[Adrenergic innervation in allergic human nasal mucosa and effect of histamine on the noradrenaline release from adrenergic fiber in nasal mucosa of guinea-pig].
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Adrenergic Fibers↗
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The surface pattern of the nasal mucosa and its relation to mucous flow--a study of chicken and herring gull nasal mucosae.
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Animals↗
Possible immediate hypersensitivity reaction of the nasal mucosa to oral contraceptives.
Nasal provocation tests with suspension of oral contraceptive drugs (OCD) as well as of their components (Estrogen, Progestin, Non-hormonal components) were performed in two groups of women, mostly suffering from perennial rhinitis or pollinosis, and all taking oral contraceptive drugs. Thirteen of the 15 patients from the first experimental group, in whom the increase of the nasal complaints was anamnestically related to the oral contraception, and three of the 34 patients from the second experimental group (without anamnestical relation to the oral contraception) demonstrated a positive nasal mucosa response after topical challenge with OCD. All OCD positively reacting patients showed also a positive nasal mucosa response after challenge with the Estrogen and one patient also after Progestin challenge. Non-hormonal components did not cause any reaction. This nasal mucosa response was interpreted as a possible allergic reaction. Type I (immedicate hypersensitivity of the nasal mucosa due to Estrogen in blood contraceptives. This response begins within 10 minutes, reaches its maximum within 30 minutes, and does not disappear completely within 60 minutes in most patients. None of the patients from control groups (atopy--without OCD; OCD takers--without atopy; male volunteers without atopy) demonstrated any positive nasal mucosa response to OCD or their components.
Contraceptives, Oral↗
Calcitonin gene-related peptide in human nasal mucosa.
To explore the potential range of functions for calcitonin gene-related peptide (CGRP) in human mucosa, we quantified human inferior turbinate nasal mucosal CGRP content by radioimmunoassay, localized CGRP-immunoreactivity by immunohistochemistry, detected 125I-CGRP binding sites by autoradiography, and tested the ability of CGRP to induce submucosal gland secretion in short-term explant culture of human nasal mucosa. Nasal mucosa contained 0.45-0.54 pmol CGRP/g wet wt (n = 18). Immunoreactive CGRP was found in nerve fibers that densely innervated the walls of small muscular arteries arterioles. Venules and venous sinusoids were innervated by individual CGRP staining fibers. Occasional CGRP-containing nerve fibers were also noted adjacent to submucosal gland acini, near the epithelial basement membrane, and between epithelial cells. Specific 125I-CGRP binding sites were concentrated on small muscular arteries and arterioles. CGRP (4 microM) did not stimulate glycoconjugate or lactoferrin release from mucosal explants. These results indicate that in the human nasal mucosa, CGRP is present in nerve fibers, which most likely represent nociceptive sensorimotor nerves that innervate vascular structures (muscular arteries, arterioles, veins and venous sinusoids). It is likely that CGRP release from sensory neurons may play a role in the regulation of vasomotor responses, but no evidence for a role of CGRP in glandular secretion was found.
Calcitonin Gene-Related Peptide↗
[Morphology of the vascular endothelium of the nasal mucosa].
In the nasal mucosa capillaries with fenestrated and continuous endothelium have been described. Fenestrated capillaries are distributed all over the tunica propria. They are increasing in number subepithelially and close to the nasal glands. Particularly subepithelially the endothelial fenestrations are facing the epithelium. This interesting, morphological feature has already been described as "polar differentiation" in capillaries of other tissues and has been interpreted as a functional differentiation. The same observations could be made in muscularised veins of the nasal mucosa. Only a few fenestrations could be detected in the endothelium of these vessels, but they were all facing the adjacent epithelium. The results indicate that the morphological peculiarities of the vascular endothelium of the nasal blood vessels are transient specialisations of this particular type of cells due to different physiological needs.
Animals↗
Nicotinic cholinergic receptor expression in the human nasal mucosa.
