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 10ü}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 19ü}5% (N=17) is reduced by 59ü}16% with iberiotoxin, by 33ü}23% with glibenclamide and inhibited by theophylline (10-5 M). In hypoxia (15% O2), pial arteriole diameters are increased by 24ü}5% (N=17) and partially decreased by the application of glibenclamide and iberiotoxin to 59ü}11% and 54ü}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