T. Mom et al., Measuring the cochlear blood flow and distortion-product otoacoustic emissions during reversible cochlear ischemia: a rabbit model, HEARING RES, 133(1-2), 1999, pp. 40-52
Impairment to the cochlear blood flow likely induces many types of sensorin
eural hearing loss. Models using several small laboratory animals have been
described in the literature that permit the simultaneous monitoring of the
cochlear blood flow with laser-Doppler flowmetry and cochlear function usi
ng evoked responses. However, these models have not permitted a direct appl
ication of the resulting knowledge to the human condition, primarily due to
differences in the translucence of the otic capsule between species. In th
e present study, to approximate conditions relevant to the human patient, t
he rabbit was utilized to develop a procedure in which laser-Doppler flowme
try could be used to measure the cochlear blood flow ill an animal with an
opaque otic capsule. At the same time, the cochlear function was monitored
non-invasively using. distortion-product otoacoustic emissions. In this man
ner. a laser-Doppler probe was positioned in the round window niche and the
cochlear function measured using distortion-product otoacoustic emissions
during a systematic series of ischemic episodes. Cochlear ischemia was prod
uced by deliberately compressing the eighth nerve complex at the porus of t
he internal acoustic meatus, for periods lasting from 1-3 min, while cochle
ar blood flow and distortion-product otoacoustic emission measures were obt
ained simultaneously before, during and following the occlusion. Results de
monstrated that the cochlear blood flow sharply decreased within 1 s after
compression onset, whereas distortion-product otoacoustic emissions showed
obstruction-induced changes after a delay of several seconds, provided that
the blood flow decreased, at least, 40%. Similarly, upon release of the co
mpression, the cochlear blood now began to recover within 1 s, whereas the
recovery of the corresponding distortion-product otoacoustic emissions was
slightly delayed. Although not apparent in the distortion-product otoacoust
ic emission recovery time course, the cochlear blood flow consistently over
shot its initial baseline value during the recovery process. Thus, although
cochlear ischemia produced changes in the distortion-product otoacoustic e
mission activity that generally followed the resulting alterations in the c
ochlear blood flow, the detailed relationship between the two measures was
complex. (C) 1999 Elsevier Science B.V. All rights reserved.