Twenty-four nasal mucosa specimens were obtained from the inferior or middle turbinates of 6 normal subjects and 18 patients with chronic sinusitis, inflammatory polyp formation, or sinus allergies. Reverse transcription-polymerase chain reaction analysis was used to identify the non-neuronal nicotinic cholinergic receptor (nAChR) subunits that were expressed in the nasal mucosa. Collectively, transcripts for alpha (alpha1, alpha2, alpha3, alpha4, alpha6, alpha7) and beta (beta2, beta3, beta4) nAChR subunit genes were detected in the respiratory mucosa. The alpha3, alpha7, and beta2 subunits were expressed in 92%, 88%, and 75% of the subjects, respectively. There was a high degree of interindividual variation in nAChR subunit gene expression among subjects. A significant univariate association was found between tissue type and beta4 expression and between gender and beta3 expression. These data suggest that cells in the nasal mucosa express the necessary messenger RNAs (mRNAs) for numerous nAChR combinations. Moreover, our identification of nAChR subunit mRNAs in the nasal mucosa extends the findings of other functional studies of nAChRs in nasal epithelial cells and implies that nicotine from tobacco products such as cigarette smoke and nicotine nasal spray may have direct cellular effects on nasal mucosa cells through activation of homogeneous or heterogeneous nAChRs. A significant number of patients receiving nicotine nasal spray have reported nasal irritation, and there are reports of transient irritation of the throat and trachea with the use of smoke-free nicotine cigarettes. These adverse respiratory effects may be due to activation of nAChRs in epithelial cells of the nose and trachea.
Adult↗
Nitroxidergic vasodilator nerve in the canine nasal mucosa.
The canine nasal mucosa was studied by in vitro bioassay. Non-adrenergic, non-cholinergic (NANC) vasodilator response to transmural electrical stimulation was observed in the presence of guanethidine and atropine. This vasodilator response was abolished by NG-nitro-L-arginine (L-NA) which is an inhibitor of nitric oxide (NO) formation but not by NG-nitro-D-arginine. The inhibitory effect of L-NA was partially reversed by treatment with L-arginine but not with D-arginine. The vasodilator response was significantly suppressed by tetrodotoxin. The present results indicate that NO may mediate neurogenic vasodilation in the canine nasal mucosa.
Animals↗
[Mast cells in the nasal mucosa of patients with nasal polyps. A histological study with lectins].
Histochemical studies done with lectins are helpful for differentiate between several carbohydrates and glycoproteins of cell structures. Mast cells predominate in the nasal polyps mucosa of these patients. Cytoplasmic granules of mastocyts reacted to all lectins employed but LTA.
Histocytochemistry↗
[The tonsils as MALT (mucosa-associated lymphoid tissue) of the nasal mucosa].
One of the most effective defense mechanisms of the nasal mucosa is its immune response leading to the synthesis of antibodies directed against inhaled antigens. In order to understand the immunology of the upper respiratory tract it is essential to know whether this response takes place within the mucosa itself or within regional lymphoid organs. The authors investigated cell populations involved in immune processes within the mucosa and as a model of a lymphoid organ, in the tonsil. Using a range of monoclonal cell surface markers, the authors concentrated on antigen-presenting cells, the B-cell differentiation, and T-cell subpopulations and their corresponding activation markers. The findings demonstrate that the normal mucosa has no organized lymphoid structures and few or no early, maturing, or activated B-lymphocyte stages. The antibody-producing plasma cells found within the mucosa can therefore not be regarded as locally formed. On the contrary, the palatine tonsils demonstrate a typical lymphoid structure and contain all activation and differentiation stages of B-lymphocytes from premature to plasma cells. This would suggest that the human nasal mucosa is not capable of providing a local immune response, but is dependent on lymphoid organs like the tonsil, as the regional "mucosa-associated lymphoid tissue" (MALT).
Antibody-Producing Cells↗
Interleukin-5 gene expression in nasal mucosa and changes in amount of interleukin-5 in nasal lavage fluid after antigen challenge.
