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PubMed1990

Activation of N-nitrosobis(2-oxopropyl)amine by liver and nasal mucosa tissue from intact and castrated male rats.

Methylation of liver and nasal mucosal DNA at the O6 position of guanine (O6-MeG) was measured in intact and castrated male rats after a dose of N-nitrosobis(2-oxopropyl)amine (BOP) (20 mg/kg; i.p.). There were no differences in O6-MeG persistence in liver DNA from either group. In the nasal mucosa more O6-MeG was detected in DNA from intact rats than in that from castrated rats. The maximum values were 61 (intact) and 35 (castrated) mumols/mol guanine. T/2 were 84 h (intact) and 24 h (castrated). These situations corresponded with changes in O6-MeG-DNAmethyl-transferase (MT) activity, which increased 6-fold in the nasal mucosa by castration resulting in less O6-MeG in the nasal mucosa. In the liver castration halved MT activity but did not produce a comparable change in O6-MeG levels. The mutagenicity of BOP in V79 cells increased almost 2-fold when a liver homogenate from castrated rats was used as the activating system. There was a comparable decline in mutagenicity when a nasal mucosa tissue homogenate from castrated rats was used.

Animals↗
PubMedDate not supplied

Histamine receptor type coupled to nitric oxide-induced relaxation of guinea-pig nasal mucosa.

1 The aim of this study was to characterize the histamine receptor type mediating relaxation of the vascular bed of the nasal mucosa from the guinea-pig, and to determine the role of cyclo-oxygenase products and nitric oxide in this relaxant response to histamine. These studies were performed in isolated nasal mucosae examined in vitro to obtain potencies of histamine receptor-type selective agonists in causing vasorelaxation and to determine affinities of histamine receptor antagonists for inhibiting histamine-induced relaxation. 2 After contraction of nasal mucosae with noradrenaline, histamine caused a maximal relaxation response that was 75 +/- 6% of the contraction caused by noradrenaline with a mean EC50 value of 4.3 +/- 0.5 microM. Neither dimaprit (H2-receptor selective) nor R-alpha-methylhistamine (H3-receptor selective) caused significant relaxation of nasal mucosae. In contrast, betahistine (H1-receptor selective) caused an 81 +/- 7% relaxation of noradrenaline-induced tone with an EC50 value of 15 +/- 1 microM. 3 pA2 experiments were performed to obtain KB values of chlorpheniramine (H1-receptor selective) and diphenhydramine (H1-receptor selective) for blocking histamine-stimulated relaxation of nasal mucosae. KB values for chlorpheniramine (0.87 nM) and diphenhydramine (7.4 nM) were consistent with their interaction at the H1-receptor type. Additionally, neither 10 microM cimetidine (H2-receptor selective) nor 1 microM thioperamide (H3-receptor selective) had any effect on the relaxation curve for histamine. 4 In the presence of 10 microM indomethacin (cyclo-oxygenase inhibitor), histamine caused a maximal relaxation response of 73 +/- 5% of the noradrenaline-induced tone with an EC50 value of 2.9 +/- 0.2 microM, which was not different from control values (EC50 = 5.0 +/- 0.4 microM; maximal relaxation = 71 +/- 6%). In contrast, 200 microM NG-nitro-L-arginine (nitric oxide synthase inhibitor) completely inhibited histamine-induced relaxation of nasal mucosae. 5 In conclusion, data from the present study suggest only the H1-receptor type mediates relaxation of nasal mucosal blood vessels to histamine, and histamine-induced relaxation of nasal mucosae is entirely dependent on nitric oxide production.

Adrenergic alpha-Agonists↗
PubMed1999

Nasal drug delivery--evaluation of an in vitro model using porcine nasal mucosa.

