Ischemia and reperfusion are involved in numerous sensorineural pathol
ogies. A model of reversible cochlear ischemia has been designed in Mo
ngolian gerbil. Selective labyrinthine ischemia of variable duration (
4-10 min) was achieved through a posterior transcranial approach. Isch
emia and reperfusion were controlled with the help of laser Doppler ve
locimetry. Functional changes were monitored every 1-10 s throughout e
xperiments, using cochlear potentials and otoacoustic emissions. After
interruption of blood flow, all signals rapidly began to decay. In co
ntrast to cochlear potentials, otoacoustic emissions always exhibited
a plateau before reaching noise floor only after approximate to 4-5 mi
n. Upon ischemia release, cochlear blood flow recovered instantly and
completely and cochlear potentials rapidly improved in most cases, in
contrast to otoacoustic emissions that underwent a delayed decay after
immediate partial recovery. The phase and group latency of otoacousti
c emissions exhibited only small changes throughout ischemia and reper
fusion, suggesting adaptive rather than damaging mechanisms. Cochlear
function returned to normal after 5 min 30 s ischemia but longer compl
ete ischemia sometimes led to irreversible damage despite the systemat
ic presence of some recovery just after ischemia release. This behavio
r suggests that reperfusion in itself can be deleterious to a sensorin
eural organ and this model can be useful for identifying the noxious m
echanisms of ischemia and reperfusion. (C) 1997 Elsevier Science B.V.