Eosinophils and their products are known to cause hyperreactivity and swelling of the nasal mucosa in subjects with nasal allergy. Interleukin-5 (IL-5) not only induces differentiation and proliferation of immature eosinophils but also causes mature cells to accumulate and activate. This study shows that IL-5 is actually produced in the human nasal mucosa by antigen challenge, and it further investigates the changes in the amount of IL-5 in nasal lavage fluids after antigen challenge. Expression of mRNA for IL-5 in nasal mucosa was investigated using the reverse transcription-polymerase chain reaction (RT-PCR) and Southern blot analysis. Among the 4 subjects with nasal allergy examined in this study, expression of mRNA for IL-5 was observed in 2 prior to antigen challenge; within 6 h after antigen challenge it was seen in 3 subjects. We also found that the amount of IL-5 in the nasal lavage fluids obtained consecutively after antigen challenge increased predominantly in the late phase, and that the number of eosinophils in the IL-5 positive group was significantly higher than that in the IL-5 negative group. These results strongly suggest that IL-5 contributes to the recruitment of eosinophils in the nasal mucosa of the subjects with nasal allergy.
Adolescent↗
Metabolism of dopamine by the nasal mucosa.
The nasal route of administration offers several advantages over oral and intravenous administration, including the ability to avoid hepatic first pass metabolism. Dopamine deficiency has been associated with several neurological disorders; it has been shown to have good systemic bioavailability and significant uptake into the CNS following intranasal administration. The purpose of these studies was to investigate the limiting role of mucosal metabolism of dopamine during nasal absorption. In vitro transport and initial rate studies were carried out using nasal mucosal explants to study dopamine permeability and metabolism. Dihydroxyphenylacetic acid (DOPAC) was the only metabolite detected. Monoamine oxidase (MAO), the enzyme responsible for DOPAC formation, was localized to the submucosal region of the nasal explants. The amount of DOPAC formed during the transport studies was less than 0.5% of the initial amount of dopamine placed into the system. Iproniazid, an MAO inhibitor, blocked DOPAC formation but had no effect on dopamine transport. The limited extent of dopamine metabolism compared to its mucosal transport demonstrates that nasal dopamine transport is not significantly reduced by mucosal metabolism and suggests that the nasal route may be promising for the efficient delivery of dopamine to the CNS.
2,4-Dinitrophenol↗
The effect of topical decongestant on blood flow in normal and infected nasal mucosa.
The nasal mucosal blood flow was determined by means of the 133Xe wash-out method in an early stage of acute rhinitis and in health and the effect of a topical decongestant (oxymetazoline) was evaluated. During an early stage of acute rhinitis, a statistically significant increase of blood flow was found. The topical decongestant in therapeutically recommended doses decreased the blood flow significantly in acute rhinitis as well as in healthy subjects. The effect was more pronounced in acute rhinitis. The effect of oxymetazoline was dose dependent and a statistically significant decrease was found in doses of about 1/50 of the therapeutically recommended. The clinical implication is that it might be possible to reduce the dose of the decongestant in order to minimize the negative side effect of a decreased blood flow.
Acute Disease↗
Histological, immunological and molecular features of a nasal mucosa primary melanoma associated with nasal melanosis.
Nasal mucosa melanoma is a rare entity that may occur together with nasal melanosis. The histological and immunological features and loss of heterozygosity analysis of such lesions have not been reported to date. In the study presented here short-term cell cultures were established from the patient's melanoma and subsequent relapses. Histology, immunohistochemistry, reverse transcription-polymerase chain reaction enzyme-linked immunosorbent assay, human leukocyte antigen analysis, microdissection with subsequent polymerase chain reaction for analysis of loss of heterozygosity were used to characterize the tumour and other cells. Melanoma of the nasal cavity was found, with a surrounding proliferation of atypical melanocytes corresponding to nasal melanosis. Immunoreactivity was found for S-100, gp100, tyrosinase and MelanA protein. Loss of heterozygosity for a p16-flanking marker was found in the tumour and the melanotic cells. Short-term cell cultures expressed tyrosinase and MUC18 at the mRNA level and intercellular adhesion molecule-1 (ICAM-1) and interleukin-12 receptor at the protein level. This is the first time short-term cell cultures have been established and analysed from such a tumour. Melanoma-associated antigens were identified within the tumour. The melanoma and the melanotic cells showed loss of heterozygosity for the p16 gene, which is implicated in melanoma development. This points to a common origin in tumorigenesis. Pathways of tumour escape, such as expression of CD54 and interleukin-10, were observed. The clinical, immunological and molecular features suggest that nasal melanosis should be followed closely.
