Ear Blood Flow Research Articles

Evaluation of hearing levels in Crimean Congo Hemorrhagic Fever with audiological and electrophysiological tests

Objective : Crimean-Congo Hemorrhagic Fever (CCHF) is a tick-borne viral disease, and Sensorineural Hearing Loss (SNHL) arises from pathologies in the cochlea or retrocochlear pathways. Viral infections, including Crimean-Congo Hemorrhagic Fever , are considered possible etiological factors for Sensorineural Hearing Loss, as endothelial damage in Crimean-Congo Hemorrhagic Fever may impair inner ear blood flow. This study aimed to differentiate between cochlear and retrocochlear hearing loss in patients with Crimean-Congo Hemorrhagic Fever and assess the reliability of Auditory Steady-State Response (ASSR) testing by comparing its results with pure-tone audiometry. Material and method: The study included 30 Crimean-Congo Hemorrhagic Fever patients (Group CCHF) and 30 healthy controls (Group C). Hearing measurements were conducted using pure tone audiometry, otoacoustic emissions, tympanometry, and Auditory Steady-State Response before the patients’ discharge. Data were analyzed using SPSS 22.0. Results: The results showed no significant difference in audiometric thresholds between the right and left ears of Group CCHF at various frequencies. However, Auditory Steady-State Response results at 1000, 2000, and 4000 Hz in the right ear and at all tested frequencies in the left ear revealed significant differences between groups (p < 0.05). Conclusion: While this study did not establish a clear link between Crimean-Congo Hemorrhagic Fever and Sensorineural Hearing Loss, it suggests the need for further research with larger samples and testing during both the active and recovery phases of Crimean-Congo Hemorrhagic Fever. Key words: Crimean Congo hemorrhagic fever; audiometry; otoacoustic emissions, tympanometry; auditory steady state response; hearing loss.

Anti-inflammatory effect of Ganluyin, a Chinese classic prescription, in chronic pharyngitis rat model

BackgroundGanluyin (GLY) is a famous classical prescription with a long history of use as a treatment for inflammatory conditions such as chronic pharyngitis (CP) in many parts of China. However, it has not been developed as a modern pharmaceutic and its anti-inflammatory mechanisms remain unclear. The aim of this study was to assess the anti-inflammatory efficacy of GLY and potential mechanisms in a rat model of CP.MethodsThe chemical profile of GLY was analyzed by HPLC-UV. We used a mouse model of ear edema and a rat model of paw edema. Specifically, xylene was used to induce edema on the surface of one ear in mice, and carrageenan was injected subcutaneously into the right hind paws of rats to induce paw edema. The paw thickness, ear weight, and ear perfusion were measured and recorded. The CP model in rats was induced by irritating the throat with 5% ammonia and was used to evaluate the therapeutic efficacy of GLY. Levels of interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor (TNF-α), and prostaglandin E2 (PGE2) were measured by ELISA in serum, and protein expression of cyclooxygenase-2 (COX-2) and nuclear factor kappa-B p65 (NF-κB p65) in the throat were detected by immunohistochemistry and Western blot to evaluate the anti-inflammatory mechanism of GLY. Hematological assays were also conducted.ResultsThere were four flavonoids identified in GLY: naringin, neohesperidin, baicalin, and wogonoside. The oral administration of GLY showed a significant inhibitory effect on xylene-induced ear swelling and ear blood flow in mice and significantly ameliorated rat right hind paw edema at doses of 6.2 and 12.4 g/kg. Mechanistic studies found that the anti-inflammatory activity of GLY was related to the inhibition of pro-inflammatory cytokines such as IL-1β, IL-6, TNF-α, and PGE2 and that GLY reduced the expression of COX-2 and NF-κB p65 proteins in the throat, attenuated throat injury, and reduced inflammatory exudates. Hematological analysis showed that treatment with GLY prevented increases in white blood cell (WBC), neutrophil (NEUT), lymphocyte (LYMPH) and monocyte (MONO) levels.ConclusionsThese studies indicated that GLY has beneficial anti-inflammatory effects on CP and that it acts through reducing pro-inflammatory factors such as IL-1β, IL-6, TNF-α, and PGE2, as well as decreasing WBC, NEUT, LYMPH and MONO levels and decreasing the expression of COX-2 and NF-κB p65 proteins. These findings may lay the groundwork for further studies of GLY as a suitable candidate for the treatment of inflammatory diseases such as CP.

