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PubMed2002

Influence of intranasal medication on the structure of the nasal mucosa.

OBJECTIVE: To study the influence of intranasal medication on the structure, pathology and reversibility of the nasal mucosa to provide a basis for the feasibility of intranasal route of drug administration. METHODS: Nasal drops of gentamicin were placed in the nasal cavity of rabbits for 3, 5, 7, 14 and 28 days. After that, the drops were stopped and drugs protecting the nasomucosa were used for one and three weeks. After being sacrificed over time, the nasomucosa of the rabbit was observed under optical and electron microscopes. RESULTS: Damage to the nasal mucosa appeared to different extents with prolonged use of nasal drops. Within 3 - 7 days of applying the drug, damages to the nasal mucosa gradually appeared, and after two and four weeks, were most serious. After stopping the drug, the nasal mucosa was gradually restored. CONCLUSION: Damages of drugs to the nasal mucosa could be restored. The intranasal route of drug administration would be feasible and clinically applicable.

Administration, Intranasal↗

PubMed1977

Effect of inflammatory mediators on nasal mucosa.

A technique used for study of permeability and vasodilation in the middle ear has been adapted to study the response of nasal mucosa to common inflammatory mediators involved in the natural production of allergic or infectious rhinitis. All of the mediators tested (histamine, prostaglandin E1, bradykinin, the C3a fraction of complement, Escherichia coli endotoxin, and lysozyme) were found to increase nasal permeability to the isotopic tracer 99mTc as the pertechnetate ion. Histamine increased the permeability of nasal mucosa to technetium-labeled plasma protein. Results indicate that the nasal mucosa is approximately ten times as permeable to the pertechnetate ion as middle ear mucosa. Nasal mucosa was also noted to be permeable to protein, even in the absence of inflammatory mediator, in contrast to prior studies of middle ear mucosa that showed little or no permeability in the absence of inflammatory mediator. In almost all cases, a corresponding change in vasodilation accompanied permeability changes.

Animals↗

PubMed1983

Metabolism of tobacco-specific nitrosamines by cultured rat nasal mucosa.

The metabolism of two nasal carcinogens, N'-nitrosonornicotine (NNN) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), was investigated using cultured nasal septa of F344 rats. The explants were cultured with 14C-labeled N-nitrosamines, and unbound metabolites present in the medium were quantitated by high-performance liquid chromatography. The results indicated that the mucosa of the nasal septum had a marked capacity to metabolize NNN and NNK to hydroxylated products which were released into the culture media. Extensive activation by alpha-carbon hydroxylation of NNN (preferentially 2'-carbon hydroxylation) and NNK was observed, whereas no deactivation by pyridine N-oxidation could be detected. Microautoradiographic studies of explants showed that binding of radioactivity occurred preferentially in the respiratory and olfactory epithelia and in the subepithelial glands of the nasal mucosa. The results suggest that reactive metabolites of NNN and NNK are formed within the target tissue rather than being transported from the liver to the nasal mucosa. The results also show that the culture of nasal septa can be used to ascertain the role of the nasal mucosa in the activation of nasal-specific carcinogens.

Animals↗

PubMed1993

Reflex vasodilatation in the cat lip elicited by stimulation of nasal mucosa by chemical irritants.

Local application of capsaicin (threshold dose 150 microM) or nicotine (threshold dose 15 mM) to the nasal mucosa as well as electrical stimulation (threshold intensity 10 V) of the nasal mucosa elicited dose- or intensity-dependent blood flow increases in the ipsilateral lower lips of the anesthetized cats. Pretreatment with 3 mM capsaicin applied locally to the nasal mucosa abolished or reduced the vasodilation in response to capsaicin, nicotine, and ammonia vapor but not to light mechanical or electrical stimulation of the nasal mucosa. The blood flow increases elicited by all above stimuli were greatly reduced by pretreatment with hexamethonium, an autonomic ganglion blocker. These results suggest that stimulation of the nasal mucosa by chemical (capsaicin, nicotine, ammonia), mechanical, or electrical methods elicits the autonomic reflex vasodilatation in the cat lower lips. Furthermore, there seem to be at least two types of afferent fibers in the nasal mucosa of the cats: one type is capsaicin-sensitive fibers, while another type is capsaicin-resistant fibers involved in reflex vasodilatation.

