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Biomedical subjects

M Merida

Publications and source records attributed to M Merida.

9 recordsLinked to original sources
PubMed1992

Characterization and autoradiographic localization of histamine H1 receptors in human nasal turbinates.

To examine the localization of histamine H1 receptors (H1R) in human nasal mucosa, the autoradiographic distribution of H1R was studied in human nasal inferior turbinates. Cryostat sections were incubated with various concentration of [3H]pyrilamine in saturation-binding studies and with 1 nmol/L of [3H]pyrilamine for autoradiography. Nonspecific binding was determined by adding 2 mumol/L of pyrilamine. Scatchard analysis demonstrated high-affinity binding sites with a maximum binding capacity of H1R of 193 +/- 46 fmol/mg of protein, and dissociation constant was 0.6 +/- 0.1 nmol/L. Autoradiograms indicated H1R exist exclusively on the endothelium of vessels. No specific labeling could be observed in the submucosal glands or epithelium. These results extend and support our previous finding that histamine directly causes vascular permeability through H1R and stimulates nasal glandular secretion indirectly through reflexes.

Autoradiography↗
PubMed1992

Double aortic arch.

In conclusion, the diagnosis of DAA should be suspected in an infant with either biphasic stridor or feeding-related respiratory distress. Radiographic studies combined with appropriate thorough endoscopic evaluation should confirm clinical suspicion. Thoracotomy with surgical division of the DAA has given excellent long-term results.

Aorta, Thoracic↗
PubMed1991

Substance P and neurokinin A in human nasal mucosa.

The tachykinins substance P (SP) and neurokinin A (NKA) were studied in human inferior turbinate nasal mucosa by radioimmunoassay, immunohistochemistry, and autoradiography and for their effect upon mucus release in an in vitro culture system in order to infer their potential functions in the upper respiratory tract. Similar amounts of SP (1.03 +/- 0.12 pmol/g wet weight; mean +/- SEM; n = 26) and NKA (0.76 +/- 0.23; n = 7) were found. NKA and SP immunoreactive nerve fibers were found in the walls of arterioles, venules, and sinusoids and as individual fibers in gland acini, near the basement membrane, and in the epithelium. [125I]SP bound to arterioles, venules, and glands. [125I]NKA bound only to arterioles. In short-term explant culture of fragments of human nasal mucosa, both 1 microM SP and 1 microM NKA stimulated release of [3H]glucosamine-labeled respiratory glycoconjugates. These results indicate that SP and NKA have similar distributions in nociceptive sensory nerves in human nasal mucosa. The distribution of [125I]SP binding sites is consistent with a role for SP as a vasodilator and mucous secretagogue. The presence of [125I] NKA binding sites on vessels suggests a primary role for NKA in regulating vasomotor tone.

Amino Acid Sequence↗
PubMed1990

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↗
PubMed1990

Bradykinin and respiratory mucous membranes. Analysis of bradykinin binding site distribution and secretory responses in vitro and in vivo.

Bradykinin (BK) and lysyl-BK (lys-BK, kallidin) have been proposed as potentially important mediators of rhinorrhea. Possible mechanisms by which BK might contribute to rhinorrhea were investigated by several approaches. (1) The autoradiographic distribution of 125I-BK binding sites in human inferior turbinate nasal mucosa was determined. (2) The effects of BK and lys-BK and antagonists on radiolabeled respiratory glycoconjugate (RGC) release from human nasal mucosa was measured. (3) The secretory effects of BK were studied in cat tracheal mucosa maintained in short-term explant culture, and in ferret trachea maintained in Ussing chambers. (4) The effects of BK on macromolecule secretion in guinea pig nasal mucosa was studied in vivo. Autoradiographic examination of human nasal mucosa revealed that 125I-BK specifically bound to small muscular arteries, venous sinusoids, and submucosal fibers. No specific binding to submucosal glands or goblet cells was noted. Human nasal fragments secreted significantly increased amounts of RGC in response to 10 microM BK (15.0% +/- 1.8 compared with control values; mean +/- standard error of the mean; n = 7; p less than 0.01 by Student's unpaired t test), 10 microM lys-BK (12.2% +/- 3.3; n = 5; p less than 0.05), and 100 microM methacholine (35.7% +/- 2.3; p less than 0.0001). The addition of 1 microM BK, or 1 microM lys-BK, did not induce release. The addition of the BK receptor antagonist des-Arg9-[Leu8]-BK (10 microM) or inhibition of arachidonic acid metabolism with 50 microM nordihydroguaiaretic acid or 65 microM ibuprofen inhibited the prosecretory effect of 10 microM BK.(ABSTRACT TRUNCATED AT 250 WORDS)

Albumins↗
PubMed1990

Neuropeptide Y (NPY) in human nasal mucosa.