An in vitro model for permeation studies using porcine nasal mucosa was developed and evaluated. The viability and integrity of the mucosa were determined by electrophysiological measurements, permeation studies involving 14C-mannitol and D-(2-3H) glucose, histological studies and a biochemical assay. Enzymatic activity in the mucosa was determined by serosal addition of ouabain. Three different types of porcine nasal mucosa (cavity mucosa, natural septum mucosa and dermatomed septum mucosa) were examined. The results showed that cavity mucosa was the most suitable; this type remained viable for up to 8 h after removal. Lower limits for electrophysiological data were defined in order to establish criteria for tissue viability. This in vitro method using porcine nasal mucosa appears potentially valuable as a tool for further permeation and mechanistic studies within nasal drug delivery research.

Administration, Intranasal↗
PubMed1995

Proliferative activity of mast cells in allergic nasal mucosa.

The proliferative activity of mast cells in the nasal mucosae of allergic (n = 14) and non-allergic (n = 18) rhinopathic patients was studied by a sequential double immunohistochemistry using anti-proliferating cell nuclear antigen (PCNA) and anti-tryptase antibodies. Two hundred to 300 tryptase-positive cells (mast cells) were studied in each allergic nasal epithelium. In case of non-allergic nasal mucosa, only a few mast cells existed in the epithelial layer. The total number of mast cells which we could detect in all patients was 168 cells. One of these cells contained PCNA. Three hundred to 500 mast cells were studied in each subepithelial layer and deep layer of lamina propria of both diseases. PCNA-positive mast cells were observed in the nasal epithelia of 10 allergic patients. In the subepithelial layer, PCNA-positive mast cells were observed eight allergic patients and four non-allergic patients, respectively. In the deep lamina propria, PCNA-positive mast cells were observed in a few patients with both diseases. The percentage of PCNA-positive mast cells of all mast cells each area ranged from 0 to 1.7%. The incidence of PCNA-positive mast cells was statistically higher in the allergic epithelium and subepithelial layer than in the deep layer of lamina propria. Moreover, that of PCNA-positive mast cells in the subepithelial layer was higher in allergic than in non-allergic nasal mucosa. Our results suggest that mast cell proliferation may contribute to the number of mast cells in the nasal epithelium and subepithelial layer of allergic patients.

Adolescent↗
PubMed2002

Expression of mRNA transcripts of the Na+/H+ and Cl-/HCO3- exchanger isoforms in human nasal mucosa.

Electrolyte transport by nasal epithelia has been suggested to be important for controlling the quantity and composition of the nasal fluid and may play an important role in the development of nasal polyps. One of a number of mechanisms involving translocation of Na+ and Cl- across cell membranes includes electroneutral processes, such as Na+/H+ exchange (NHE) and Cl-/HCO3- exchange (AE). The present study evaluated the presence of mRNAs for various members of the human NHE and AE gene families in human inferior turbinate mucosa and nasal polyp using reverse transcriptase polymerase chain reaction and in situ hybridization. The mRNA for NHE1 was detected in human turbinate mucosa and nasal polyp while the mRNAs for NHE2 and NHE3 could not be detected in any of the samples examined. Of the AE isoforms, AE2 mRNA was expressed in inferior turbinate mucosa but not in nasal polyp. In situ hybridization revealed that NHE1 mRNA in the turbinate mucosa and nasal polyp was localized in the epithelial layer and submucosal glands. AE2 mRNA was also expressed in the epithelial layer and submucosal glands of inferior turbinate mucosa. Taken together, these results indicate that the expression of AE2 mRNA is altered in nasal polyp compared with inferior turbinate mucosa, suggesting that the altered expression of these genes in nasal polyp may cause impaired electrolyte and water transport across the epithelial cells.

Adult↗
PubMed2004

Effect of glucocorticoid on upregulation of histamine H1 receptor mRNA in nasal mucosa of rats sensitized by exposure to toluene diisocyanate.