Ammonia↗

PubMed2003

Epithelial cells of nasal mucosa express functional gap junctions of connexin 43.

OBJECTIVE: Recent studies have suggested that inositol triphosphate is transmitted through the gap junction of adjacent epithelial cells and communicates the intracellular calcium wave that controls the beating of cilia. Therefore, gap junction-mediated intercellular communication may modulate the metachronal ciliary beating of respiratory mucosa. MATERIAL AND METHODS: The expression and function of gap junctions were evaluated in nasal mucosa using immunofluorescent staining, Western blotting and Lucifer Yellow dye coupling in both whole nasal mucosa and cultured nasal epithelial cells. RESULTS: Among connexins (Cxs) 26, 32 and 43, only Cx43 was found in the nasal mucosa, in both the epithelial cells and submucosa tissue. Using Western blotting, Cx43 protein was found in protein extracts of both whole mucosa and cultured epithelial cells. The Cx43 protein content increased twofold between the 3rd and 6th days of culture. Lucifer Yellow dye, microinjected into single cultured epithelial cells, had spread to the adjacent cells. CONCLUSION: Cx43 is present in nasal mucosa. The expression of Cx43 on epithelial cells increases after culture. The dye-coupling study in epithelial cells indicated that the signal may be transmitted to neighboring cells via a gap junction composed of Cx43. Thus, Cx43 may be involved in the regulation of metachronal ciliary beating in ciliated epithelial cells and growth or differentiation in nasal tissue.

Blotting, Western↗

PubMed1991

Alterations of adrenoceptors in the nasal mucosa of allergic patients in comparison with nonallergic individuals.

Nasal hyperreactivity in nasal allergy may be due to changes of the characteristics in adrenergic receptors. Radioligand receptor-binding studies with the antagonists, 3H-prazosin (alpha 1-adrenoceptor), 3H-rauwolscine (alpha 2-adrenoceptor), and 125I-(-)-Cyanopindolol (beta-adrenoceptor) were performed in homogenates of nasal mucosa of allergic and nonallergic (NA) patients to investigate this hypothesis. The heterogeneous NA group was subdivided into control individuals and patients with chronic sinusitis and vasomotor rhinitis. No significant differences in affinities or densities of alpha 1- and alpha 2-adrenoceptors could be demonstrated in allergic patients in comparison with NA and control individuals. The beta-adrenoceptor density was significantly reduced in allergic patients in comparison with that of control individuals. Neither changes in agonist binding or in the effect of Gpp(NH)p on the agonist binding to beta-adrenoceptors could be observed in allergic patients. The subtype selective antagonist, LK203-030, demonstrated the presence of a homogeneous population of beta 2-adrenoceptors in human nasal mucosa of both NA and allergic patients. In vitro, autoradiography demonstrated specific 125I-(-)-Cyanopindolol labeling of the epithelium in NA and allergic patients. In conclusion, no changes in characteristics of alpha 1- or alpha 2-adrenoceptors in the nasal mucosa could be demonstrated in nasal allergy. However, a decreased number of beta-adrenoceptors may reflect a beta-adrenergic abnormality in nasal allergy.

Autoradiography↗

PubMed2000

Validation of excised bovine nasal mucosa as in vitro model to study drug transport and metabolic pathways in nasal epithelium.

The present work aims at the validation of excised bovine nasal mucosa as an in vitro model to address transport and metabolism pathways relative to the nasal mucosal uptake of therapeutic peptides. Preservation of the viability of the excised tissue in the course of in vitro studies of up to 3 h was demonstrated by (i) positive viability staining, (ii) constant transepithelial electrical resistance (42 +/- 12 Omega cm(2)), (iii) constant rates of metabolic turnover, and (iv) linear permeation profiles of therapeutic peptides and (3)H-mannitol. Using 1-leucine-4-methoxy-2-naphthylamide as a model substrate, we observed no difference between bovine and human nasal aminopeptidase activity. By a series of therapeutic peptides, no direct correlation was found between their effective permeability coefficients (from 0. 1 x 10(-5) to 5 x 10(-5) cm s(-1)) and their respective molecular masses (from 417 to 3,432 Da), indicating that other factors dominate nasal permeability. For instance, the permeabilities of metabolically labile peptides were concentration dependent and saturable, as demonstrated for two short thymopoietin fragments, Arg-Lys-Asp (TP3) and Arg-Lys-Asp-Val (TP4). By permeation studies using gonadorelin and two gonadorelin derivatives, buserelin and Hoe 013, without and in the presence of the chemical enhancer bacitracin, we also verified the ability of the model to assess chemical enhancer effects and their reversibility. In conclusion, our work demonstrates the potential of the investigated in vitro model, excised bovine nasal mucosa, to explore mechanistic aspects of nasal transport and metabolism of therapeutic peptides.

