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PubMed2006

The permeation of nalmefene hydrochloride across different regions of ovine nasal mucosa.

The permeability of nalmefene hydrochloride (NH) across different regions of ovine nasal mucosa was investigated in vitro. Five different regions of ovine nasal mucosa (superior turbinate mucosa, middle turbinate mucosa, inferior turbinate mucosa, posterior septum mucosa, and anterior septum mucosa) were studied. The results showed that the permeability coefficients of NH through different regions of nasal mucosa were different, and the suitable regions for the absorption of NH were the middle turbinate mucosa, the posterior septum mucosa and the superior turbinate. At the same time, the middle turbinate mucosa was the largest region among the five regions, thus it was the main absorption region for NH. The high uniformity of the middle turbinate mucosa also made it the most suitable model for the permeation of NH in vitro.

Animals↗
PubMed1992

Kinetics and enzyme involvement in the metabolism of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in microsomes of rat lung and nasal mucosa.

The rat lung and nasal cavity are two target organs for carcinogenesis by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). In order to characterize further the enzymes involved in the bioactivation of NNK, detailed kinetic and inhibitory studies were conducted with rat lung and nasal mucosa microsomes, and the results were compared with previous studies. The enzymes in rat lung microsomes catalyzed the alpha-hydroxylation, pyridine N-oxidation and carbonyl reduction of NNK. The apparent Km for the formation of the NNK-derived keto aldehyde, NNK-N-oxide, the NNK-derived keto alcohol and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol were 28.8, 10.4, 7.0 and 178.1 microM respectively. In rat nasal microsomes, alpha-hydroxylation was the predominant pathway and the rate was approximately 200 times higher than that in lung microsomes. The apparent Kms for keto aldehyde and keto alcohol formation in rat nasal microsomes were 9.6 and 10.1 microM respectively. The cytochrome P450 inhibitors metyrapone and carbon monoxide markedly inhibited the metabolism of NNK in both rat lung and nasal microsomes. In rat lung microsomes, alpha-naphthoflavone and monospecific antibodies against P450s 1A2, 2A1 and 2B1 inhibited the formation of keto aldehyde by 39, 46, 64 and 23% respectively. In rat nasal microsomes, alpha-naphthoflavone and antibodies against P450s 1A2, 2A1 and 3A inhibited the metabolism of NNK by 80, 35, 20 and 14% respectively. The results indicate that cytochromes P450 play a major role in the metabolic activation of NNK in rat lung and nasal microsomes, and that there are tissue-related differences in NNK metabolism.

Animals↗
PubMed2000

[Effects of nitric oxide on ciliary beat frequency in the human nasal mucosa].

OBJECTIVE: To investigate the effect of nitric oxide on ciliary beat frequency in human nasal mucosa. METHOD: A primary culture model of human nasal mucosa epithelial cells was established and the effect of nitric oxide on ciliary beat frequency was observed by videomicroscopy method. The data were statistically analyzed using t-test. RESULT: L-arginine significantly increased ciliary beat frequency from (400 +/- 48) beats/min to (793 +/- 68) beats/min (n = 9, P < 0.001), D-arginine had no similar effect, while NOS blocker L-NAME inhibited the effect of L-arginine. CONCLUSION: Cells cultured by our method could synthesize NOS that made L-arginine produce NO that could increase ciliary beat frequency in the human nasal mucosa.

Arginine↗
PubMed1982

N-Demethylation of aminopyrine by the nasal mucosa in mice and rats.

N-demethylation of aminopyrine was demonstrated in the nasal mucosa of C57 Bl mice and Sprague-Dawley rats by measurements of the 14CO2 formed at incubation of 14C-aminopyrine with tissue-slices. The metabolism of aminopyrine by the nasal mucosa was induced by phenobarbital pretreatment and susceptible to inhibition with metyrapone and SKF 525 A suggesting the presence of cytochrome P-450-dependent enzyme system in the tissue. Immediately after injection of 14C-aminopyrine in rats a uniform distribution of radioactivity in the body was recorded. After thirty minutes, however, a preferential localization of radioactivity was found in the nasal mucosa and in the liver. By pretreatment with metyrapone the uptake of radioactivity in the nasal mucosa and in the liver was blocked suggesting that the observed accumulation of radioactivity is due to metabolites.

Aminopyrine N-Demethylase↗
PubMed2007

Rhinitis medicamentosa: electron microscopic changes of human nasal mucosa.

