Clinical treatment of vascular inner ear diseases

Hultcrantz, Elisabeth

doi:10.1016/s0196-0709(88)80039-5

Cited by 34 publications

(14 citation statements)

References 39 publications

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“…Strong evidence shows that vascular disease or dysfunction is a major contributing factor to hearing loss (Hultcrantz, 1988;Nuttall, 1999;Schuknecht, 1982). The cochlear spiral modiolar artery (SMA) is of particular importance, because it supplies nearly all blood flow to the cochlea (Axelsson, 1988).…”

Section: Introductionmentioning

confidence: 99%

ACh-induced depolarization in inner ear artery is generated by activation of a TRP-like non-selective cation conductance and inactivation of a potassium conductance

et al. 2008

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Adequate cochlear blood supply by the spiral modiolar artery (SMA) is critical for normal hearing. ACh may play a role in neuroregulation of the SMA but several key issues including its membrane action mechanisms remain poorly understood. Besides its well-known endothelium-dependent hyperpolarizing action, ACh can induce a depolarization in vascular cells. Using intracellular and whole-cell recording techniques on cells in guinea pig in vitro SMA, we studied the ionic mechanism underlying the ACh-depolarization and found that: 1) ACh induced a DAMP-sensitive depolarization when intermediate conductance K Ca channels were blocked by charybdotoxin or nitrendipine. The ACh-depolarization was associated with a decrease in input resistance (R input ) in high membrane potential (V m ) (~−40 mV) cells but with no change or an increase in R input in low V m (~−75 mV) cells. ACh-depolarization was attenuated by background membrane depolarization from ~−70 mV in the majority of cells; 2) ACh-induced inward current in smooth muscle cells embedded in a SMA segment often showed a U-shaped I/V curve, the reversal potential of its two arms being near E K and 0 mV respectively; 3) ACh-depolarization was reduced by low Na + , zero K + or 20 mM K + bath solutions; 4) ACh-depolarization was inhibited by La 3+ in all cells tested, by 4-AP and flufenamic acid in low V m cells, but was not sensitive to Cd 2+ , Ni 2+ , nifedipine, niflumic acid, DIDS, IAA94, linopirdine or amiloride. We conclude that ACh-induced vascular depolarization was generated mainly by activation of a TRP-like non-selective cation channel and by inactivation of an inward rectifier K + channel.

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Section: Introductionmentioning

confidence: 99%

ACh-induced depolarization in inner ear artery is generated by activation of a TRP-like non-selective cation conductance and inactivation of a potassium conductance

et al. 2008

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“…Improving the circulation in the cochlea that may have been altered following certain types of insults or trauma can help in the recovery process (Hultcrantz, 1988); however, the results from another study showed that vasodilators do not alter tinnitus (Hulshof & Vermeij, 1987).…”

Section: Treatment Modelsmentioning

confidence: 99%

Tinnitus in Patients with Sensorineural Hearing Loss : Management, Quality of Life and Treatment Strategies

Zarenoe

2016

Linköping University Medical Dissertations

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“…[50][51][52][53][54][55][56] Vestibular effects may be due to vascular sludging or microinfarcts in either the vestibular periphery or CNS, but symptoms can occur without strokes evident by neuroimaging. Because these disorders can damage the vestibular end organ or CNS in a manner similar to more typical strokes, they could present as with AVS patients with vestibular neuritis or stroke.…”

Section: Cardiovascular Respiratory Rheological and Hematologic DImentioning

confidence: 99%

Medical and Nonstroke Neurologic Causes of Acute, Continuous Vestibular Symptoms

Edlow

Newman‐Toker

2015

Neurologic Clinics

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Clinical treatment of vascular inner ear diseases

Cited by 34 publications

References 39 publications

ACh-induced depolarization in inner ear artery is generated by activation of a TRP-like non-selective cation conductance and inactivation of a potassium conductance

ACh-induced depolarization in inner ear artery is generated by activation of a TRP-like non-selective cation conductance and inactivation of a potassium conductance

Tinnitus in Patients with Sensorineural Hearing Loss : Management, Quality of Life and Treatment Strategies

Medical and Nonstroke Neurologic Causes of Acute, Continuous Vestibular Symptoms

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