Hepatocyte growth factor suppresses ischemic cerebral edema in rats with microsphere embolism

The present study was aimed at determining whether human recombinant hepatocyte growth factor (HGF) ameliorates cerebral edema induced by microsphere embolism (ME). Rats were injected with 700 microspheres (48μm in diameter). Continuous administration of HGF at 13μg/3 days/animal into the right vent...

Full description

Saved in:
Bibliographic Details
Published inNeuroscience letters Vol. 448; no. 1; pp. 125 - 129
Main Authors Takeo, Satoshi, Takagi, Norio, Takagi, Keiko, Date, Ichiro, Ishida, Kumi, Besshoh, Shintaro, Nakamura, Toshikazu, Tanonaka, Kouichi
Format Journal Article
LanguageEnglish
Published Shannon Elsevier Ireland Ltd 19.12.2008
Elsevier
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:The present study was aimed at determining whether human recombinant hepatocyte growth factor (HGF) ameliorates cerebral edema induced by microsphere embolism (ME). Rats were injected with 700 microspheres (48μm in diameter). Continuous administration of HGF at 13μg/3 days/animal into the right ventricle was started from 10min after embolism to the end of the experiment by using an osmotic pump. On day 3 after the ME, the rats were anesthetized, and their brains were perfused with an isotonic mannitol solution to eliminate constituents in the vascular and extracellular spaces. Thereafter, tissue water and cation contents were determined. A significant increase in tissue water content of the right hemisphere by ME was seen. This ME-induced increase in water content was associated with increases in tissue sodium and calcium ion contents and decreases in tissue potassium and magnesium ion contents of the right hemisphere. The treatment of the animal with HGF suppressed the increases in water and sodium and calcium ion contents, but not the decreases in potassium and magnesium ion contents. These results suggest that HGF suppresses the formation of ischemic cerebral edema provoked intracellularly in rats with ME.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
ObjectType-Article-1
ObjectType-Feature-2
ISSN:0304-3940
1872-7972
DOI:10.1016/j.neulet.2008.10.026