Metabolic changes in rats with photochemically induced cerebral infarction and the effects of batroxobin: a study by magnetic resonance imaging, 1H- and 31P-magnetic resonance spectroscopy.
Metabolic changes in rats with photochemically induced cerebral infarction and the effects of batroxobin were investigated 1, 3, 5 and 7 days after infarction by means of magnetic resonance imaging (MRI), 1H- and 31P-magnetic resonance spectroscopy (MRS). A region of T2 hyperintensity was observed in left temporal neocortex in infarction group and batroxobin group 1, 3, 5 and 7 days after infarction. The volume of the region gradually decreased from 1 day to 7 days after infarction. The ratio of NAA/Cho + Cr in the region of T2 hyperintensity in the infarction group was significantly lower than that in the corresponding region in the sham-operated group 3, 5 and 7 days after infarction respectively (P < 0.05). Lac appeared in the region of T2 hyperintensity in the infarction group 1, 3, 5 and 7 days after infarction, but it was not observed in the corresponding region in sham-operated group at all time points. Compared with the sham-operated group, the ratios of beta ATP/PME + PDE and PCr/PME + PDE of the whole brain in the infarction group were significantly lower 1, 3 and 5 days after infarction respectively (P < 0.05), and the ratio of beta ATP/PCr also was significantly lower 1 day after infarction (P < 0.05). Batroxobin significantly decreased the volume of the region of T2 hyperintensity 1 and 3 days after infarction (P < 0.05), significantly increased the ratio of NAA/Cho + Cr in the region 5 and 7 days after infarction (P < 0.05), significantly decreased the ratios of Lac/Cho + Cr and Lac/NAA in the region 5 and 7 days after infarction (P < 0.05), and significantly increased the ratios of beta ATP/PME + PDE and beta ATP/PCr in the whole brain 1 day after infarction (P < 0.05). The results indicated that the infracted region had severe edema, increased Lac and apparent neuronal dysfunction and death, and energy metabolism of the whole brain decreased after focal infarction, and that batroxobin effectively ameliorated the above-mentioned abnormal changes.
Guan
X
X
Chinese Military Postgraduate Medical College, Beijing 100853.
Wu
W
W
Kuang
P
P
Kuang
P
P
Gao
Y
Y
Guan
L
L
Li
L
L
Mao
X
X
Liu
M
M
D000818:Animals; D001224:Aspartic Acid / Q000031:analogs & derivatives* / Q000378:metabolism*; D012103:Batroxobin / Q000494:pharmacology*; D002544:Cerebral Infarction / Q000209:etiology / Q000378:metabolism*; D008279:Magnetic Resonance Imaging; D008297:Male; D010777:Photochemistry; D017319:Photosensitizing Agents; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012395:Rose Bengal
D017319:Photosensitizing Agents; D012395:Rose Bengal; D001224:Aspartic Acid; C000179:N-acetylaspartate; D012103:Batroxobin