cerebral blood flow in rats (53). The active constituents of G. biloba responsible
for increasing cerebral blood flow appeared to be the non-flavonoid compounds
(54); ginkgolide B may be responsible for this action owing to its PAF-antagonist
activity (55, 56). Furthermore, intravenous administration of a standardized
G. biloba extract and ginkgolide B to rats showed that the extract, but not
ginkgolide B, decreased the brain’s use of glucose (57).
The constituents of G. biloba responsible for its anti-ischaemic activity remain
undefined. The flavonoids, ginkgolides, and bilobalide have all been suggested,
but it is possible that other constituents may be responsible.
An extract of G. biloba was effective in the in vivo treatment of cerebral
oedema, a condition of excessive hydration of neural tissues owing to damage
by neurotoxic agents (such as triethyltin) or trauma (58–60). Bilobalide appeared
to play a significant role in the antioedema effect (61, 62). Oral or subcutaneous
administration of an extract of G. biloba to rats with acute and chronic phases
of adriamycin-induced paw inflammation partially reversed the increase in
brain water, sodium, and calcium and the decrease in brain potassium associated
with sodium arachidonate-induced cerebral infarction (63).
Mice treated with a standardized extract of G. biloba (100 mg/kg, orally for
4–8 weeks) showed improved memory and learning during appetitive operant
conditioning (64).