OBJECTIVE: Histamine is a major chemical mediator in the development of nasal allergy, which is characterized by nasal hypersensitivity. In this study, we used rats sensitized by exposure to toluene diisocyanate (TDI) as an animal model of nasal hypersensitivity and examined changes in expression of histamine H1 receptor (H1R) in the nasal mucosa. The effect of glucocorticoid on upregulation of H1R in nasal mucosa induced by TDI was also examined. MATERIAL AND METHODS: In rats sensitized by exposure to TDI, nasal allergy-like behavior was scored during a 10-min period after TDI provocation. The expression of H1R in the nasal mucosa was determined by means of a real-time quantitative reverse transcriptase polymerase chain reaction and a [3H]mepyramine binding assay. RESULTS: In TDI-sensitized rats, nasal allergy-like behavior, such as sneezing and watery rhinorrhea, was induced after intranasal application of TDI and nasal hypersensitivity to histamine was significantly increased. The level of H1R mRNA expression and the specific binding of [3H]mepyramine in the nasal mucosa were significantly increased after intranasal application of TDI in TDI-sensitized rats. Pretreatment with dexamethasone significantly reduced both nasal allergy-like behavior and the upregulation of H1R induced by TDI in the rats. CONCLUSION: As shown in TDI-sensitized rats, our findings suggest that the upregulation of H1R in the nasal mucosa is one of the mechanisms responsible for nasal hypersensitivity behavior and nasal hypersensitivity to histamine and that the therapeutic effects of dexamethasone are, in part, due to its inhibitory action on the upregulation of H1R.

Animals↗
PubMedDate not supplied

Histochemical demonstration of peripheral autonomic innervation in canine nasal mucosa by retrograde axonal transport of horseradish perioxidase.

The peripheral autonomic nervous pathways of the nasal mucosa in dogs were investigated by the horseradish peroxidase (HRP) method. HRP was applied to the nasal mucosa, caudal nasal nerve, ethmoidal nerve, vidian nerve and pterygopalatine ganglion in 20 dogs, and retrogradely labelled neurons were observed in the superior cervical ganglion (SCG) and the pterygopalatine ganglion (PPG) by the blue reaction method. It was suggested that the vidian nerve, the maxillary branch of the trigeminal nerve, the caudal nasal nerve, the pterygopalatine nerve and the ethmoidal nerve contained the postganglionic sympathetic fibres which originated in SCG and terminated in the nasal mucosa. Moreover, other sympathetic pathways, such as those around the blood vessels, were also suggested to be a main route. It was suggested that the postganglionic parasympathetic fibers originating in PPG travelled along the caudal nasal nerve and the ethmoidal nerve.

Animals↗
PubMed1996

Differential expression of vascular cell adhesion molecule mRNA and protein in nasal mucosa in response to IL-1 or tumor necrosis factor.

IL-1 and tumor necrosis factor (TNF) are cytokines that share many overlapping functions, including induction of expression of the vascular cell adhesion molecule (VCAM) by endothelial cells. However, because most studies of cytokine induction of adhesion molecules have used human umbilical vein endothelial cells (HUVECs) and not microvascular endothelial cells, the functional significance of such observations to sites of allergic inflammation, such as the nasal mucosa, are at present unknown. We have therefore used nasal mucosa to compare the functional response of these microvascular endothelial cells with HUVECs. HUVECs or nasal mucosal explants were stimulated in vitro with varying concentrations of IL-1 or TNF for 0 to 48 hours, and VCAM mRNA and protein expression were determined by means of immunostaining and in situ hybridization. TNF and IL-1 were equivalent in their ability to induce VCAM mRNA and protein expression by HUVECs. In contrast, TNF was significantly more potent than IL-1 in inducing VCAM mRNA and protein expression by nasal mucosal microvascular endothelial cells. The recovery of significant amounts of IL-1 after incubation of recombinant IL-1 with nasal mucosa, as well as the ability of IL-1 to induce intercellular adhesion molecular expression by nasal mucosa, suggests that neither degradation of IL-1 nor downregulation of IL-1 receptors in nasal mucosa is likely to explain the inability of IL-1 to induce VCAM expression by nasal mucosa. These studies suggest that microvascular endothelial cells in the nasal mucosa differ functionally from HUVECs and that TNF may be more important than IL-1 in induction of VCAM expression in the nasal mucosa.