Research progress of vascular pulsatile tinnitus

Pulsatile tinnitus (PT) is relatively rare, which accounts for approximately 4% of patients with tinnitus. It originates from mostly vascular structures within the cranial cavity, head and neck region or thoracic cavity, and is transmitted to the cochlear by bony or vascular structures and the blood flow, stimulating patient's hearing. It can be the patient's subjective feelings, there can be objective performance.Vascular PT is more common than non-vascular PT. Vascular PT can be further classified by vessel of origin as arterial and venous ones, and the latter is more commonly seen clinically.It's rhythm is synchronous with patients' pulse, and its tinnitus frequency is less than 600 Hz. The cause of pulsatile tinnitus is complex and diverse, and 56 cases are reported in the literature. Objective tinnitus or somatosensory, associated with tympanic membrane myoclonus, ear blood flow changes adjacent to blood vessels and other in vivo factors. While subjective tinnitus lacks a clear source of the body. PT's pathogenesis has not been fully understood yet, so intensive study targeting PT is of great importance. This review focuses on the pathophysiological mechanisms,etiology,clinical manifestation, diagnosis and progress of treatment of vascular PT.

TRPA1 activation leads to neurogenic vasodilatation: involvement of reactive oxygen nitrogen species in addition to CGRP and NO.

Background and PurposeTransient receptor potential ankyrin‐1 (TRPA1) activation is known to mediate neurogenic vasodilatation. We investigated the mechanisms involved in TRPA1‐mediated peripheral vasodilatation in vivo using the TRPA1 agonist cinnamaldehyde.Experimental ApproachChanges in vascular ear blood flow were measured in anaesthetized mice using laser Doppler flowmetry.Key ResultsTopical application of cinnamaldehyde to the mouse ear caused a significant increase in blood flow in the skin of anaesthetized wild‐type (WT) mice but not in TRPA1 knockout (KO) mice. Cinnamaldehyde‐induced vasodilatation was inhibited by the pharmacological blockade of the potent microvascular vasodilator neuropeptide CGRP and neuronal NOS‐derived NO pathways. Cinnamaldehyde‐mediated vasodilatation was significantly reduced by treatment with reactive oxygen nitrogen species (RONS) scavenger such as catalase and the SOD mimetic TEMPOL, supporting a role of RONS in the downstream vasodilator TRPA1‐mediated response. Co‐treatment with a non‐selective NOS inhibitor L‐NAME and antioxidant apocynin further inhibited the TRPA1‐mediated vasodilatation. Cinnamaldehyde treatment induced the generation of peroxynitrite that was blocked by the peroxynitrite scavenger FeTPPS and shown to be dependent on TRPA1, as reflected by an increase in protein tyrosine nitration in the skin of WT, but not in TRPA1 KO mice.Conclusion and ImplicationsThis study provides in vivo evidence that TRPA1‐induced vasodilatation mediated by cinnamaldehyde requires neuronal NOS‐derived NO, in addition to the traditional neuropeptide component. A novel role of peroxynitrite is revealed, which is generated downstream of TRPA1 activation by cinnamaldehyde. This mechanistic pathway underlying TRPA1‐mediated vasodilatation may be important in understanding the role of TRPA1 in pathophysiological situations.

Long-term administration of vasopressin can cause Ménière’s disease in mice

Conclusion: A new murine model of Ménière’s disease has been developed, based on long-term administration of vasopressin. Induction of vestibular dysfunction in the present animal model can cause additional stress, by reducing inner ear blood flow. Latanoprost, a selective agonist for the FP prostanoid receptor, may become a new remedy for Ménière’s disease. Objective: The purpose of this study was to develop a more suitable animal model, with a closer resemblance to the pathophysiological process in Ménière’s disease. Methods: Adult CBA/J or ICR mice were treated by subcutaneous injection of vasopressin for 5 days up to 8 weeks. Morphological analyses were performed of the cochlea, vestibular end organs and endolymphatic sac. The effect of latanoprost on the development of endolymphatic hydrops was also examined. Results: All experimental animals showed mild to moderate endolymphatic hydrops, increasing in severity as the vasopressin treatment was prolonged. Animals treated with vasopressin for 8 weeks showed severe endolymphatic hydrops with partial loss of outer hair cells and spiral ganglion cells. These animals also had a reversible vestibular dysfunction following intratympanic injection of epinephrine. Latanoprost inhibited the development of endolymphatic hydrops caused by vasopressin.