Absorption↗

PubMed1992

Immunoglobulin E distribution in atopic nasal mucosa.

The distribution of B lymphocytes and immunoglobulins G, A, M, and E in nasal mucosa was studied in frozen biopsy sections of nasal turbinate from 16 allergic patients and 8 controls. The immunoperoxidase technique was used with monoclonal and polyclonal antibodies. Comparative analyses of serum immunoglobulin levels were also performed. Few B lymphocytes were observed in the nasal mucosa linings in specimens from allergic and non-allergic patients. In both groups, high positivity for IgG and IgA was observed in the nasal mucosa linings in the specimens. IgM concentration was minimal in both groups. IgE was absent in the nasal turbinate specimens of nonallergic subjects, but was present discontinuously in low concentrations in 7 of the 16 allergic patients. There was no significant difference between allergic and nonallergic patients in the tissue and serum IgG, IgA, and IgM concentrations found. IgE was detected slightly in the nasal mucosa of patients with high IgE serum concentrations (greater than 1000 IU/mL) as well as in patients with very low IgE serum concentration readings. This result raises some doubt on the hypothesis concerning the local production of IgE.

Adolescent↗

PubMed1990

Biotransformation enzymes in the rodent nasal mucosa: the value of a histochemical approach.

An increasing number of chemicals have been identified as being toxic to the nasal mucosa of rats. While many chemicals exert their effects only after inhalation exposure, others are toxic following systemic administration, suggesting that factors other than direct deposition on the nasal mucosa may be important in mechanisms of nasal toxicity. The mucosal lining of the nasal cavity consists of a heterogeneous population of ciliated and nonciliated cells, secretory cells, sensory cells, and glandular and other cell types. For chemicals that are metabolized in the nasal mucosa, the balance between metabolic activation and detoxication within a cell type may be a key factor in determining whether that cell type will be a target for toxicity. Recent research in the area of xenobiotic metabolism in nasal mucosa has demonstrated the presence of many enzymes previously described in other tissues. In particular, carboxylesterase, aldehyde dehydrogenase, cytochromes P-450, epoxide hydrolase, and glutathione S-transferases have been localized by histochemical techniques. The distribution of these enzymes appears to be cell-type-specific and the presence of the enzyme may predispose particular cell types to enhanced susceptibility or resistance to chemical-induced injury. This paper reviews the distribution of these enzymes within the nasal mucosa in the context of their contribution to xenobiotic metabolism. The localization of the enzymes by histochemical techniques has provided important information on the potential mechanism of action of esters, aldehydes, and cytochrome P-450 substrates known to injure the nasal mucosa.

Aldehydes↗

PubMed1993

Lack of effect of ammonium glycyrrhizinate on the morphology of ovine nasal mucosa in vitro.

Glycyrrhetinic acid derivatives are reported to be nasal absorption promoters (1). Effects of ammonium glycyrrhizinate (AMGZ) on the in vitro morphology of ovine nasal mucosa were therefore examined by light and electron microscopy. Nasal mucosa was stripped from the submucosa and mounted in Ussing chambers. Exposure of the apical surface to 2% ammonium glycyrrhizinate (24 mM) for 90 min caused no histopathological changes to the nasal epithelium. Epithelial integrity remained intact as evidenced by the continued presence of morphologically intact junctional complexes. No sloughing of the epithelial layer from the basement membrane was observed, and cilia and microvilli were not affected by treatment with AMGZ. The results indicate that short-term exposure in vitro to ammonium glycyrrhizinate caused no overt morphological damage to ovine nasal mucosa.