Cells, Cultured↗
PubMedDate not supplied

Characteristics of capillary permeability in nasal mucosa.

The transendothelial passage of horseradish peroxidase (HRP) and colloidal carbon and diffusion of HRP in pericapillary space, injected intravenously into rats, was studied at the light microscopic and ultrastructural level in the nasal mucosa. In the lamina propria of the mucosa in the middle third of the nasal septum of rats, the capillaries directly beneath the epithelium were mostly with fenestrae, while the capillaries around the nasal gland were without the fenestrae. The permeability of the capillaries in the lamina propria of the nasal mucosa was very high and some of the endothelial cells were wide open, like liver sinusoid, allowing free passage of carbon pasrticles. Marked transendothelial passage was also noted at ten seconds after HRP infusion through the capillaries without fenestrae located around the nasal gland. On the other hand, no extracapillary leakage of HRP was noted even at 150 seconds after its infusion in the capillaries without fenestrae located in the muscles. The permeability of small venules located in the lamina propria of nasal mucosa also was extremely high. The reasons for the greater permeation of HRP through capillaries of nasal mucosa are as follows. First, the endothelial cell junction was loose in the nasal mucosa and in some capillaries endothelium had holes like liver sinusoid. Second, interstitium surrounding the capillary was loose in nasal mucosa.

Animals↗
PubMed1987

Retrograde axonal transport of true blue dye by the peripheral autonomic nerves in canine nasal mucosa.

In this study we employed retrograde axonal transport of (E)-2,2'-vinylendi-benzofuran-5-carboxamidin-diaceturate+ ++ or true blue (TB) to study the peripheral autonomic innervation of the canine nasal mucosa. After injection of TB into the nasal mucosa, labeled neurons were found in the ipsilateral sphenopalatine ganglion (SPG) and the superior cervical ganglion (SCG). There were no labeled neurons in the middle cervical or stellate ganglia. This indicated that the origin of the postganglionic sympathetic fibers of the nasal mucosa was only from the ipsilateral SCG. When TB was injected into the nasal mucosa of dogs following a caudal or ethmoidal neurectomy, labeled neurons could still be found in the SPG and SCG. When TB was injected into the nasal mucosa of dogs following ethmoidal and vidian neurectomies or with maxillary neurectomy added, some labeled neurons could still be found in both the ipsilateral SPG and SCG. These results support the concept that another pathway--perhaps perivascular--exists for postganglionic sympathetic fibers other than the vidian and ethmoidal nerves. Labeled neurons were still observed in SPG when TB was applied to the canine nasal mucosa following neurectomy of either the ethmoidal or the caudal nasal nerve. However, retrograde labeled neurons could not be found in SPG following simultaneous neurectomies of the ethmoidal and caudal nasal nerves. These results show that the postganglionic parasympathetic fibers originating in the SPG travel along the ethmoidal and caudal nasal nerves.

Animals↗
PubMed1998

Characterization and localization of thromboxane A2 receptor in human and guinea-pig nasal mucosa using radiolabelled (+)-S-145.