Detection Rates of the Labyrinthine Artery in Patients with ISSHL by 7‐T MRI

Objectives: Disturbance of inner ear blood flow has been considered to be one of the possible causes of idiopathic sudden sensorineural hearing loss (ISSNHL); however, imaging evaluation of the labyrinthine artery has not been reported to date. The aim of this study was to compare the detection rates of labyrinthine artery in subjects with and without ISSNHL using 7-T magnetic resonance imaging (MRI). Methods: In 10 patients (5 males and 5 females) with ISSHL (ISSNHL group) and 14 volunteers (8 males and 5 females) with normal hearing (Control group), 7-T MRI (Discovery MR950, GE Medical Systems) was performed with 3D time-of-flight spoiled gradient echo (3D TOF SPGR) sequence for the comparison of detection rates of the labyrinthine artery. Results: MRI scan was performed from 11 days to 49 days after onset. Among 10 patients with ISSNHL, 3 showed complete recovery and the rest showed partial recovery. The labyrinthine artery was depicted in 20 of 20 ears (100%) in the ISSHL group and 27 of 28 (96.4%) ears in the Control group. There was no significant difference in detection rates. Conclusions: The present study is the first to report depiction of the labyrinthine artery by 7-T MRI. Our preliminary results indicate occlusion of the labyrinthine artery would be rare in the pathogenesis of ISSNHL and also demonstrate the labyrinthine artery could be detected by ultra-high field MRI.

The role of transient receptor potential ankyrin 1 (TRPA1) receptor activation in hydrogen-sulphide-induced CGRP-release and vasodilation

Activation of transient receptor potential ankyrin 1 (TRPA1) and vanilloid 1 (TRPV1) channels on capsaicin-sensitive sensory neurons causes release of inflammatory neuropeptides, including calcitonin gene-related peptide (CGRP). We investigated whether the hydrogen sulphide (H2S)-evoked CGRP release from sensory neurons of isolated rat tracheae and H2S-induced increases in the microcirculation of the mouse ear were mediated by TRPA1 receptor activation.Allylisothiocyanate (AITC) or the H2S donor sodium hydrogen sulphide (NaHS) were used as stimuli and CGRP release of the rat tracheae was measured by radioimmunoassay. AITC or NaHS were applied to the ears of Balb/c, C57BL/6, TRPA1 and TRPV1 receptor gene knockout mice and blood flow was detected by laser Doppler imaging.Both AITC and NaHS increased CGRP release from isolated rat tracheae, and both responses were inhibited by the TRPA1 antagonist, HC-030031, but was not affected by the TRPV1 receptor blocker, BCTC. Application of AITC or NaHS increased the cutaneous blood flow in the mouse ears. Similarly to the effect of AITC, the vasodilatory response to NaHS was reduced by HC-030031 or in TRPA1 deleted mice. In contrast, genetic deletion of TRPV1 did not affect the increase in the ear blood flow evoked by AITC or NaHS.We conclude that H2S activates TRPA1 receptors causing CGRP release from sensory nerves of rat tracheae, as well as inducing cutaneous vasodilatation in the mouse ear. TRPV1 receptors were not involved in these processes. Our results highlight that TRPA1 receptor activation should be considered as a potential mechanism of vasoactive effects of H2S.

Regional blood flow changes underlying the hypotensive action of 5‐HT:Studies using Doppler and Microsphere technologies

Serotonin (5‐hydroxytryptamine, 5‐HT) causes a sustained decrease in mean arterial pressure (MAP) and elicits a fall in total peripheral resistance (TPR) in normal conscious rats. We hypothesized that the decrease in TPR induced by 5‐HT is caused by relaxation (direct or indirect) of arteries serving one or more major regional vascular beds. Alzet pumps containing vehicle or 5‐HT (25 ug/kg/min) were implanted in male Sprague‐Dawley rats and 24 hours later the rats were anesthetized and underwent: 1) ear and tail blood flow measurements using Doppler to determine cutaneous vascular contribution; or 2) left ventricular injection of fluorescent microspheres (300,000 yellow green microspheres) to determine global organ blood flow. Infusion of 5‐HT increased ear (69.1±20.5% time‐controlled vehicle) and tail (23.5±2.5%) blood flow (Doppler) while elevating small intestinal (50% increase) flow (microsphere) over vehicle‐infused rats. In the microsphere experiments there was no alteration in blood flow by 5‐HT infusion (vs vehicle) in spleen, liver, lung, right or left kidney, leg muscle, abdominal skin, visceral fat or brain, and right and left kidney flows were statistically similar (R; 3.78±0.69 vs L: 4.00±0.74 ml/min/g tissue, p> 0.05). These findings define the cutaneous and splanchnic vasculature as regions of interest to study the mechanism of 5‐HT ability to lower MAP and TPR. NIH HL081115.