OBJECTIVE: Prolonged application of nasal vasoconstrictors causes rhinitis medicamentosa (RM). Nasal obstruction is induced by rebound swelling when the decongestive effect has disappeared. The aim of this study was to demonstrate ultrastructural changes in RM. STUDY DESIGN AND SETTING: Tissue samples of inferior turbinates from 22 patients with RM and 10 patients without rhinitis were taken during nasal surgery. Ultrathin sections were investigated by using a transmission electron microscope (TEM). RESULTS: The TEM findings revealed severe epithelial damages such as loss of ciliated cells. In the subepithelial region, the vascular endothelium showed gaps and ruptures of basal lamina. CONCLUSION: RM is a drug-induced damage of human nasal mucosa. Loss and destruction of ciliated epithelial cells are the morphologic correlation of the disturbed mucociliary clearance. In addition, vascular endothelium revealed ultrastructural changes. This could be caused by an increased vascular permeability with consecutive interstitial edema. SIGNIFICANCE: This study demonstrated new morphological aspects of rhinitis medicamentosa.

Adult↗
PubMed1983

Ultrastructure of human nasal mucosa.

This thesis describes the ultrastructure of human nasal mucosa, based upon surgical biopsy specimens. The intent of the study is to characterize the normal ultrastructure of human nasal mucosa with emphasis upon the difference between olfactory and respiratory epithelia. Other nasal epithelia (anterior, sinus, and posterior) are reviewed briefly for comparison only. Several pathological examples of the olfactory and respiratory epithelia are also briefly presented for contrast.

Epithelium↗
PubMed1996

[Study on distributions of somatostatin in rat nasal mucosa and trigeminal ganglion].

To explore the regulatory mechanism of the release of neuropeptides in nasal mucosa, the distributions of somatostatin (SOM) and SOMmRNA-immunoreactivities (IR) in cryostat sections of rat nasal mucosa and trigeminal ganglion (TG) cells were investigated using immunohistochemistry (ABC technique) and in situ hybridization histochemistry. The recombinant PSP65 plasmid (400 SOMcDNA) in vitro worked as a plate for the preparation of SOMmRNA single strand (cRNA) probe, which was labelled with digoxigenin. The results showed that neither of these two substances reacted positively in nasal mucosa but positive SOM-IR and SOMmRNA-IR signals were definitely seen in TG cells. In contrast with SOM immunohistochemistry, SOMmRNA-IR positive granules tended to be located in the cytoplasm of TG cells, with a clearer background and a higher resolution rate. The significance of SOMmRNA in TG cells was briefly discussed. It was concluded that SOMmRNA in TG cells might be involved in the regulation of the release of neuropeptides in nasal mucosa.

Animals↗
PubMed1988

Effect of long-term use of reserpine, a sympathetic neuron blocker, on muscarinic cholinergic receptors in the guinea pig nasal mucosa.

To evaluate whether hypofunction of the sympathetic nervous system induced by long-term reserpine treatment affects the parasympathetic system in the nasal mucosa in the receptor level, a receptor binding assay was performed using the nasal mucosa of guinea pigs which had chemical denervation produced by intraperitoneal injection of 0.1 mg/body reserpine once daily for 4 weeks. The maximum number of muscarinic cholinergic receptor bindings to diquinuclidinyl benzilate (3H-QNB) in the nasal mucosa of the reserpine-treated guinea pigs was increased by 46% as compared with that in the control (p less than 0.05). The present experiment shows that hypofunction of the sympathetic system in the nasal mucosa induced by reserpine may affect the parasympathetic system in the nasal mucosa.

Animals↗
PubMed2001

Analysis of human papillomavirus in schneiderian papillomas as compared to chronic sinusitis and normal nasal mucosa.

Schneiderian papillomas (SPs) are tumours arising from the surface epithelium (schneiderian epithelium) of the nasal cavity and paranasal sinuses. Evidence points toward a viral etiology, specifically human papillomavirus (HPV). Although substantial data indicate HPV as a likely etiology, little is known about the role of HPV in benign nasal pathologies or in normal nasal mucosa. The objective of this study was to characterize the relationship between HPV and SP, chronic sinusitis (CS), and normal nasal mucosa. A case-control study was undertaken, matching patients with SP to patients with CS. Patients with normal nasal mucosa served as a control group. All patients had their tissues analyzed for the presence of various HPV subtypes using line blot assay. A total of 168 patients were identified (74 SP, 74 CS, 20 control). Of these, 70 (41.7%) had detectable deoxyribonucleic acid and 9 of 70 (12.9%) had detectable HPV of subtypes 6, 11, and 16. None had detectable HPV type 18. Significant differences were detected in the presence of HPV in the CS, SP, and control groups, as well as in the presence of low- versus high-risk subtypes among investigation and control groups. Significant differences exist in HPV infectivity among SP, benign nasal pathologies such as CS, and normal nasal mucosa. Human papillomavirus plays an important role, at least in part, in the development of SP, with types 6, 11, and 16 being more pivotal than other types. Line blot assay is a useful technique in identifying HPV in SP.

