Sensitivity of the Endocochlear Potential Level to Cochlear Blood Flow during Hypoventilation

Abstract

To study the relationship between endocochlear DC potential (EP) and cochlear blood flow (CoBF) under hypoxic conditions, we recorded the EP and CoBF from the basal turn of the cochlea in 21 guinea pigs. Hypoventilation for 10 minutes was induced by reducing the respiratory rate and volume. During hypoventilation, the EP declined in most of the cases to an intermediate level of the positive range in a few minutes. At the midpoint of the 10-minute hypoventilation, angiotensin II (5 μg/kg or 1 mL/kg) was infused for 60 seconds to raise the systemic blood pressure. In this experimental manipulation of systemic blood pressure, the CoBF and EP generally rose transiently. We determined the sensitivity of the EP to a CoBF change (Δ) by calculating the ΔEP/ΔCoBF. More specifically, we analyzed the relationship between the ΔEP/ΔCoBF and the EPi (EP level just before angiotensin II infusion). The ΔEP was equal to the maximum EP level after angiotensin II infusion minus the EPi. The ΔCoBF was equal to the maximum CoBF value after angiotensin II infusion minus the CoBF value just before infusion. The ΔEP/ΔCoBF increased most in the range near 70% of the EPi. That is, the ΔEP/ΔCoBF was greater and the EPi was lower in the range above 70% of the EPi. To elucidate this linear correlation in the range above 70% of the EPi, we must consider several factors. In the supplementary experiments for blood gas analysis using 11 guinea pigs, most of the data of the EPi in the range above 70% were found to be obtained under conditions of a Pao2 of more than 12 mm Hg. As to the sensitivity increase of the EP to the ΔCoBF above mentioned, we propose that among several factors in the stria vascularis during hypoxemia, the activation of glycolysis in aerobic metabolism may be involved. As another possible factor, we postulate the increase in the reactive rate of the enzymatic activities that are linked with EP production and respond to the elevated cyclic adenosine monophosphate activity induced by the sympathicotonic state due to hypercapnia.