In Vivo Antipyretic, Analgesic, and Anti-inflammatory Activities of the Brown Alga Ecklonia cava Extracts in Mice

Dichloromethane, ethanol, and boiling water extracts of the brown alga Ecklonia cava were examined in vivo for their antipyretic, analgesic, and anti-inflammatory activities in mice. These activities were evaluated by yeast-induced pyrexia, tail-flick test, and phorbol myristate acetate-induced inflammation (edema, erythema, and blood flow). Ethanol extract of E. cava (0.4 mg/ear) inhibited the inflammatory symptoms of mouse ear edema, erythema, and blood flow by 82.6%, 69.0%, and 65.4%, respectively. This extract also demonstrated potent analgesic activity. No acute toxicity was observed after p.o. administration of each extract (5 g/kg bw). These in vivo data are in agreement with the claims of the health care industry and indigenous medicine that E. cava is an effective remedy for inflammation-related symptoms.

Fibro-Vascular Coupling in the Control of Cochlear Blood Flow

BackgroundTransduction of sound in the cochlea is metabolically demanding. The lateral wall and hair cells are critically vulnerable to hypoxia, especially at high sound levels, and tight control over cochlear blood flow (CBF) is a physiological necessity. Yet despite the importance of CBF for hearing, consensus on what mechanisms are involved has not been obtained.Methodology/Principal FindingsWe report on a local control mechanism for regulating inner ear blood flow involving fibrocyte signaling. Fibrocytes in the super-strial region are spatially distributed near pre-capillaries of the spiral ligament of the albino guinea pig cochlear lateral wall, as demonstrably shown in transmission electron microscope and confocal images. Immunohistochemical techniques reveal the inter-connected fibrocytes to be positive for Na+/K+ ATPase β1 and S100. The connected fibrocytes display more Ca2+ signaling than other cells in the cochlear lateral wall as indicated by fluorescence of a Ca2+ sensor, fluo-4. Elevation of Ca2+ in fibrocytes, induced by photolytic uncaging of the divalent ion chelator o-nitrophenyl EGTA, results in propagation of a Ca2+ signal to neighboring vascular cells and vasodilation in capillaries. Of more physiological significance, fibrocyte to vascular cell coupled signaling was found to mediate the sound stimulated increase in cochlear blood flow (CBF). Cyclooxygenase-1 (COX-1) was required for capillary dilation.Conclusions/SignificanceThe findings provide the first evidence that signaling between fibrocytes and vascular cells modulates CBF and is a key mechanism for meeting the cellular metabolic demand of increased sound activity.

Anesthesiology: From Patient Safety to Population Outcomes

Anesthesiology: From Patient Safety to Population Outcomes

Peripheral photoplethysmography variability analysis of sepsis patients

Sepsis is associated with impairment in autonomic regulatory function. This work investigates the application of heart rate and photoplethysmogram (PPG) waveform variability analysis in differentiating two categories of sepsis, namely systemic inflammatory response syndrome (SIRS) and severe sepsis. Electrocardiogram-derived heart period (RRi) and PPG waveforms, measured from fingertips (Fin-PPG) and earlobes (Ear-PPG), of Emergency Department sepsis patients (n=28) with different disease severity, were analysed by spectral technique, and were compared to control subjects (n=10) in supine and 80° head-up tilted positions. Analysis of covariance (ANCOVA) was applied to adjust for the confounding factor of age. Low-frequency (LF, 0.04-0.15Hz), mid-frequency (MF, 0.09-0.15Hz) and high-frequency (HF, 0.15-0.60Hz) powers were computed. The normalised MF power in Ear-PPG (MFnu(Ear)) was significantly reduced in severe sepsis patients with hyperlactataemia (lactate>2mmol/l), compared to SIRS patients (P<0.05). Moreover, in a group of normal controls, MFnu(Ear) was not altered by head-up tilting (P>0.05), suggesting that there may be a link between 0.1Hz ear blood flow oscillation and tissue metabolic changes in sepsis, in addition to autonomic factors. The study highlighted the value of PPG spectral analysis in the non-invasive assessment of peripheral vascular regulation in sepsis patients, with potential implications in monitoring the progression of sepsis.

