Anatomical and immunohistochemical considerations on the microinnervation of trachea in humans.
ABSTRACT The anatomy of the tracheal microinnervation is understudied in humans; the purpose of our study was to fill this gap by working on human adult tracheas, to compare the results with those obtained from animal studies, and to checking whether or not these studies are suitable to be translated from comparative to the human anatomy. The study was designed as a qualitative one. The present work was performed on human adult tracheas dissected out in 15 human adult cadavers. Microdissections were performed in eight tracheas and revealed the outer peritracheal plexus, segmentally supplied and distributed to trachea and esophagus, with longitudinal intersegmentary anastomoses but also with bilateral interrecurrential anastomoses previously undescribed in anatomy. Seven different tracheas were transversally cut and paraffin embedded. Histological stains (HE, toluidine blue, luxol fast blue, Giemsa on tissues and trichrome Gieson) and immunohistochemistry using primary antibodies for nNOS, neurofilament, SMA and the cocktail of citokeratines CK AE1-AE3+8/18 were done. According to the histological individual variation, the neural layers of the posterior wall of the human trachea could be considered as it follows: (a) an outer neural layer, ganglionated, associated with the connective covering layers, adventitia and the posterior fibroelastic membrane (external elastic lamina); (b) a submucosal ganglionated neural layer, mainly with juxtaglandular microganglia that may expand, as glands do, through the outer covering layers; (c) intrinsic nerves of the transverse trachealis muscle; (d) the neural layer intrinsic to the longitudinal elastic band (internal elastic lamina) and supplied from the inner submucosa; (e) the neural plexus of the lamina propria, with scarcely distributed neurons. We also bring here the first evidences for the in vivo nNOS phenotype of mast cells that were identified, but not exclusively, within the trachealis muscle.
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ABSTRACT: Intrinsic nerve plexuses of the rat trachea and extrapulmonary bronchi were examined by immunohistochemistry. Three nerve plexuses--peritracheal and peribronchial, intramuscular, and submucosal--were found in the wall of the trachea and bronchi. Nerve cell bodies were located in the peritracheal and peribronchial nerve plexuses. They occurred singly or formed ganglia in the plexus, and regional differences in cell numbers were found in the cervical and thoracic portions of the trachea and in the extrapulmonary bronchia. In total, 83.5 +/- 28.3 ganglia (mean +/- SD, 57-131, n=5) and 749.8 +/- 221.1 nerve cell bodies (540-1,080, n=5) were found in the nerve plexus. The mean densities of ganglia were 0.31, 0.97 and 1.15/mm2, and the mean densities of the nerve cell bodies were 1.82, 9.26 and 11.54/mm2 in the cervical region, thoracic region of trachea, and extrapulmonary bronchi, respectively. Almost all nerve cell bodies in ganglia were positive for choline acetyltransferase and neuropeptide Y (NPY), and a few cells were positive for vasoactive intestinal peptide (VIP). In addition, in cholinergic nerves, a few nerve fibers in the smooth muscles were positive for substance P (SP), calcitonin gene-related peptide (CGRP), and VIP, and a moderate number of fibers were positive for NPY. Tyrosine hydroxylase-immunoreactive nerve fibers were observed around blood vessels and within nerve bundles in the tunica adventitia. In the epithelium, nerve fibers were positive for SP and CGRP. Our results indicate that postganglionic neurons form three layers of cholinergic plexuses in the rat trachea and extrapulmonary bronchi, and that all of these possess intrinsic and extrinsic peptidergic innervation.Archives of Histology and Cytology 04/2004; 67(1):41-55. · 0.60 Impact Factor
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ABSTRACT: Neurally-mediated relaxation of smooth muscle in human, guinea-pig, cat, and pig airways is largely attributed to a nonadrenergic, noncholinergic mechanism. While the specific transmitter(s) of this relaxant system have not been conclusively identified, vasoactive intestinal peptide and nitric oxide have emerged as likely mediators in airway smooth muscle. Both vasoactive intestinal peptide and nitric oxide relax guinea-pig, pig and human smooth muscle. Vasoactive intestinal peptide is present in nerve fibers associated with airway smooth muscle in humans and several animal species. In guinea-pigs, vasoactive intestinal peptide is released during electrical field stimulation of airway strips and the release correlates with the nonadrenergic relaxation. This relaxation is markedly reduced after incubation of tracheal tissue with a specific VIP antibody and by immunization to vasoactive intestinal peptide. Similarly, nonadrenergic relaxations induced by electrical field stimulation are reduced in human, pig, guinea-pig and bovine airways by nitric oxide synthesis inhibitors. Vasoactive intestinal peptide is present in nerve cell bodies of airway ganglia, suggesting that these nerves in airway smooth muscle originate from intrinsic neurons. It is stored in dense-core vesicles of nerve terminals near airway smooth muscle, suggesting that preformed vasoactive intestinal peptide is released by fusion of the vesicles with the cell membrane of the nerve terminal. Nitric oxide is probably generated by a novel mechanism involving de novo synthesis at the nerve terminal during neural activation by the action of the enzyme nitric oxide synthase.(ABSTRACT TRUNCATED AT 250 WORDS)Neuroscience 07/1993; 54(4):839-43. · 3.12 Impact Factor
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ABSTRACT: Asthma is a leading cause of morbidity in children. Risk factors include chronic exposure to allergens and air pollution. While chronically activated mast cells contribute to the pathophysiology of asthma in part through their proteases such as chymase and tryptase, previous studies of airway mast cell abundance and distribution in asthmatics have been inconsistent. To determine whether repeated episodic exposures to environmental pollutants during postnatal lung development alter airway mast cell abundance and distribution, we exposed infant rhesus monkeys to a known human allergen, house dust mite antigen (HDMA), and/or a known environmental pollutant, ozone (O(3)), and quantitatively compared the abundance of tryptase- or chymase-positive mast cells in three airway levels. Mast cells are resident in multiple compartments of the airway wall in infant rhesus monkeys raised from birth in filtered air. Tryptase- and chymase-positive cells were most abundant in trachea and least in terminal bronchioles. The majority of tryptase-positive and almost all chymase-positive cells were in extracellular matrix and smooth muscle bundles. Chronic exposure to HDMA elevated the abundance of both tryptase- and chymase-positive cells in the trachea and intrapulmonary bronchi. Neither exposure to O(3) nor HDMA + O(3) increased mast cell accumulations in the airway wall. We conclude that during postnatal airway development (1) mast cells are a resident airway cell population even in the absence of toxic air contaminants; (2) aeroallergen exposure alters large airway mast cell distribution and abundance, increasing chymase-positive mast cells; and (3) this response is attenuated by exposure to oxidant air pollutants.Toxicological Sciences 07/2010; 116(1):313-22. · 4.33 Impact Factor