Tristan Messager, Jean Michel de Bray, Pierre Jallet, Elmar Rump and
Jean Jacques Le Jeune
Unite de Vectorisation Particulaire, UPRES-EA no 2169, Faculte
de Medecine, Universite d'Angers, Rue Haute de Reculee, 49045 Angers, France
Abstract: The exact mechanisms of cerebral arterial hypoxia are
not perfectly defined. Our purpose is to adapt and validate, with drugs
well known in rats and rabbits, a closed cranial window technique in gerbils.
The method was used with seventeen gerbils to measure diameter changes of
the pial arterioles under normoxia (after the topical application of agonists
and antagonists of ATP-sensitive and Ca2+-dependent potassium
channels), as well as under hypoxia. In normoxia, aprikalim (10-6
M), a direct activator of ATP-sensitive potassium channels, increases the
diameter of pial arterioles by 10±2% (N=17). This effect is inhibited by
glibenclamide (10-6 M), but not affected by iberiotoxin (10-6
M), a specific inhibitor of Ca2+-dependent potassium channels.
The adenosine-induced dilation by 19±5% (N=17) is reduced by 59±16% with
iberiotoxin, by 33±23% with glibenclamide and inhibited by theophylline
(10-5 M). In hypoxia (15% O2), pial arteriole diameters
are increased by 24±5% (N=17) and partially decreased by the application
of glibenclamide and iberiotoxin to 59±11% and 54±5%, respectively. These
data are similar to those obtained in other species and validate the closed
cranial window technique on gerbils. They indicate that, as for rats and
rabbits, both ATP-sensitive and Ca2+-dependent potassium channels
are present in gerbil pial vessels and play a role in hypoxia.
Keywords: Hypoxia, Potassium channel, Adenosine, Pial arteriole, Closed
cranial window