Effect of inner ear blood flow changes in Ménière's model mice

Conclusions. The endolymphatic sac (ES) is important for inner ear fluid homeostasis. A dysfunctional ES can cause vertigo attacks following additional stress such as a sudden change in endolymphatic volume and/or pressure, or restricted inner ear blood flow. Objective. The purpose of this study was to elucidate the mechanism of vertigo attacks in Ménière's disease. Materials and methods. Adult CBA/J mice were given an intratympanic injection of lipopolysaccharide and an intraperitoneal injection of aldosterone. These ‘model’ animals had epinephrine or sodium nitroprusside (SNP) instilled into the middle ear cavity. Cochleae, vestibules, and endolymphatic sacs were studied morphologically by light microscopy. Results. The injection of epinephrine into the model animals reduced the endolymphatic hydrops in the cochlea, but also produced mild hydrops in the vestibule, which was never observed in untreated (control) animals. The ES did not react to epinephrine in the normal way. Injection of SNP did not cause any changes.

Effect of inner ear blood flow changes on the endolymphatic sac

Conclusions. That the endolymphatic sac (ES) reacts to changes in inner ear blood flow may be important for homeostasis of the inner ear fluid volume and pressure. Objectives. To elucidate the effect of changes in inner ear blood flow on the ES and to learn more about the volume and pressure regulatory function of the ES. Materials and methods. Epinephrine or sodium nitroprusside (SNP) was injected into the middle ear cavity of adult CBA/J mice. The ES were analyzed morphologically by light microscopy. Results. Epinephrine reduced the luminal size of the ES leading to an accumulation of intraluminal homogeneous substance. Injection of SNP increased the size of the ES lumen, accompanied by a collapse of the lateral intercellular space (LIS) and dense perisaccular tissue. These changes were almost reversed 4 h after injection.

A new animal model for Ménière's disease

Conclusion. A new murine model for the study of Ménière's disease has been developed by treatment with both lipopolysaccharide (LPS) and aldosterone. Induction of vestibular dysfunction in the hydropic animal model may entail additional stress such as reduced inner ear blood flow, and sudden acute changes in endolymph volume and/or pressure. Objective. The purpose of this study was to develop a more suitable animal model, showing closer resemblance to the pathophysiological process in Ménière's disease. Materials and methods. Adult CBA/J mice were treated by intratympanic injection of LPS, intraperitoneal injection of aldosterone, or injection of both LPS and aldosterone. Morphological analyses were performed in the cochlea and endolymphatic sac. Results. All experimental animals showed mild to moderate endolymphatic hydrops. Those treated with both LPS and aldosterone showed reversible vestibular dysfunction after the intratympanic injection of epinephrine.

Vascular endothelial growth factor receptor tyrosine kinase inhibitor PTK787/ZK 222584 inhibits both the induction and elicitation phases of contact hypersensitivity

Vascular endothelial growth factor (VEGF) and its endothelial cell receptors (VEGFR) have been shown to be involved in the pathogenesis of the contact hypersensitivity (CHS) reaction. Previous studies have demonstrated that anti-VEGFR-2 antibody significantly suppresses the elicitation phase of CHS but does not affect the induction phase. PTK787/ZK 222584 (1-[4-chloroanilino]-4-[4-pyridylmethyl] phthalazine succinate; PTK/ZK) is a potent inhibitor of VEGFR tyrosine kinases. To test the effect of PTK/ZK on the induction and elicitation phases of CHS separately, we used an established method of CHS assay-sensitization and challenge in BALB/c mice. Either 50 mg/kg/day PTK/ZK or vehicle serving as a control was administered orally in the induction or elicitation phases separately. In the afferent phase, flow cytometry of skin-draining lymph node cells revealed that the migration of Langerhans cells was suppressed in the mice treated with PTK/ZK at sensitization. The degrees of ear swelling at 24 and 48 h were significantly diminished in mice treated with PTK/ZK at sensitization (P < 0.05). In the efferent phase, the degrees of ear swelling at 24 h (P < 0.01) and 48 h (P < 0.05), ear blood flow at 24 and 48 h (P < 0.01), and production of VEGF in the epidermis at 24 h (P < 0.05) were significantly suppressed in mice treated with PTK/ZK at elicitation. These findings and previous demonstrations suggest that both VEGF R-1 and VEGF R-2 are needed during the induction phase, and that VEGFR-2 has a pivotal role in the elicitation phase of the CHS reaction.

Sphingosine-1-phosphate modulates spiral modiolar artery tone: A potential role in vascular-based inner ear pathologies?