Case-Control Studies↗
PubMedDate not supplied

Effect of cooling on electrical field stimulation and norepinephrine-induced contraction in isolated hypertrophic human nasal mucosa.

BACKGROUND: Exposure to cold causes cutaneous vasoconstriction to reduce body heat loss, while the nasal cavity warms up the inspired cold air. This suggests cooling might evoke a different response in nasal mucosa blood vessels than in cutaneous blood vessels. Thus, the aim of this study was to evaluate the effect of cooling (to 24 degrees C) on the vascular response of isolated nasal mucosa. METHODS: An in vitro isometric contraction of nasal mucosa excised from patients suffered from chronic nasal congestion was continuously recorded. Either electrical field stimulation (EFS) or exogenous norepinephrine (NE) was applied to the turbinate mucosa strip at 37 and 24 degrees C, and the influence of cooling (to 24 degrees C) was evaluated. RESULTS: EFS (1, 2, 4, and 8 Hz) produced frequency-dependent contractions at 37 and 24 degrees C. Cooling did not alter the magnitude but significantly prolonged the duration of EFS-induced contraction. Exogenous NE (10(-8) to 10(-4) M) produced concentration-dependent contractions at 37 and 24 degrees C. Cooling significantly enhanced the contractile responses evoked by NE between 3 x 10(-6) and 1 x 10(-4) M. CONCLUSION: Cooling (to 24 degrees C) prolonged the EFS-induced and enhanced NE (3 x 10(-6) to 1 x 10(-4) M)-induced contraction of isolated human nasal mucosa.

Adolescent↗
PubMed2000

alpha(1)-adrenoceptor subtypes and effect of alpha(1A)-adrenoceptor agonist NS-49 on guinea pig nasal mucosa vasculature.

It is now clear that alpha(1)-adrenoceptors comprise a heterogeneous family. In the present study, we characterized the alpha(1)-adrenoceptor subtype in the nasal mucosa vasculature of guinea pigs. A rectangular strip of guinea pig nasal mucosa was suspended in an organ bath containing Krebs' bicarbonate solution. Changes in tension were recorded isometrically. Concentration-response curves for agonists were obtained in a cumulative manner. Noradrenaline produced the greatest contraction of the nasal mucosa vasculature. NS-49 ((R)-(-)-3'-(2-amino-1-hydroxyethyl)-4'-fluoromethane sulfonanilide hydrochloride) and oxymetazoline worked as partial agonists. The intrinsic activities of NS-49 and oxymetazoline were 0.50+/-0.22 and 0.29+/-0.17, respectively, compared with noradrenaline (=1.00). Prazosin and the putative alpha(1A)-adrenoceptor antagonists WB-4101 (2-(2,6-dimethoxyphenoxyethyl)aminomethyl-1,4-benzodioxane) and 5-methylurapidil antagonized the response to noradrenaline competitively (pA(2) for prazosin<9.0). Conversely, putative alpha(1B) and alpha(1D)-adrenoceptor antagonists (spiperone and BMY7378 (8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4, 5]decane-7,9-dione), respectively) did not antagonize competitively. These results suggest that the alpha(1A)-subtype is predominant and that the alpha(1L) (or alpha(1N)) subtype may also be present in the guinea pig nasal mucosa vasculature. Furthermore, NS-49 might prove to be a nasal mucosa vasoconstrictor, which will improve nasal obstruction.

Adrenergic alpha-1 Receptor Agonists↗
PubMed1990

Morphological basis for impaired protective efficiency by the nasal mucosa in infants with and without recurrent acute otitis media: a light and electron microscopy study.

The structure of the nasal mucosa in biopsy specimens from the inferior turbinate in 'normal healthy' infants (n = 27) was compared with that in age-matched infants (n = 59) with increased frequency of recurrent acute otitis media (RAOM). Light and transmission electron microscopic examination revealed that the healthy infants, i.e., the control subjects, had almost as extensive structural changes in their nasal mucosa as those with RAOM. Only 1 infant in each group was considered to have normal nasal mucosa from a morphological point of view. The high frequencies of structural abnormalities in the nasal mucosa in infants, healthy or with RAOM, is likely to be due to frequent infections causing damage so often and to such high extent that the repair processes became insufficient and thus did not restore the structure of the nasal mucosa. Mucosal lining defects may decrease the resistance to infections, resulting in frequent relapses further adding to the mucosal damage, i.e., a self-ongoing circle.

