Noise exposure levels in stock car auto racing.

Noise-induced hearing loss associated with the workplace has been well described. Far less is known, however, about the risks to hearing from recreational sources of noise. We investigated the popular sport of stock car racing as a potentially significant source of noise exposure, and we conducted a sound-level survey at a National Association for Stock Car Auto Racing (NASCAR) event.

Nitric oxide in glutamate-induced compound action potential threshold shifts.

Objective: Investigate the role of NO as a neurotransmitter in the gerbil cochlea and the effects of (7-NI) on compound action potential (CAP) threshold elevations induced by l-glutamate, an agonist at the NMDA glutamate receptor subtype, to further elucidate the role of NO in cochlear excitotoxicity.

Method: In anesthetized gerbils, CAP thresholds were recorded before and after cochlear perfusions with a control solution of artificial perilymph (APS) and a test solution of L-glutamate (GA) in three experimental groups.

Results: The control group showed no CAP threshold elevations (p<0.

Immune modulatory oligonucleotides in the prevention and treatment of OVA-induced eustachian tube dysfunction in rats.

Background: Otitis media with effusion (OME) is often associated with allergies. Immune modulatory oligonucleotides (IMO) mediate allergic inflammation and may therefore be efficacious in the treatment of airway inflammation.

Objective: To evaluate the role of an IMO via transtympanic mucosal application in prevention and treatment of ovalbumin-induced OME.

Immune modulatory oligonucleotides in prevention of nasal allergen-induced Eustachian tube dysfunction in rats.

Objectives: Develop a model of nasal allergen-induced Eustachian tube dysfunction (ETD) in a rat and investigate the role of immune modulatory oligonucleotides (IMOs) in the prevention of nasal allergen-induced ETD.

Study Design And Setting: Prospective, randomized study. Brown Norway rats were sensitized to ova albumin (OVA) and randomized to receive pretreatment with IMOs or phosphate-buffered saline.

The role of immunomodulatory oligonucleotides in prevention of OVA-induced Eustachian tube dysfunction.

Objective: To evaluate the potential role of immunomodulatory oligonucleotides (IMO) in the prevention of OVA-induced Eustachian tube dysfunction (ETD) in a rat model.

Methods: Brown-Norway rats were sensitized to ovalbumin (OVA) and randomized to receive pre-treatment with IMO or phosphate buffered saline (PBS). After systemic sensitization, subjects received a transtympanic OVA challenge followed by evaluation of the Eustachian tube's dynamic function.

The role of soluble interleukin-4 receptor and interleukin-5 antibody in preventing late-phase allergy-induced eustachian tube dysfunction.

Objectives: We investigated the role of soluble interleukin (IL)-4 receptors (sIL-4R) and IL-5 antibodies (IL-5Ab) in preventing allergic eustachian tube dysfunction (ETD) and middle ear effusion (MEE).

Study Design: Brown-Norway rats were sensitized to ovalbumin (OVA) and challenged transtympanically. Two groups of rats received either IL-4R or IL-5Ab transtympanically 1 hour before challenge.

Gastroesophageal reflux and eustachian tube dysfunction in an animal model.

Objective: To explore the possible relationship between gastroesophageal reflux and eustachian tube dysfunction in an animal model.

Study Design: Randomized trial.

Methods: Twenty Sprague-Dawley rats were randomly assigned into two groups, the control (phosphate-buffered saline, n = 10) and experimental (hydrochloric acid [HCl]/pepsin, n = 10) groups.

Effect of intranasal histamine challenge on Eustachian tube function.

Objective: To show a relationship between intranasal histamine challenge, the development of middle ear effusion and Eustachian tube (ET) dysfunction in a rat model.

Methods: Non-allergic Sprague-Dawley rats weighing between 450-600 g were randomly assigned to receive an intranasal infusion of 16 microl of 10% histamine or normal saline. ET function was assessed by using the forced-response test to measure passive and active opening and closing pressures at time intervals of 6, 10, 14, 18, 22, and 26 min and 24 h post-infusion.

Eustachian tube dysfunction after tobacco smoke exposure.