Animals↗

PubMed1998

[Effect of topical corticosteroids and topical antihistaminics on ciliary epithelium of human nasal mucosa in vitro].

A normal ciliary beat frequency of ciliated cells is necessary for the mucociliary clearance of the nose and paranasal sinuses. An in vitro investigation was performed to evaluate the influence of topical corticosteroids and antihistamines on the ciliary beat frequency of human nasal mucosa. The nasal sprays examined contained the corticosteroids budesonide or fluticasone propionate and the topical antihistamines azelastine or levocabastine. All tests were performed on cell cultures of human nasal mucosa during constant conditions. Three of the four nasal sprays tested contained benzalkonium chloride as preservative. An irreversible cessation of ciliary movement was observed in all cells exposed to nasal sprays containing benzalkonium chloride in a 50 per cent solution. The nasal spray containing budesonide was benzalkonium chloride-free and caused minor but fully reversible decreases in ciliary beat frequency after 20 min. As benzalkonium chloride can cause complete standstill of ciliary beat frequency in vitro in human nasal mucosa, we recommend that this preservative should not be used anymore in topical nasal medications.

Administration, Topical↗

PubMed1997

[Transmission electron microscopic study on eosinophil degranulation in nasal mucosa in allergic rhinitis].

To observe the ultrastructure of eosinophil (EOS) degranulation in nasal mucosa in allergic rhinitis, nasal mucosa biopsies from patients with perennial allergic rhinitis (PAR, n = 13) pollinosis (PS, n = 9) subjects and normal controls (n = 3) were processed and the ultrastructure changes of EOS degranulation were examined under transmission electron microscope and routine histopathological observation. The ultrastructure of EOS degranulation in nasal mucosa collected from PAR and PS patients in their remission period differed from that in their attacking period, though there was no distinct differences in the distribution patterns of EOS. Increased cell membrane projections, eminent cytoplasm vacuolization, inconsistent density of granules with its crystalloid being lost, plus tissue edema and damage of collagen fibers in adjacent areas of degranulating EOS were among the most important ultrastructural changes of EOS in attacking period. The interrelations of EOS, mast cells (MC) and T-lymphocytes play important roles in the pathogenesis of allergic rhinitis.

Adult↗

PubMed1990

Neuropeptide Y: presence in sympathetic and parasympathetic innervation of the nasal mucosa.

The occurrence of neuropeptide Y (NPY), vasoactive intestinal polypeptide (VIP) and peptide histidine isoleucine (PHI) in the sympathetic and parasympathetic innervation of the nasal mucosa was studied in various species including man. A dense network of NPY-immunoreactive (IR) fibres was present around arteries and arterioles in the nasal mucosa of all species studied. NPY was also located in nerves around seromucous glands in pig and guinea-pig, but not in rat, cat and man. The NPY-IR glandular innervation corresponded to about 20% of the NPY content of the nasal mucosa as revealed by remaining NPY content determined by radioimmunoassay after sympathectomy. These periglandular NPY-positive fibres had a distribution similar to the VIP-IR and PHI-IR nerves but not to the noradrenergic markers tyrosine hydroxylase (TH) or dopamine-beta-hydroxylase (DBH). The NPY nerves around glands and some perivascular fibres were not influenced by sympathectomy and probably originated in the sphenopalatine ganglion where NPY-IR and VIP-IR ganglion cells were present. The venous sinusoids were innervated by NPY-positive fibres in all species except the cat. Dense NPY and DBH-positive innervation was seen around thick-walled vessels in the pig nasal mucosa; the latter may represent arterio-venous shunts. Double-labelling experiments using TH and DBH, and surgical sympathectomy revealed that the majority of NPY-IR fibres around blood vessels were probably noradrenergic. The NPY-positive perivascular nerves that remained after sympathectomy in the pig nasal mucosa also contained VIP/PHI-IR. The major nasal blood vessels, i.e. sphenopalatine artery and vein, were also densely innervated by NPY-IR fibres of sympathetic origin. Perivascular VIP-IR fibres were present around small arteries, arterioles, venous sinusoids and arterio-venous shunt vessels of the nasal mucosa whereas major nasal vessels received only single VIP-positive nerves. The trigeminal ganglion of the species studied contained only single TH-IR or VIP-IR but no NPY-positive ganglion cells. It is concluded that NPY in the nasal mucosa is mainly present in perivascular nerves of sympathetic origin. In some species, such as pig, glandular and perivascular parasympathetic nerves, probably of VIP/PHI nature, also contain NPY.

