Electrically Stimulated Increases in Cochlear Blood Flow: I. Frequency and Intensity Effects

Abstract

Charge-balanced, sinusoidal current was passed differentially between the apex and round window of the guinea pig cochlea. Cochlear blood flow was measured using a laser Doppler flow monitor. Systemic blood pressure was monitored from a cannula within the common carotid artery. Electrical stimulation increased cochlear blood flow, while systemic blood pressure was unaffected. A cochlear blood flow response parameter, normalized for transient changes in systemic blood pressure, was defined. The magnitude of the response parameter was found to be frequency selective and was also found to be an increasing function of current intensity, with maximum responses obtained with 500 Hz sinusoids. This cochlear blood flow response was not observed in dead animals; was present in preparations paralyzed with gallamine hydrochloride; and was correlated with an increase in cochlear red blood cell velocity, as directly observed by intravital microscopy. These observations imply that electrical stimulation induces a local vasodilation within the temporal bone. The fact that decreased cochlear blood flow was never observed with current injection implies that ischemia is not a likely mechanism of electrically induced tissue damage within the inner ear. The mechanism of this cochlear blood flow response is addressed in a companion report.

Physiopathology of the cochlear microcirculation

“…Many of these functions are well-documented in previous reviews (Axelsson, 1988; Axelsson et al, 1987; Kimura, 1986; Lawrence, 1980; Miller et al, 1988; Miller et al, 1995a; Nakashima et al, 2003; Nuttall, 1988; Seidman et al, 1999b; Sillman et al, 1989; Wangemann, 2002b). This review has focused on regulation of blood flow in the microvasculature, as dysfunction of cochlear blood flow and disruption of the cochlear BLB are shown to result in hearing impairment in animal models.…”

“…One mechanism for hearing loss is disruption of the vascular barrier in the stria vascularis (Cadoni et al, 2002; Fattori et al, 2001; Naarendorp et al, 1998; Ottaviani et al, 1999), with subsequent loss of endocochlear potential (Lin et al, 1997; Ruckenstein et al, 1999). Study of the vascular system in the inner ear has a long and rich history, which has been well-documented in previous reviews (Axelsson, 1988; Axelsson et al, 1986; Kimura, 1986; Lawrence, 1980; Miller et al, 1988; Miller et al, 1995a; Nakashima et al, 2003; Nuttall, 1988; Seidman et al, 1999b; Sillman et al, 1989; Wangemann, 2002a). Animal models of cochlear microcirculation have provided a good understanding of cell-mediated CoBF homeostasis, and further studies will extend this basic understanding to clinical studies, which directly address vascular-related hearing disorders.…”

8-Iso-Prostaglandin F_2α, a Product of Noise Exposure, Reduces Inner Ear Blood Flow

“…Agents were assessed in terms of their effects on cochlear VC, defined as the ratio of CBF to BP, with decreased values of VC indicating constriction of the cochlear vasculature [for additional analysis of CBF/BP as a measure of VC, see ref. Sillman et al, 1989;Ren et al, 1993a].…”

“…However, in an organ with such a small volume as the cochlea, it is often difficult to avoid the influence of systemic cardiovascular effects, such as blood pressure and cardiac output, on measurements of blood flow. The CBF response normalized for transient BP changes, as defined by Sillman et al [1989], has been used in this and other studies of CBF to provide a measure of the local resistance/compliance to flow and the local effects of agents on the cochlear vasculature.…”

Hydrops-Induced Changes in Cochlear Blood Flow

“…13 -IS Bipolar stimulation was used between a platinum-iridium ball electrode (0.2 nun diameter) placed on the round window and another electrode placed in a small fenestra in the bone at the apex ofthe cochlea. The ES was produced by charge-balanced, sinusoidal, capacity-coupled constant current stimulation at 500 Hz with intensities from 10 to 300 tJA peak-to-peak, as previously 00scribed.…”