Objective: To examine the effects of tobacco smoke exposure on eustachian tube (ET) function.

Study Design: ET pressures of Sprague Dawley Rats (n = 16) were measured after 1, 7, and 15 exposures and in control animals. Passive opening pressure, passive closing pressure, active clearance of positive pressure, and active clearance of negative pressure were measured.

Transient inflammation and dysfunction of the eustachian tube secondary to multiple exposures of simulated gastroesophageal refluxant.

Gastroesophageal reflux is a common problem in the newborn and preschool periods. Recent research suggests that it may be related to eustachian tube dysfunction and otitis media with effusion. The purpose of this experiment was to investigate the relationship between simulated gastroesophageal reflux and eustachian tube dysfunction.

Late-phase allergy and eustachian tube dysfunction.

Objective: This study investigated the role of late-phase allergy in the development of otitis media with effusion.

Methods: Brown Norway rats were sensitized to ovalbumin and later challenged transtympanically. Eustachian tube ventilatory function was assessed 2, 4, 8, 24, 28, and 32 hours postchallenge by measuring passive opening and closing pressures, active clearance of positive and negative middle ear pressure, and mucociliary clearance.

Function of the eustachian tube after weekly exposure to pepsin/hydrochloric acid.

Objective: To determine the effects of repeated pepsin/hydrochloric acid (HCl) exposure on the eustachian tube (ET).

Study Design And Setting: ET function was studied in 22 rats. Group I (control) rats received transtympanic phosphate buffered saline solution; groups II (0.

Action of histamine on eustachian tube function.

Introduction: The role of allergy in eustachian tube dysfunction is controversial. In this study, allergy was simulated by exposure to histamine, and eustachian tube function testing was performed in an experimental rat model.

Methods: Ventilatory function was assessed by measuring passive opening and closing pressures of the eustachian tube after challenge with either transtympanic or intranasal histamine.

An animal model for the study of genetic predisposition in the pathogenesis of middle ear inflammation.

Objectives: Chronic otitis media with effusion (COME) is the most prevalent inflammatory disease in children and is associated with numerous adverse long-term sequelae. Many factors have been associated with an increased risk of developing COME, one of which may be a genetic predisposition to the disease. To study the role that genetics play in the pathogenesis of COME, we used an animal model to compare the middle ear inflammatory responses in two different strains of rats (Lewis and Fisher).

Nitric oxide is a mediator of the late-phase response in an animal model of nasal allergy.

The presence of nitric oxide (NO) in the nose is well documented; however, the role of this molecule in nasal physiology is still poorly understood. Our laboratory has previously demonstrated that NO is a mediator of the immediate secretory response to an intranasal histamine challenge in a rat model of nasal allergy. Histamine challenge, however, does not elicit a late-phase response (LPR).

Cytotoxic changes in hair cells secondary to pneumococcal middle-ear infection.

To determine whether the bacterial toxins associated with otitis media could induce morphologic changes in the organ of Corti, we inoculated the middle-ear cavities of healthy guinea pigs with either Streptococcus pneumoniae or sterile saline and then examined the organ of Corti histologically at 1, 2, and 3 weeks postinoculation. We found that the outer hair cells (OHCs) in the infected ears underwent several changes that were dependent on both the length of time following inoculation and also the position of the OHCs in the cochlea. At 2 weeks postinoculation, 7.

Allergy increases susceptibility to otitis media with effusion in a rat model. Second place--Resident Clinical Science Award 1998.

To investigate the possible relationship between allergy and otitis media with effusion (OME), we investigated the hypothesis that allergen presentation to the middle ear causes functional disruption of the eustachian tube predisposing to the development of OME. Thirteen of 19 Brown-Norway rats were sensitized to ovalbumin, and the remaining 6 served as nonallergic controls. To mimic subclinical exposure to allergen, we transtympanically injected ovalbumin at a dose (0.

Systemic reactivation of otitis media with effusion in a rat model.

Objective: This study addresses the interaction of bacterial antigens, specifically peptidoglycan-polysaccharide (PG-PS) and lipopolysaccharide (LPS), in the induction and reactivation of mucoid middle ear effusions.