1. TxA2 receptor (TP-receptor) antagonists such as S-1452 and Bay u 3405 have been shown to be effective in alleviating nasal blockage in patients with allergic rhinitis as well as guinea-pig allergic rhinitis models. The present study was conducted to examine the existence and localization of the TP-receptor in human and guinea-pig nasal mucosa by in vitro receptor binding autoradiography using radiolabelled (+)-S-145, which is a potent and specific TP-receptor antagonist with an extremely slow dissociation rate. 2. We ascertained the binding specificity of [3H]-(+ )-S-145 in human and guinea-pig platelet membranes by comparing the ability of four TP-receptor ligands of U-46619, (+)-S-145, I-(+)-S-145 and Bay u 3405 to displace the specific binding of [3H]-(+)-S-145 and [3H]-U-46619. The rank order of potency (Ki) for the displacement was correlated highly with that determined from [3H]-U-46619 binding to the same preparations. 3. Quantitative autoradiography using a radioluminographic imaging plate system, in which the radioactivity of [3H]-(+)-S-145 is expressed as photostimulated luminescence (PSL) per area (mm2), revealed that specific binding of [3H]-(+)-S-145 to human and guinea-pig nasal mucosa was saturable. Scatchard analysis showed about three fold higher affinity and two fold greater maximal binding to the nasal mucosa of humans than that of guinea-pigs: the KD and Bmax values in human mucosa were 2.82+/-0.35 nM and 6.47+/-0.33 PSL mm(-2) and those in guinea-pig mucosa were 8.23+/-1.93 nM and 3.37+/-0.66 PSL mm(-2), respectively. 4. Specific [3H]-(+)-S-145 binding to cryostat sections of human and guinea-pig nasal mucosa was displaced by another TP-receptor antagonist, Bay u 3405, and a TP-receptor agonist, U-46619. The order of potency (Ki value: nM) was (+)-S-145 (2.5) > Bay u 3405 (15.4) > > U-46619 (359.6) in human nasal mucosa and (+)-S-145 (22.8) > U-46619 (49.8) approximately Bay u 3405 (62.1) in guinea-pig nasal mucosa. These rank orders showed rather good correlation with those obtained for the respective platelet membranes. 5. Autoradiographs of human nasal mucosa demonstrated that specific [125I]-(+)-S-145 binding sites mainly exist on the smooth muscle layers of venous sinusoids and arterioles in the lamina propria, with few or no binding sites in the epithelium and nasal gland. 6. We concluded that radiolabelled (+)-S-145 can be used as a TP-receptor ligand for autoradiographic study, and that the TP-receptor is exclusively located on smooth muscle layers of venous sinusoids and arterioles in the nasal mucosa. The potent vasoconstrictive activity of TxA2 may cause reduction of local blood flow followed by mucosal oedema probably through mechanisms of vascular injury such as ischaemia-reperfusion.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1992

Neuropeptide Y is a vasoconstrictor in human nasal mucosa.

Neuropeptide Y (NPY) is a neurotransmitter in sympathetic nerve fibers in human nasal mucosa. Like norepinephrine, NPY acts as a vasoconstrictor. An established method of nasal provocation was used to determine the effects of topically applied NPY on nasal resistance to airflow measured by anterior rhinomanometry, the protein content of nasal secretions, and the protein content of bradykinin-induced secretions. NPY (2.3 nmol) reduced the resistance to inspiratory airflow by 57 +/- 18% (P < 0.001) in 10 normal subjects and by 50 +/- 17% (P < 0.05) in 12 subjects with perennial rhinitis. In nasal provocations, NPY in doses of 0.1-10 nmol had no effect on vascular (albumin), glandular (lysozyme, glycoconjugate), or total proteins present in lavaged nasal secretions. Because the vasoconstrictor properties of NPY may only be apparent in the presence of increased vascular permeability and albumin exudation, bradykinin (BK) nasal provocation was performed. BK (500 nmol) significantly increase total protein (10- to 20-fold), albumin (10- to 30-fold), and glycoconjugate (2- to 5-fold) in lavage fluid. NPY (2.3 nmol) reduced BK-induced total protein by 59 +/- 15% (P < 0.05) and albumin by 63 +/- 17% (P < 0.02) but had no significant effect on glandular secretion. Therefore exogenous administration of NPY to the human nasal mucosa reduced nasal airflow resistance and albumin exudation without affecting submucosal gland secretion. NPY agonists may be useful for the treatment of mucosal diseases characterized by vasodilation, vascular permeability, and plasma exudation.

Adult↗
PubMed1989

Hemophilus influenzae adherence to and absorption from the nasal mucosa of guinea pigs.