Neuropeptide Y (NPY), a potent vasoconstrictor peptide found in sympathetic neurons, was analyzed in human inferior turbinate nasal mucosal tissue. NPY content determined by radioimmunoassay was 3.13 +/- 0.79 pmol/g tissue (n = 6) in mucosa extracted with ethanol-acetic acid. NPY-immunoreactive nerves were found around small muscular arteries, arterioles, arteriovenous anastomoses, and as free fibers near arteriolar and venous vessels. They formed a plexus around the arterial vessels, and were also present between vascular smooth muscle cells. Few NPY fibers were present near glands or the epithelium. [125I]NPY binding sites were localized by autoradiography to small muscular arteries, arterioles, and a few venous sinusoids. In explant culture experiments, 4 microM NPY did not stimulate release of [3H]glucosamine-labeled glycoconjugates or lactoferrin (a product of serous cells) from nasal mucosal fragments. Degradation of NPY by a tissue homogenate was rapid (t1/2 = 13.5 +/- 2.3 min). The degradation was inhibited by thiorphan and phosphoramidon, inhibitors of neutral endopeptidase activity. NPY released from sympathetic neurons may play a role as a constrictor of arterial vessels and regulate vasomotor tone in the human nasal mucosa.

Arteries↗
PubMed1990

Gastrin-releasing peptide in human nasal mucosa.

Gastrin-releasing peptide (GRP), the 27 amino acid mammalian form of bombesin, was studied in human inferior turbinate nasal mucosa. The GRP content of the mucosa measured by radioimmunoassay was 0.60 +/- 0.25 pmol/g tissue (n = 9 patients; mean +/- SEM). GRP-immunoreactive nerves detected by the immunogold method of indirect immunohistochemistry were found predominantly in small muscular arteries, arterioles, venous sinusoids, and between submucosal gland acini. 125I-GRP binding sites determined by autoradiography were exclusively and specifically localized to nasal epithelium and submucosal glands. There was no binding to vessels. The effects of GRP on submucosal gland product release were studied in short-term explant culture. GRP (10 microM) significantly stimulated the release of the serous cell-specific product lactoferrin, and [3H]glucosamine-labeled glycoconjugates which are products of epithelial goblet cells and submucosal gland cells. These observations indicate that GRP released from nerve fibers probably acts on glandular GRP receptors to induce glycoconjugate release from submucosal glands and epithelium and lactoferrin release from serous cells, but that GRP would probably not affect vascular permeability.

Autoradiography↗
PubMed1990

Vasoactive intestinal peptide in human nasal mucosa.

Vasoactive intestinal peptide (VIP), which is present with acetylcholine in parasympathetic nerve fibers, may have important regulatory functions in mucous membranes. The potential roles for VIP in human nasal mucosa were studied using an integrated approach. The VIP content of human nasal mucosa was determined to be 2.84 +/- 0.47 pmol/g wet weight (n = 8) by RIA. VIP-immunoreactive nerve fibers were found to be most concentrated in submucosal glands adjacent to serous and mucous cells. 125I-VIP binding sites were located on submucosal glands, epithelial cells, and arterioles. In short-term explant culture, VIP stimulated lactoferrin release from serous cells but did not stimulate [3H]glucosamine-labeled respiratory glycoconjugate secretion. Methacholine was more potent than VIP, and methacholine stimulated both lactoferrin and respiratory glycoconjugate release. The addition of VIP plus methacholine to explants resulted in additive increases in lactoferrin release. Based upon the autoradiographic distribution of 125I-VIP binding sites and the effects on explants, VIP derived from parasympathetic nerve fibers may function in the regulation of serous cell secretion in human nasal mucosa. VIP may also participate in the regulation of vasomotor tone.

Cells, Cultured↗