
N. Sadato ◽  
...  
2002 ◽  
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Nobuyuki Maruoka ◽  
Tetsuhito Murata ◽  
Naoto Omata ◽  
Yasuhisa Fujibayashi ◽  
Yoshiharu Yonekura ◽  
...  

2007 ◽  
Vol 28 (3) ◽  
pp. 672-678 ◽  
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Tetsuhito Murata ◽  
Naoto Omata ◽  
Yasuhiro Takashima ◽  
Yasuhisa Fujibayashi ◽  
...  

2007 ◽  
Vol 114 (9) ◽  
pp. 1155-1159 ◽  
Author(s):  
N. Maruoka ◽  
T. Murata ◽  
N. Omata ◽  
Y. Takashima ◽  
Y. Fujibayashi ◽  
...  

2004 ◽  
Vol 143 (3) ◽  
pp. 388-396 ◽  
Author(s):  
Uwe Christians ◽  
Sven Gottschalk ◽  
Jelena Miljus ◽  
Carsten Hainz ◽  
Leslie Z Benet ◽  
...  

1998 ◽  
Vol 249 (2-3) ◽  
pp. 155-158 ◽  
Author(s):  
Tetsuhito Murata ◽  
Atsuo Waki ◽  
Naoto Omata ◽  
Yasuhisa Fujibayashi ◽  
Norihiro Sadato ◽  
...  

2000 ◽  
Vol 20 (2) ◽  
pp. 350-358 ◽  
Author(s):  
Naoto Omata ◽  
Tetsuhito Murata ◽  
Yasuhisa Fujibayashi ◽  
Atsuo Waki ◽  
Norihiro Sadato ◽  
...  

Dynamic changes in the regional cerebral glucose metabolic rate induced by hypoxia/reoxygenation or ischemia/reperfusion were investigated with a positron autoradiography technique. Fresh rat brain slices were incubated with [18F]2-fluoro-2-deoxy-D-glucose ([18F]FDG) in oxygenated Krebs-Ringer solution at 36°C, and serial two-dimensional time-resolved images of [18F]FDG uptake in the slices were obtained. In the case of loading hypoxia (oxygen deprivation)/pseudoischemia (oxygen and glucose deprivation) for various periods of time, the net influx constant ( K) of [18F]FDG at preloading and after reoxygenation/pseudoreperfusion (post-loading) was quantitatively evaluated by applying the Patlak graphical method to the image data. Regardless of the brain region, with hypoxia lasting ≥20 minutes, the postloading K value was decreased compared with the unloaded control, whereas with pseudoischemia of ≤40 minutes, approximately the same level as the unloaded control was maintained. Next, the neuroprotective effect against hypoxia/pseudoischemia loading induced by the addition of a free radical scavenger or an N-methyl-D-aspartate (NMDA) antagonist was assessed by determining whether a decrease in the postloading K value was prevented. Whereas with 20-minute hypoxia, both agents exhibited a neuroprotective effect, in the case of 50-minute pseudoischemia, only the NMDA antagonist did so, with the free radical scavenger being ineffective. These results demonstrate that hypoxia causes irreversible neuronal damage within a shorter period than ischemia, with both free radicals and glutamate suggested to be involved in tandem in the neurotoxicity induced by hypoxia, whereas glutamate alone is involved in ischemic neurotoxicity.


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