Adrenergic Fibers↗

PubMed1985

Intranasal inoculation of chickens with encapsulated or nonencapsulated variants of Haemophilus paragallinarum: electron microscopic evaluation of the nasal mucosa.

Chickens were inoculated intranasally with encapsulated or nonencapsulated strains of Haemophilus paragallinarum. The nasal mucosa of the chickens were examined, using scanning and transmission electron microscopy. In chickens given the encapsulated variant, marked loss of cilia and microvilli, infiltration of leukocytes, and deposition of a mucopurulent substance were seen on the surface of the nasal mucosa; the number of microvillous cells were markedly increased, and infiltration of mast cells into the lamina propria of the mucous membrane was observed. Numerous encapsulated organisms were found near cilia and on microvillous cells, and the capsule surrounding the organisms appeared to mediate attachment of the organisms to the cilia. In contrast, the nasal mucosa of the chickens given the nonencapsulated variants changed little morphologically. A few nonencapsulated organisms were found near cilia. Colonization of the nasal mucosa by encapsulated organisms probably was essential to induce the morphologic changes seen in the nasal mucosa.

Animals↗

PubMed1993

Quantification of resident inflammatory cells in the human nasal mucosa.

BACKGROUND: To define the normal resident inflammatory cell population in the nasal mucosa, surgical specimens of human nasal turbinates were immunohistologically stained for various cell markers. METHODS: Freeze-dried paraffin-embedded sections were stained for lymphocyte cell-surface markers, and Carnoy's fixed sections were stained for mast cells and immunoglobulins. The numbers of stained cells were microscopically counted. RESULTS: T cells (CD3+ cells) were abundant in the lamina propria, and the number of CD4+ cells and CD8+ cells accounted for two thirds and one third of CD3+ cell number, respectively. Cells that stained for the alpha-chain of the interleukin-2 receptor (activated cells, CD25+) were limited and accounted for only 0.6% of CD3+ cell number. B cells (CD22+ cells) and monocytes and macrophages (CD14+ cells) were observed less frequently than T cells. Many immunoglobulin-producing cells were found in close proximity to the submucosal glands, and those cells were predominantly IgA+. Mast cells were widely distributed in the nasal mucosa, and about one third of these cells were stained for IgE molecules. Nonmast cells bearing IgE were rarely observed. CONCLUSION: Thus the dominant cell in the nasal mucosa is a CD3+, CD4+, CD25-lymphocyte.

Animals↗

PubMed1995

Lymphocyte subsets of the nasal mucosa in perennial allergic rhinitis.

T cells have been considered to play a primary role in IgE-mediated atopic diseases, yet little is known about the T-cell subsets in the nasal mucosa of patients with perennial allergic rhinitis. To elucidate the characteristics of T cells at the site of allergic inflammation, we analyzed the proportions, phenotypes, stages of differentiation, and distribution of T-cell subsets in the nasal mucosa of 15 patients with house-dust-mite perennial allergic rhinitis (PAR) and 14 patients with chronic infective rhinitis (CIR), using flow cytometry and immunohistochemistry. We also examined the T-cell subsets in the peripheral blood (PBL) in conjunction with those of the nasal mucosa in 10 patients with PAR and in nine patients with CIR. Our results revealed no obvious difference in the percentage of nasal CD3+ T cells, CD8+ T cells, and alpha beta T cells in the PAR and CIR patients. In contrast, CD4+ T cells (p < 0.05), CD3+4-8- double-negative T cells, (p < 0.01), and gamma delta T cells (p < 0.01) were significantly increased in the nasal mucosa of PAR patients. A majority of the CD4+ T cells in the nasal mucosa of PAR patients coexpressed the CD45RO surface molecule, and a predominant proportion of CD4+ T cells in the nasal coexpressed the CD45RO surface molecule, and a predominant proportion of CD4+ T cells in the nasal epithelium were CD45RO+. The ratio of CD4+ CD45RO+:CD4+ CD45RA+ T cells in the allergic patients' nasal mucosa was significantly greater than that in autologous peripheral blood (p < 0.01). The proportion and stages of activation and differentiation of T-cell subsets in the allergic patients' nasal mucosa were independent of those in the peripheral blood. An increase in the proportion of natural killer (NK) cells was observed in the nasal mucosa of CIR patients. Taken together, our results suggest that nasal T cells exhibit distinct patterns of distribution, differentiation, and activation in different inflammatory conditions of the nose. PAR is characterized by a selective increase in CD4+ memory T cells, CD3+4-8- double-negative T cells, B cells, and gamma delta T cells in the nasal mucosa. The increase in CD4+ memory T cells in the allergic nasal epithelium may have critical implications in the pathogenesis of PAR.

