Biomedical subjects
Publications and source records attributed to H C Baggett.
We conducted a retrospective study of neonatal leukocytosis induced by prostaglandin E(1). Among 45 neonates with congenital heart disease, leukocyte counts increased during PGE(1) infusion. We conclude that PGE(1) infusion is a predictable cause of leukocytosis in newborns with congenital heart disease.
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Enlargement of the cochlear aqueduct is a controversial topic, with experienced investigators doubting its existence because of a lack of published cases. We describe the CT appearance of an enlarged cochlear aqueduct in a patient with advanced congenital inner ear anomalies and congenital hearing loss. The intent of this article is to present the CT appearance of a presumably enlarged cochlear aqueduct and to underscore the need to examine this structure in patients with congenital hearing loss.
OBJECTIVE: To understand the actions of glucocorticoids on the development and progression of endotoxin-mediated otitis media with effusion. METHODS AND DESIGN: The middle ears of 20 Sprague-Dawley rats were exposed to 35 microL of either 300-mOsm Krebs-Ringer solution (control; n = 5) or lipopolysaccharide, 1 mg/mL, dissolved in Krebs-Ringer solution (n = 15). Among the group that received lipopolysaccharide, 10 rats were randomly selected to receive dexamethasone (1 mg/kg intramuscularly), either 2 hours (n = 5) or 24 hours (n = 5) before the introduction of lipopolysaccharide. Middle ear fluid was sampled after 2, 4, and 6 hours of exposure. OUTCOME MEASURES: Middle ear fluid volume and albumin content were determined as measures of vascular extravasation. Histological sections of the middle ear mucosa were used to quantify the degree of leukocyte exudation. Data were analyzed by 1- or 2-way analysis of variance with the significance level set at P < .05. RESULTS: Lipopolysaccharide exposure caused a significant increase in the mean +/- SEM middle ear fluid volume from 29.9 +/- 0.99 to 45.8 +/- 1.4 microL between the 2- and 6-hour samplings. Lipopolysaccharide exposure caused a significant increase in the albumin content of middle ear fluid from 70.1 +/- 19.2 to 271.0 +/- 93.1 micrograms between the 2- and 6-hour samplings. Both increases were significant compared with controls. Lipopolysaccharide also caused a significant increase in leukocytes localized to the middle ear mucosa. Pretreatment of animals with dexamethasone for either 2 or 24 hours inhibited the lipopolysaccharide-induced changes. There were no differences between 2- and 24-hour pretreatment with dexamethasone. CONCLUSIONS: Dexamethasone inhibits the development of endotoxin-induced otitis media with effusion.
Rhinorrhea is a troublesome symptom of rhinitis seen commonly by otolaryngologists. The sources of nasal fluid production are glandular secretions and exudation from submucosal blood vessels. This study was designed to investigate the role of nitric oxide in neurogenically mediated vascular exudation in the nose. A rat model of the nasonasal reflex was developed in which one nasal cavity was challenged with histamine while albumin exudation was measured on the contralateral side. Histamine challenge was associated with a significant rise in albumin leakage, indicating an increase in vascular permeability. Perfusion with a nitric oxide synthase inhibitor (N-nitro-L-arginine methyl ester (L-NAME)) in the nasal cavity contralateral to nasal challenge was found to block albumin exudation on that side. This inhibition was overcome by the addition of L-arginine, the natural substrate of nitric oxide synthase, to the perfusate. Treatment of the ipsilateral nasal cavity with L-NAME did not significantly decrease the contralateral response. These findings indicate that NO is an important mediator of the effector arm of the nasonasal reflex that increases vascular permeability but is not involved in the sensory nerve afferent pathway. Further elucidation of the role of NO in nasal physiology may lead to novel pharmacotherapeutic approaches to the treatment of allergic and nonallergic rhinorrhea.
The mechanisms that regulate mucin release in chronic otitis media with effusion, a leading cause of hearing loss in children, remain largely unknown. We developed an animal model using Sprague-Dawley rats to determine the factors responsible for mucin production in chronic otitis media with effusion. N-nitro-L-arginine methyl ester (L-NAME), a competitive inhibitor of nitric oxide synthase, was used to investigate the role of nitric oxide in mucin secretion by the middle ear epithelium. All rats underwent eustachian tube obstruction. In the first set of rats, the middle ear was then injected transtympanically with 35 microl of either 300 mOsm Krebs-Ringer bicarbonate buffer (control group) or 1 mg/ml lipopolysaccharide in Krebs-Ringer (experimental group 1). In a second set of rats, the middle ear space was injected with lipopolysaccharide and then infused at a continuous rate for 7 days with either Krebs-Ringer (experimental group 2) or 1 mmol/L L-NAME in Krebs-Ringer (experimental group 3) through an osmotic infusion pump. After 7 days the volume of effusion and the quantity of mucin collected were significantly greater in lipopolysaccharide-exposed ears than in controls. In addition, antimucin immunostaining demonstrated mucous cell hyperplasia in response to lipopolysaccharide. The lipopolysaccharide-induced production of mucin and mucous cell hyperplasia was inhibited in ears treated with lipopolysaccharide and L-NAME. These results suggest that nitric oxide is a mediator in the pathway of mucin secretion in chronic otitis media with effusion.
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Acetylcholine (ACh), muscarine and methacholine all decreased the short-circuit current (Isc) measured across isolated canine lingual epithelia bathed in symmetrical solutions of Krebs-Henseleit buffer when added to the serosal, but not mucosal, solutions. Atropine inhibited the ACh-induced decrease in Isc whereas serosal solutions of 1 mM hexamethonium or 1 mM nicotine did not. Addition of a membrane-permeable analogue of cAMP also reduced Isc and, in the presence of this analogue, the decrease in Isc produced by ACh was markedly reduced. These data suggested the presence of muscarinic acetylcholine receptors in the serosal membranes of isolated canine lingual epithelia. The decrease in Isc induced by ACh may involve the inhibition of Ba(2+)-inhibitable K+ currents, as the addition of 100 microM BaCl2 to the serosal solution inhibited Isc and also completely inhibited the response produced by ACh. These findings suggest that responses of sensory fibres in lingual epithelia elicited by ACh may involve an interaction of ACh with epithelial cells rather than a direct interaction of ACh with receptors on sensory nerves.