The adherence to and the absorption from nasal mucosal epithelium of type b and non-typeable strains of Hemophilus influenzae were studied in guinea pigs. H. influenzae bacteria were administered to the nose as 4 x 10(7) organisms in 1.0 ml saline. The outer membrane vesicles (OMV) of H. influenzae were used in the absorption study. Scanning electron microscopic studies showed that H. influenzae cells attached to both ciliated and non-ciliated cells of the nasal mucosa. Histological studies showed that OMV were absorbed through the nasal mucosa, mainly from ciliated cells. Further, penetration of OMV through the nasal mucosa of immunized animals was reduced when compared with that of non-immunized ones.

Animals↗
PubMed1990

[An observation of the effect of sulfur dioxide on rat nasal mucosa].

This paper reports the effect of SO2 on rat nasal mucosa. The rats were forced to inhale SO2 and the effect on the nasal mucosa observed. The rats were divided into four groups. The first group inhaled 10ppm SO2; the second group 20ppm; the third group 40 ppm and the fourth group served as control. The observation lasted for 6 months. It was found that the nasal mucosa in the control group remained columnar ciliated. In the experimental groups, during the early stage (groups I, II) of exposure, there was no significant morphological change in epithelium. Then (groups I, II) the epithelium changed into cuboidal with complete disappearance of cilia, only some short and slender microvilli remained. While in the late stage (group III), the epithelium had transformed into squamous stratified and the amount of mucosal glands reduced.

Animals↗
PubMed1987

Enzyme histochemistry of the rat nasal mucosa embedded in cold glycol methacrylate.

The nasal passages are anatomically complex, and while there have been a number of descriptions of nasal structure in many species, there is very little information available on the distribution of enzymes in the nasal mucosa. In rodents, this delicate mucosa is the first site within the respiratory tract to be exposed during inhalation toxicology studies designed to assess human risks from such exposures. However, the nasal mucosa presents problems for histologic preparation because it is encased in brittle bones. Because of recent interest in the nose as a target site, and findings from biochemical studies which indicate that the nose is very active metabolically, studies were carried out to determine the value of cold glycol methacrylate (GMA) processing for localization of nasal enzymes. For these studies, liver and kidney were used as positive controls. Published histochemical procedures for acid and alkaline phosphatase, adenosine triphosphatase, glucose-6-phosphatase, gamma-glutamyl transpeptidase, and naphthyl butyrate esterase were applied, with modifications, to undecalcified nasal passages of Fisher-344 rats. Frozen sections exhibited excellent enzyme preservation but very poor morphology, while GMA gave good enzyme preservation and excellent morphology. For GMA, acetone fixation generally resulted in the best preservation of enzyme activity. It was concluded that cold GMA processing provides a useful approach to studies of nasal enzyme distribution and that this technique of value for inhalation toxicology studies. Details of enzyme distribution in the squamous, respiratory, and olfactory epithelia, associated glands, and other structures of the nose of the rat are described and discussed.

Acid Phosphatase↗
PubMed1986

Characterization of alpha-adrenoceptors in the vasculature of the canine nasal mucosa.