Adult↗

PubMed1995

[Study of monocyte chemotactic and activating factor in the human nasal mucosa].

Recently monocyte chemotactic and activating factor (MCAF) has been reported to be a potent histamine releasing factor (HRF) for human basophils. In this study we investigated the localization and biological activity of MCAF in human nasal mucosa. To investigate the localization of MCAF within the nasal mucosa we performed specific immunohistochemical staining of sections of large pieces of the inferior turbinate obtained by conchotomy from patients with nasal allergy and without nasal allergy and compared them. Sections of nasal mucosa from allergic subjects stained with anti-MCAF mAb demonstrated the presence of many MCAF-positive cells in the lamina propria especially around small vessels and excretory gland, but only a few positive cells were found in the nasal mucosa of normal subjects. We cultured allergic nasal mucosa and sinus mucosa from patients with chronic inflammation for 2 days and detected MCAF by western blot analysis of the culture supernatants. One portion separated from sinus mucosa supernatant by column chromatography also released histamine from human basophils. Mean release was 3-4% and the difference from the control was statistically significant (p < 0.05). In the human nasal mucosa it seemed to exist IgE independent histamine releasing system sustained by MCAF producing cells. These results suggested that MCAF is one of the important mediators causing histamine release in the late phase reaction and in protracted inflammation of the nasal mucosa.

Adult↗

PubMedDate not supplied

A new in vitro method of decongestant assay of nasal mucosa: a preliminary report.

BACKGROUND: The calculation of cell planar surface area, successfully used for glomerular mesangial cell-altered contractility, also is a reasonable methodology to assess nasal mucosal contractility. A simple technique that works particularly well with vasoconstriction-inducing agents has been introduced to test the effects of several drugs on patient turbinate nasal mucosa in vitro. This report will introduce this technique and present some of the initial findings. METHODS: We tested epinephrine, norepinephrine, pseudoephedrine HCl, and methoxamine, respectively, for effectiveness as a vasoconstricting drug. We also tested the effectiveness of verapamil as a vasodilating drug. A piece of nasal mucosa approximately 3 x 4 mm in size was mounted with a 27-gauge needle and submersed in a 4-mL muscle bath in a Petri dish at room temperature. The bath consisted of 4 mL of Kreb's solution. We recorded the decrease of nasal mucosa planar surface area in response to the application of vasoconstricting agents, as measured using a digital microscope connected to a Pentium III with morphometric software, as the estimated degree of contraction. A photograph of the same mucosa was taken every 3 minutes for a total period of 18 minutes. RESULTS: Nasal mucosa that was mounted in a muscle bath in a Petri dish and treated with a small dose of a nasal decongestant was l observed to contract. Drug dosage determined the degree of nasal mucosa contraction. Nasal mucosa similarly prepared but treated with a vasodilating agent, such as verapamil, exhibited a relaxation response only when pretreated with a vasoconstricting agent, such as methoxamine. Both vasoconstricting and vasodilating drugs induce dose-related responses in planar surface calculation. CONCLUSION: In this study, drug dosage determined the degree of nasal mucosa contraction. We also found that the rate of contraction and percent of contraction were dose dependent. We believe this new method will prove useful in studying the effects of drugs on nasal blood vessels.

Dose-Response Relationship, Drug↗