Adult↗
[Vasoconstriction of dog nasal mucosa caused by histamine].
Nasal mucosa was obtained from 12 dogs. The vasoconstrictive effect of histamine was measured with physiological recorder. The results showed that vasoconstriction of the nasal mucosa caused by histamine could be blocked by H1 antihistamines or verapamil and not by H2 or alpha antagonists. It suggests that the effect of histamine on nasal mucosa might be mediated by H1 receptor through activation of calcium channel and not by releasing noradrenaline.
Animals↗
Lack of DNA binding in the rat nasal mucosa and other tissues of the nasal toxicants roflumilast, a phosphodiesterase 4 inhibitor, and a metabolite, 4-amino-3,5-dichloropyridine, in contrast to the nasal carcinogen 2,6-dimethylaniline.
The phosphodiesterase 4 inhibitor Roflumilast (B9302-107) (RF) and its metabolite 4-amino-3,5-dichloropyridine (ADCP) produced nasal toxicity in preclinical safety studies with rats. The purpose of this study was to assess the possible formation of DNA adducts, by RF and ADCP, in the nasal mucosa, liver and testes of male rats using the 32P-postlabeling assay. For comparison, rats were exposed to the DNA-reactive carcinogens 2,6-dimethylaniline (DMA), also known as 2,6-xylidine, a nasal carcinogen, and the aromatic amine carcinogens 4,4'-methylene-bis(2-chloroaniline) (MOCA), which yields monocyclic DNA adducts, and 2-acetylaminofluorene (2-AAF). In the case of RF, possible sources of DNA adducts include the parent molecule and its ADCP moiety by enzymatic N-hydroxylation and sulfation, reactions typical of carcinogenic aromatic amines. 4-Acetoxylamino-3,5-dichloropyridine (N-acetoxy-ADCP), a chemically activated derivative of ADCP, was prepared and used to modify DNA which was then used to establish the chromatographic conditions with which to reliably detect whether or not such adducts were formed metabolically from RF and ADCP. Similarly, a standard N-hydroxy-DMA was prepared, but the corresponding N-acetoxy derivative was unstable and decomposed during synthesis. Both N-hydroxy-DMA and N-acetoxy-ADCP were mutagenic in the Salmonella typhimurium Ames assay using strain TA100 without an exogenous bioactivation system, with the former being more potent. N-hydroxy-ADCP was essentially inactive in this assay. For the 32P-postlabeling assay, male Wistar rats were exposed to the test substances and carrier control compounds by intragastric instillation at the selected dose levels for 7 days. Subsequently, the nasal mucosa, liver, and testes of the rats exposed to the test or control compounds were extirpated, the DNA extracted and the samples postlabeled. The patterns of adducts formed with the test compounds were compared to those formed in N-acetoxy-ADCP- and N-hydroxy-DMA-adducted DNA, which were assayed by both nuclease P1 and butanol enhancement methods. Based upon the similarity of results from the two enhancement methods, only the former was used for the in vivo studies. No evidence was obtained for the formation of DNA adducts from RF or its metabolites, specifically ADCP, under the conditions of these assays despite the ability to detect adducts from DNA modified chemically with N-acetoxy-ADCP and DNA adducts from the other compounds in their target organs. In the absence of a pattern of compound-related spots, we conclude that RF does not form DNA adducts having the potential to initiate neoplasia in these three tissues.
