Mannitol and dextran increase cochlear blood flow in normotensive and spontaneously hypertensive rats.

Pharmacologic treatments for otopathologies of possible vascular origin are aimed at enhancing vascular transport and are intended to increase cochlear blood flow (CBF). In the current study, normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHRs) were given intravascular infusions of mannitol (20%), dextran 70 (6%), or control saline. In general, the results clearly indicate that both osmotic agents effectively increase CBF, as measured by laser Doppler flowmetry. However, the mechanism of action of these agents is less clear.

Autoregulation of cochlear blood flow in normotensive and spontaneously hypertensive rats following intracerebroventricularly mediated adjustment of blood pressure.

Previous studies in our laboratory (Quirk et al., 1988) noted significantly impaired elevations in cochlear blood flow (CoBF) during systemic infusion of the potent vasoconstrictive agent angiotensin II (AII) in the spontaneously hypertensive rat (SHR) as compared with the normotensive Wistar-Kyoto (WKY) rat, despite similar increases in systemic blood pressure. We interpreted these results to suggest that SHRs have an exaggerated autoregulatory mechanism that controls blood supply to the cochlear vessels. However, an alternative explanation for these findings concerns the potential influence of the elevated baseline blood pressure of the SHR on CoBF. Specifically, if there is an absolute threshold blood pressure that triggers an autoregulatory response in the cochlea, then the SHRs would reach that threshold sooner than normotensive animals because they begin at a baseline blood pressure that is well above that of the WKY rat. The present study addressed this possibility by pharmacologically reducing SHR blood pressure to WKY baseline blood pressure and raising WKY to SHR baselines, followed by the infusion of previously utilized doses of AII. The results are consistent with previous findings and support our interpretation of an exaggerated autoregulation of cochlear blood supplying the SHR.

The effects of pentoxifylline on cochlear blood flow in normotensive and spontaneously hypertensive rats.

Normotensive and spontaneously hypertensive rats (SHRs) were given arterial infusions of saline and pentoxifylline in doses of 1.5, 2.0, and 3.0 mg/kg/min. Blood pressure decreased in a dose related fashion with increasing doses of pentoxifylline. Cochlear blood flow, measured via laser Doppler flowmeter, increased with infusion of pentoxifylline in members of both rat strains, but to a greater extent in SHRs than in normotensive animals. The mechanism of action appears to be decreased red blood cell rigidity which allows increased penetration of red blood cells into microvessels of the cochlea.