Methods: Twenty-seven rats underwent eustachian tube obstruction before inoculation of the middle ear bulla with PG-PS. Three weeks later, after resolution of all middle ear effusions, 6 rats were randomly selected and euthanized as the first control group (control I).

Mucin production in the middle ear in response to lipopolysaccharides.

Objective: This study examined the response of middle ear tissue to establish the lowest dose of lipopolysaccharide to induce mucin production in a rat otitis media model.

Methods: Twenty-six male Sprague-Dawley rats' eustachian tubes were obstructed before transtympanic inoculation of the bulla tympanica with 35 microL of Krebs Ringer or 1, 10, 100, or 1000 microgram/mL lipopolysaccharide. After 7 days the effusion and a lavage were collected for mucin ELISA measurement, and tissue was collected for histologic evaluation.

Non-insulin-dependent diabetic microangiopathy in the inner ear.

Unlabelled: Hearing loss has long been associated with diabetes mellitus. Microangiopathy, associated with thickening of the basement membranes of small vessels, has been implicated as a major source of multiple system organ disease.

Objective: This study was designed to evaluate changes in basement membrane thickness in the inner ear of laboratory animals suffering from non-insulin-dependent diabetes mellitus (NIDDM) with, and without, exposure to moderate intensity noise exposure in an attempt to extrapolate the same disease process in humans.

Role of nitric oxide in kainic acid-induced elevation of cochlear compound action potential thresholds.

Nitric oxide (NO) has specifically been found to mediate the effects of excitatory amino acids in the central nervous system (CNS). Excitatory amino acids are the primary neurotransmitters at the cochlear hair cell afferent nerve synapse. Recent studies in our laboratory demonstrate that NO synthase is an active enzyme in the spiral ganglion cells of the cochlea.

Sodium nitroprusside/nitric oxide causes apoptosis in spiral ganglion cells.

Objective: In the cochlea, excitatory amino acid receptor overstimulation induces toxicity in spiral ganglion neurons by an unknown mechanism. In the central nervous system, excitatory amino acid-induced toxicity is mediated by nitric oxide, which induces apoptosis in neurons. This study tested the hypothesis that cochlear nitric oxide-mediated toxicity is the result of induction of apoptosis in spiral ganglion neurons.

Inhibition of nitric oxide synthase causes elevation of hearing thresholds.

Objective: Nitric oxide mediates the effects of excitatory amino acids in the central nervous system. The excitatory amino acids are thought to be the neurotransmitters at the cochlear hair cell-afferent nerve synapse. Nitric oxide synthase is present in spiral ganglion cells.

Interaction between hypertension and diabetes mellitus in the pathogenesis of sensorineural hearing loss.

The purpose of this study is to support the hypothesis that diabetic end-organ damage of the cochlea is augmented in the setting of hypertension. A historical perspective reviewing the effects of diabetes and hypertension as causative factors in the development of sensorineural hearing loss, as well as the basic epidemiology and pathophysiology of the renal and vascular effects of diabetes and hypertension, is presented. The results of audiologic findings in insulin-dependent diabetic patients, both normotensive and hypertensive, were analyzed and correlated with the results of animal studies to support the hypothesis that sensorineural hearing loss in patients and cochlear hair cell loss in animal studies result from the effects of hypertension in conjunction with insulin-dependent diabetes mellitus.

Role of tumor necrosis factor and interleukin-1 in endotoxin-induced middle ear effusions.

In a rat model, we investigated the role of tumor necrosis factor (TNF) and interleukin-1 (IL-1) in endotoxin-induced middle ear effusions (MEEs). After the eustachian tube was obstructed, the middle ear was transtympanically injected with 35 microL of either 1) 1 mg/ mL lipopolysaccharide (LPS); 2) LPS and 100 micrograms TNF binding protein (TNFbp); 3) LPS and 1 microgram IL-1 receptor antagonist (IL-1ra); or 4) LPS, TNFbp, and IL-1ra. Every 2 hours, the fluid within the middle ear was collected, and the quantity of albumin in the fluid, an index of vascular leakage, was determined by enzyme-linked immunosorbent assay.