Acute Disease↗
PubMed2006

[Effect of radiation on nasal mucosa and the microvascular casting of guinea pig].

OBJECTIVE: To study the histopathologic and microvascular changes in nasal mucosa of guinea pigs following a series of irradiation. METHOD: A total of 84 healthy guinea pig were divided into two groups randomly: the irradiation group (n=72) and the control group (n=12). The animals of the irradiation group were exposed nasally to linear accelerator X-rays at 5.0 Gy once a week for three weeks. At 0.5, 1, 2, 3, 5, 6 month after X-irradiation 12 animals from each group were sacrificed at each time point. The animals of control group did not be irradiated and were sacrificed after 6 month. Their middle nasal turbinate mucosa of 6 animals from each group was observed under optical microscope and scanning electron microscope and the another 6 animals was made microvascular corrosion casts. RESULT: In the irradiation group, the early histopathological transformation was acute inflammatory reaction, nasal mucosa tissues congesting, partial nasal mucosa necrosis or shedding. The inflammation cells infiltrated into the submucosa. The acute inflammatory reaction declined as the time went by. Then the nasal mucosa repaired step by step. But parts of the area were squamous epithelium instead of the normal ciliary structure. Through scanning electron microscope, we found the capillary of nasal mucosa expanded and congested, the vascular endothelial cell swelled. As the time went by, the capillary became deformation and tore and the microvascular networks broke off. All changes which led to capillary density descended. Although partial area had new capillary, but the structure was disordered and had no microcirculation function. CONCLUSION: The nasal mucosa injury, the squamous metaplasia and the microvascular networks broke off can form a pathological basis of dysfunction after irradiation.

Animals↗
PubMed2004

Stability of PEGylated salmon calcitonin in nasal mucosa.

The purpose of this study was to evaluate the stabilization of salmon calcitonin (sCT) by PEGylation in nasal mucosa. Degradation of native sCT in the homogenates of rat nasal mucosa was investigated by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS). The initial cleavage of sCT was due to tryptic-like endopeptidase activity, and the subsequent degradation followed the sequential pattern of aminopeptidase activity. To prepare PEGylated sCT resistant to the proteolytic degradation, the lysine residues susceptible to tryptic activity were selectively PEGylated by controlling reaction pH. The PEGylated sCT showed strong resistance against enzymatic degradation in rat nasal mucosa, with 56-fold prolonged half-life compared with that of native sCT. In the MALDI-TOF MS spectrum, the PEGylated sCT did not show any degradation peak for incubation of 120 min in the homogenates of rat nasal mucosa. The improved stability may be responsible for enhancing nasal absorption of PEGylated sCT.

Animals↗
PubMed1987

Neuropeptide Y and non-adrenergic sympathetic vascular control of the cat nasal mucosa.

Neuropeptide Y (NPY) coexists with noradrenaline (NA) in a population of perivascular nerves in the cat nasal mucosa. In the present study, NPY was found to exert non-adrenergic nasal vasoconstrictor actions. Postganglionic sympathetic nerve stimulation induced a release of NPY-like immunoreactivity (LI) concomitant with vasoconstriction in the nasal mucosa. About 60 and 70% of the vasoconstrictor responses upon sympathetic stimulation at 2 and 10 Hz, respectively, remained after pretreatment with phenoxybenzamine and propranolol which abolished the effects of exogenous NA. Preganglionic denervation one week prior to the experiments did not change the vasoconstrictor response to sympathetic nerve stimulation or the NA or NPY contents of the nasal mucosa. The levels of NPY-LI in the superior cervical ganglion were however reduced. After reserpine treatment, which depleted the nasal NA content by almost 90% and the NPY content by 50%, a vasoconstrictor response to nerve stimulation was still present. After reserpine treatment combined with preganglionic denervation, nerve stimulation simultaneously induced an increased output of NPY-LI and a marked long-lasting vasoconstriction which was not influenced by phenoxybenzamine and propranolol. The reserpine-induced depletion of NA was not influenced by preganglionic denervation while the reduction in the nasal content of NPY-LI was prevented. In conclusion, NPY could be a non-adrenergic mediator of sympathetic vascular effects in cat nasal mucosa.

Animals↗
PubMed1987

Prostaglandins, leukotrienes, and other arachidonic acid metabolites in nasal polyps and nasal mucosa.

