A reversible ischemia model in gerbil cochlea.
A completely reversible cochlear-ischemia animal model was developed, and an initial study of ischemia/reperfusion-induced cochlear function change is presented. The bulla of the anesthetized gerbil was opened through a ventral approach and the anterior inferior cerebellar artery and its branches were exposed. Cochlear blood flow (CBF) from the basal turn of the cochlea was monitored with a laser Doppler flowmeter. An electrically isolated microclamp was used to occlude the labyrinthine artery (LA). During LA clamping, the cubic distortion product (DP) was continuously recorded. The LA was repeatedly clamped for different durations in all animals, and CBF consistently showed full recovery after clamp release. No obvious change in vessel diameter or flow pattern was observed under a stereomicroscope. Mean blood pressure did not show significant change during clamping. Immediately upon LA clamping, CBF decreased rapidly nearly to zero. After clamp release, CBF demonstrated an immediate rapid increase, followed by a secondary gradual recovery to baseline. CBF recovery patterns were clamp duration-related. Within a few seconds of occlusion, DP decreased and reached a minimum of approximately 24% of the initial level in less that 30 s. Following reperfusion of the cochlea, DP gradually increased, decreased again, then slowly recovered. Time delay between CBF reperfusion and the first increase of DP was proportional to clamping duration, and the increased amplitudes demonstrated a negative relationship to clamp duration. We assume that the first decrease in DP during clamping was caused by ischemia in the cochlea; the second decrease, during the cochlear reperfusion, could be a form of reperfusion-induced change in cochlear function. This ischemia/reperfusion model in gerbil cochlea demonstrates excellent repeatability and reversibility. Since DP and other measurements can be used to dynamically monitor cochlear or hair cell functions, this model is useful in studies of auditory physiology and pathophysiology.
Ren
T
T
Kresge Hearing Research Institute, Department of Otolaryngology, University of Michigan Medical School, Ann Arbor, 48109-0506, USA. renty@med.umich.edu
Brown
N J
NJ
Zhang
M
M
Nuttall
A L
AL
Miller
J M
JM
D000818:Animals; D001158:Arteries; D003051:Cochlea / Q000098:blood supply* / Q000473:pathology / Q000502:physiology; D015834:Cochlear Diseases / Q000503:physiopathology; D004195:Disease Models, Animal; D007758:Ear, Inner / Q000098:blood supply; D005849:Gerbillinae; D006198:Hair Cells, Auditory / Q000166:cytology / Q000502:physiology; D007511:Ischemia / Q000503:physiopathology*; D017078:Laser-Doppler Flowmetry; D017084:Otoacoustic Emissions, Spontaneous; D012039:Regional Blood Flow / Q000502:physiology; D015427:Reperfusion Injury / Q000503:physiopathology*; D015203:Reproducibility of Results