The mechanisms regulating spiral modiolar artery (SMA) tone are not known, yet their characterization is pivotal for understanding inner ear blood flow regulation. Sphingosine-1-phosphate (S1P), known to stimulate vasoconstriction in several vascular beds, is a candidate regulator of SMA tone with potential pathophysiological relevance. Gerbil SMAs were isolated, cannulated and pressurized (30 mm Hg transmural) for experimentation under near-in vivo conditions. For functional experiments, vascular diameter and intracellular Ca2+ were simultaneously measured. Standard RT-PCR and immunohistochemical techniques were also employed. mRNA transcripts encoding sphingosine kinase, S1P phosphohydrolase and three S1P receptors (S1P(1-3)) were detected in the SMA. S1P induced dose-dependent vasoconstriction of the SMA (EC50 = 115 nmol/L), and enhanced the apparent Ca2+-sensitivity of the contractile apparatus. Noradrenaline did not elicit vasoconstriction. The Rho kinase inhibitor Y27632 (1 micromol/L) reversed S1P-induced vasoconstriction and the S1P-mediated enhancement of Ca2+-sensitivity. RhoA was observed to translocate to the plasma membrane in response to stimulation with 30 micromol/L S1P. We conclude that all key signalling pathway constituents are present at the mRNA level for S1P to act as an endogenous regulator of SMA tone. S1P stimulates potent, RhoA/Rho kinase-dependent SMA vasoconstriction and Ca2+ sensitization. The high sensitivity to S1P suggests that SMA vasoconstriction is likely to occur under pathological conditions that increase intramural S1P concentrations (i.e., inflammation). From a clinical perspective, the present study identifies new potential therapeutic targets for the treatment of vascular-based, "stroke-like" inner ear pathologies: the enzymes responsible for S1P bioavailability and the S1P receptors.

Inhibition of medullary raphé/parapyramidal neurons prevents cutaneous vasoconstriction elicited by alerting stimuli and by cold exposure in conscious rabbits

In conscious rabbits, microinjection of muscimol into the medullary raphé/parapyramidal region decreased fluctuation (coefficient variation) of resting ear blood flow (from 62 ± 8 to 25 ± 4%, P < 0.01, n = 8). The muscimol injection also prevented falls in ear blood flow that normally occur in response to alerting stimuli and to cold exposure. Thus, raphé/parapyramidal neurons constitute an important brainstem center for mediating cutaneous vasoconstriction initiated by alerting stimuli and by cold exposure.

耳症状初発の限局型ウェゲナー肉芽腫症例

Wegener's granulomatosis is a distinct clinicopathologic entity characterized by granulomatosis vasculitis of the respiratory tract accompanied by glomerulonephritis. We report a case of a 56-year-old female with localized Wegener's granulomatosis presenting as otitis media. The patient complained of right ear pain. Antibiotic treatment was ineffectual and right sensorineural deafness and right facial palsy became apparent. Perinuclear anti-neutrophil cytoplasmic antibody (p-ANCA) was positive, but cytoplasmic anti-neutrophil cytoplasmic antibody (c-ANCA) was negative. The histopathologic appearance of granulation tissue in her tympanic and nasal cavity indicated inflammatory granulation involving multinucleated giant cells and epithelioid cells. The disease did not involve her lung or kidney, so it was diagnosed as localized Wegener's granulomatosis. Glucocorticoid treatment with cyclophosphamide improved the right hearing loss and facial palsy. CRP and p-ANCA became negative.Early diagnosis of Wegener's granulomatosis is difficult because of atypical manifestations of the disease, but ANCA measurements may be effective in the diagnosis. The present case suggests that inner ear blood flow impairment due to p-ANCA-associated small vessel vasculitis induces hearing loss.

Contribution of stapedial artery to blood flow in the cochlea and its surrounding bone

This study was performed to elucidate the contribution of the stapedial artery (SA) – which has been considered to be independent of the vertebrobasilar system – to blood flow in the ear by observing ear blood flow in Sprague–Dawley rats. A laser-Doppler (LD) probe was positioned on the bony wall of the cochlear basal turn after removal of the middle ear mucosa. The LD output was measured while either or both the SA and the anterior inferior cerebellar artery (AICA) were occluded. The LD output decreased to 70.6±2.5% (mean±S.D.) of the baseline value following SA occlusion, and to 58.0±7.8% following AICA occlusion in 12 animals. The rebound phenomenon of blood flow, which is a type of autoregulation, was only observed after releasing AICA occlusion. Simultaneous occlusion of the SA and AICA decreased the LD output to 27.0±5.5% of the baseline value. The role of the contribution of the SA and AICA to the LD output is discussed.