Prostaglandins (PGs) and leukotrienes (LTs) are known to play an important role in allergic inflammatory reactions. The triad of aspirin sensitivity, nasal polyposis, and asthma led us to suspect that PGs, LTs and other arachidonic acid metabolites may be involved in the pathogenesis of nasal polyps. The purpose of this study was to determine arachidonic acid metabolites and to measure concentrations of PGs and LTs in nasal polyps and nasal mucosa. Samples of nasal polyps and nasal mucosa were obtained at the time of polypectomies and nasal procedures. Metabolites of arachidonic acid in tissue were determined by incubation of tissue-homogenates with 14C-arachidonic acid and analyses with thin-layer chromatography and high performance liquid chromatography (HPLC). Levels of PGE2, 6-keto-PGF1 alpha, thromboxane (Tx)B2, 15-hydroxyeicosatetraenoic acid (HETE), LTC4, LTB4 were measured by radioimmunoassay. The predominant arachidonic acid metabolite in both nasal polyps and mucosa with 15-HETE. The HPLC analysis showed that the predominant metabolite in nasal polyp was 15-HETE, especially in polyps from aspirin sensitive patients. Levels of 15-HETE and PGE2 were higher in polyps from patients with a history of allergy than from nonallergic patients. Levels of LTC4 and LTB4 in nasal polyps were determined. The findings of this study will help to explain biochemical basis of the pathogenesis of aspirin-sensitive nasal polyps and to develop better medical treatment for them.

6-Ketoprostaglandin F1 alpha↗
PubMed1993

Histamine content, synthesis and degradation in human nasal mucosa.

Histamine content and enzyme activities of histamine metabolism, histidine decarboxylase (HDC), histamine N-methyltransferase (HMT) and histaminase (diamine oxidase, DAO) in human nasal mucosa were determined with a highly sensitive and specific fluorescent method which was combined with high performance liquid chromatography. Histamine content and HDC activity were determined in 10 specimens of nasal polyp, nine specimens of maxillary sinus and five specimens of inferior turbinate. HMT and histaminase activities were determined in 15 specimens of nasal polyp, nine specimens of maxillary sinus and five specimens of inferior turbinate obtained during surgical therapy. Histamine and activities of HDC, HMT and histaminase were detected in all specimens except the case of histaminase activity in one specimen of nasal polyp. The mean values of histamine content and activities of HDC, HMT and histaminase of human nasal mucosa were 137.3 nmol/g wet weight, 26.3 fmol/min/mg protein, 26.4 pmol/min/mg protein and 0.5 pmol/min/mg protein, respectively. Histamine content in the mucosal tissue of the maxillary sinuses was significantly higher than that of nasal polyps or inferior turbinates. There were no significant differences in HDC activities among three kinds of nasal mucosa. Activities of HMT and histaminase, including their kinetic constants (Km and Vmax values for histamine) indicated that HMT has a greater potential than histaminase for histamine degradation in the human nasal mucosa. The presence of these enzymes suggests that these activities constitute an important modulating factor in histamine mediated allergic and inflammatory reactions in human nasal mucosa.

Adolescent↗
PubMed1998

Monocyte chemotactic and activating factor/monocyte chemoattractant protein-1-mediated histamine release from human nasal mucosa.

OBJECTIVES: To demonstrate the existence and localization of monocyte chemotactic and activating factor or monocyte chemoattractant protein-1 (MCAF/MCP-1) in human nasal mucosa and to verify its activity as a histamine-releasing factor. DESIGN: Detection of MCAF/MCP-1 in culture supernatants of nasal mucosa using Western blot analysis and assay of histamine release from basophils induced by these culture supernatants. Detection of MCAF/MCP-1 expression in nasal mucosa of patients with perennial allergic rhinitis using immunohistochemistry. PATIENTS: Twenty-one patients with house dust mite allergy, 7 nonallergic patients, and 5 patients with chronic inflammatory sinusitis participated in the study. All the allergic patients had positive test results for mite nasal allergy, detected by a clinical history, a nasal provocation test, and determination of specific mite IgE antibodies by a radioallergosorbent test. RESULTS: In Western blot analysis of supernatants of explant culture of human nasal mucosa, the band corresponding to approximately 13 to 15 kd was observed. This band was considered to be MCAF/MCP-1. These supernatants induced histamine release from basophils (approximately 3%-5% in net histamine release), and anti-MCAF/MCP-1 antibody inhibited this histamine-releasing activity. Immunoreactivity of MCAF/MCP-1 was observed in the nasal submucosa but not in the epithelium. Immunoreactive cells of MCAF/MCP-1 were also stained with the antibody, which recognizes monocytes and macrophages. CONCLUSIONS: These results suggest that MCAF/MCP-1, which is produced constantly by monocytes and macrophages and is stored in human nasal mucosa, possibly participates in the protracted histamine release from basophils and in the pathogenesis of perennial allergic rhinitis.

Adolescent↗