3',5'-Cyclic-AMP Phosphodiesterases↗
Quantitative assessment of aerial ammonia toxicity to the nasal mucosa by use of the nasal lavage method in pigs.
Effects of atmospheric ammonia (NH3) on the nasal mucosa and somatic growth were investigated in pigs exposed to 4 NH3 concentrations (0; 25; 50; and 100 ppm) for 6 days in a specifically designed air-pollutant exposure chamber. Nasal lavage (NAL) was applied to quantify the ammonia-induced inflammatory response by measuring the number of neutrophils and the albumin (porcine serum albumin) concentration in the NAL liquid. In control pigs, these variables remained unchanged throughout the exposure period. In all other groups, an important ammonia concentration-related increase was recorded. The equation of the linear regression line established between the mean values of the number of neutrophils (x 10(3)) per milliliter of NAL liquid (y) recorded at the end of the exposure period and the ammonia concentrations (ppm) was: y = 69.7 + 3.3 [NH3] (r = 0.979; P < 0.020). The increase in the neutrophil count was significant (P < 0.05) at concentrations as low as 25 ppm. For albumin concentration nanograms per milliliter, the corresponding equation was: y = 574 + 14.3 [NH3] (r = 0.953; P < 0.045). However, the first significant change (P < 0.05) in this variable was only obtained for the higher concentration (100 ppm). In exposed pigs, a concentration-related depression of somatic growth was observed. The equation of the regression line plotted relating the individual values of the changes in body weight gain recorded over the exposure period expressed as percentage of the initial body weight (y) and the ammonia concentration was: y = 3.507-0.203 [NH3] + 0.001 [NH3]2 (r = 0.55; P < 0.010).(ABSTRACT TRUNCATED AT 250 WORDS)
Air Pollution, Indoor↗
[Quantitative analysis of color of the nasal mucosa].
The color of the nasal mucosa was quantitatively studied. Chromaticity of the nasal mucosa was indicated by two parameters, x (red component in RGB) and y (green in RGB) values, measured with a chromameter (MINOLTA Co., CS-100). According to preliminary studies in normal subjects, the following conditions were thought to make the method suitable for measuring the color of the nasal mucosa. 1) The chromameter can be held in the hand. 2) Brightness of the nasal mucosa should be kept as constant as possible. 3) The inferior turbinate mucosa is easier to measure than the septal one. In the preliminary study there was no significant difference in chromaticity measurements among the examiners. Chromaticity of the inferior turbinate was compared among patients with perennial nasal allergy (PNA, n = 19), with cedar pollinosis (CP, n = 11), and normal subjects serving as a control (n = 15). The x values in the PNA and CP groups were significantly lower than those in the control group (p < 0.01), and the y values were significantly higher (p < 0.02). The results agreed with the macroscopic observations made by trained rhinologists. The x values increased when azelastin was administered in five of the PNA group. This increase was related to improvement of their subjective symptoms. Quantitative analysis of the nasal mucosal color could be useful for objective evaluation of the clinical course of allergic rhinitis.
Color↗
Electron microscopy findings in the nasal mucosa of a patient with stenosis of the nasal vestibule.
The nasal mucosa humidifies, warms and filters inspired air before it passes to the lower respiratory tract. In order to maintain the physiological activity of the respiratory epithelium, a certain amount of airflow is required. This report describes electron microscopy findings in the nasal mucosa of a patient who had decreased airflow through the nose due to stenosis of the nasal vestibule. Electron microscopic examination of the nasal mucosa revealed stratified squamous epithelium composed of markedly degenerated cells. The findings of abnormal mucosal structure highlight another negative consequence of nasal obstruction in addition to abnormal physiological function of the nose. The negative impact of diminished airflow on the nasal mucosa should be considered in any case where the patient has a condition that can lead to partial or total loss of airflow through the nose.
Adolescent↗