alpha-Adrenoceptors present in the vasculature of the nasal mucosa in beta-adrenoceptor blocked dogs have been characterized pharmacologically using selective alpha 1- and alpha 2-adrenoceptor agonists and antagonists. In pentobarbitone-anaesthetized dogs, intra-arterial (i.a.) administration of the selective alpha 1-agonists cirazoline and phenylephrine, the selective alpha 2-agonist UK-14,304 and the mixed alpha 1/alpha 2-agonists adrenaline, noradrenaline and oxymetazoline produced dose-related nasal vasoconstrictor responses (as measured by decreases in nasal cavity pressure). The rank order of agonist potency was adrenaline greater than oxymetazoline = UK-14,304 greater than noradrenaline greater than cirazoline greater than phenylephrine. The nasal response to cirazoline was inhibited by the selective alpha 1-adrenoceptor antagonist prazosin but not by the new, potent selective alpha 2-adrenoceptor antagonist RX811059. In contrast, UK-14,304 was inhibited only by RX811059. Either prazosin or RX811059 reduced the effect of the mixed agonist adrenaline. In spinal dogs, the noradrenaline-evoked fall in nasal cavity pressure was reduced by either prazosin or RX811059. Prazosin attenuated markedly the nasal vasoconstrictor response to electrical stimulation of postganglionic fibres emerging from the superior cervical ganglion (SNS) whereas RX811059 was ineffective. Administration of the neuronal re-uptake inhibitor cocaine potentiated the effect of i.a. noradrenaline but reduced marginally the maximal response to SNS. After cocaine, RX811059 enhanced the effect of SNS and attenuated the response to noradrenaline. Prazosin reduced effectively the responses to both SNS and noradrenaline after cocaine. Pretreatment with the alpha 2-agonist UK-14,304 did not affect the response to noradrenaline in the nasal cavity but evoked a persistent (up to 2 h) reduction in the response to SNS. RX811059 antagonized the inhibitory effect of UK-14,304. These results demonstrate that both postjunctional alpha 1- and alpha 2-adrenoceptors mediating vasoconstriction are present in the canine nasal mucosa. In addition, sympathetic neurones innervating the nasal mucosa are characterized by a very efficient re-uptake process and contain prejunctional alpha 2-adrenoceptors.

Adrenergic alpha-Agonists↗
PubMed1996

[Immune complex detection in nasal mucosa of patients with chronic and permanent nasal obstruction].

Thirty patients with rhinologic problems and in which the main symptom was "Permanent Nasal Blockade" were studied. We found that they presented a "Permanent and Total Chronic Nasal Blockade"-an entity defined by us as a permanent chronic obstruction of the nasal cavities that would be the clinical and anatomopathologic expression and the immunological terminal phase of "Chronic Rhinitis", leading to Chronic Respiratory Nasal Insufficiency. The main symptoms of these "buccal breathers" were: throat dryness, night snores, nasal resonance of the voice, mechanic and secondary disturbances derived from mouth breathing, such as pharingitis, laryngitis, bronchitis, bronchial asthma and a tendency towards emphysema; dystrophia of the facial bones, disminution of the intellectual capacity, irritability, lack of concentration; disturbances of the circulatory function (alterations of the cardiac rhythm and of the blood pressure). The patients were adolescents and young adults in which allergic and infectious causes dominated the etiology, showed by family allergic and personal atopic antecedents, positive intradermic tests for aeroallergenes and bacteria and corroborated by increase of immunoglobulin E and of blood eosinophiles. The methods of diagnosis used to verify the "Permanent and Total Chronic Nasal Blockade" were: X-rays, lineal tomography; rhinomanometry and rhinofibrolaringoscopy. The anatomopathologic results obtained by nasal biopsy showed a lymphomonocitary infiltrate around arterioles and venules: signs of vasculitis. All this led us to search for immunocomplexes. The presence of positive immunocomplexes surrounding the vessels contributed to a more precise focusing of the physiopathology, diagnosis and treatment of "Permanent and Total Chronic Nasal Blockade".

Adolescent↗
PubMed1994

The early development of sino-nasal mucosa.

The development of human nasal mucosa was studied in 20 fetal heads between 8 and 24 weeks of gestation. Initially the nasal cavity is lined by a single layer of flattened cells, which produces two to three layers of undifferentiated spherical cells. Olfactory epithelium lines the cranial portion of the human fetal nasal cavity at 8 weeks of gestation. Pseudostratified ciliated cuboidal or columnar epithelium appears at 9 weeks of gestation in the nasal cavity and between 14 and 16 weeks of gestation in the primitive ethmoid sinuses and maxillary sinus infundibulum. Goblet cells and glandular acini appear between 12 and 14 weeks of gestation. Initially these goblet cells/glands are found predominantly in the anterior nasal cavity but are more evenly distributed at 24 weeks of gestation. The epithelial development of the nasal septum generally precedes that of the lateral nasal wall. This study documents nasal mucosal maturation and associated anatomic development in the human fetus.

Embryonic and Fetal Development↗