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Cochlear blood flow autoregulation in Wistar-Kyoto rats
W S Quirk1, H A Dengerink, J K Coleman
1Kresge Hearing Research Institute, University of Michigan, Ann Arbor 48109-0506.
Hearing Research
|August 1, 1989
Summary
Cochlear blood flow in Wistar-Kyoto rats is autoregulated. Angiotensin II (AII) infusion directly into the cochlear artery reduces blood flow, suggesting AII
Area of Science:
- Otoacoustic emissions and inner ear physiology
- Vascular physiology and autoregulation
- Renal and cardiovascular pharmacology
Background:
- Cochlear blood flow (CoBF) is crucial for inner ear function.
- Autoregulation mechanisms in the cochlea are not fully understood.
- The role of angiotensin II (AII) in cochlear hemodynamics requires further investigation.
Purpose of the Study:
- To investigate the autoregulation of cochlear blood flow (CoBF) in Wistar-Kyoto rats (WKY).
- To determine the specific role of angiotensin II (AII) in modulating CoBF.
- To explore the involvement of vascular angiotensin receptors in CoBF regulation.
Main Methods:
- Intra-arterial infusion of vasoactive agents (angiotensin II, phenylephrine) in WKY rats.
- Laser Doppler flowmetry to measure cochlear blood flow (CoBF).
- Direct infusion of AII into the anterior inferior cerebellar artery (AICA) and administration of angiotensin receptor antagonist (sarthran).
Main Results:
- Systemic infusion of AII and phenylephrine initially increased CoBF, followed by a return to baseline despite elevated blood pressure, indicating autoregulation.
- Direct AICA infusion of AII significantly reduced CoBF without altering systemic blood pressure.
- Sarthran pretreatment attenuated AII-induced reductions in CoBF, implicating angiotensin receptors.
Conclusions:
- Cochlear blood flow (CoBF) in Wistar-Kyoto rats exhibits autoregulation.
- Angiotensin II (AII) directly causes vasoconstriction in cochlear vasculature.
- Vascular angiotensin receptors play a role in the autoregulation of CoBF.