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PubMedDate not supplied

Incidence of short trachea in patients with myelomeningocele.

Short trachea, typically due to reduced tracheal cartilage ring number, produces high tracheal bifurcation which can be demonstrated in radiographs with evaluable air bronchograms. Accidental bronchial intubation with sequelae has been reported in short trachea patients who have tracheal intubation. Short trachea is associated with a number of syndromes, including DiGeorge anomaly and several types of congenital heart disease and skeletal dysplasias. Review of chest radiographs of 87 patients with myelomeningocele revealed that 31 (36%) had short tracheas. Two patients had a total of 3 episodes of bronchial intubation. This degree of association of short trachea with myelomeningocele, the frequency of myelomeningocele, and the number of surgical procedures performed on many such patients suggest that special attention to the short trachea is warranted in myelomeningocele patients because of the risk of accidental bronchial intubation and subsequent sequelae. Twelve (14%) of the myelomeningocele patients lacked radiographic evidence of the presence of twelfth ribs and 11 (13%) had hypoplasia of the twelfth ribs.

Adolescent↗
PubMed2000

The lack of compound 48/80-induced contraction in isolated trachea of mast cell-deficient Ws/Ws rats in vitro: the role of connective tissue mast cells.

In the rat trachea, two types of mast cells have been identified, connective tissue mast cells and mucosal mast cells. Their different characteristics may account for their different biological functions. The role of connective tissue mast cells in tracheal contraction as one feature of the immediate reaction of asthma was studied in vitro in isolated trachea, using tissue derived from mast cell-deficient (Ws/Ws) rats, heterozygous (Ws/+) rats and control (+/+) rats, and compound 48/80 as a potent inducer of mast cell degranulation. The contractile response of tracheas from the three types of rats was also studied upon exposure to the following spasmogens: histamine, 5-hydroxytryptamine (5-HT), and carbachol. Histamine content in tissues reflected the differing mast cell numbers in strips from the three rat types. It was found that carbachol and 5-HT elicited tracheal contraction in a similar manner in strips from the three types of rats. Histamine had no contractile effect. Compound 48/80, at a dose of 25 microg/ml, elicited contraction in tracheas from both control (+/+) and heterozygous (Ws/+), but not in trachea from Ws/Ws rats. Compound 48/80-induced contractions in tracheas from +/+ rats were inhibited by 0.1 microM ketanserin and 0.1 microM nedocromil, but not by 0.1 microM mepyramine. Enzyme histochemistry confirmed that the degranulation occurred in connective tissue mast cells, but not in mucosal mast cells. We concluded that connective tissue mast cells play an important role in rat tracheal contraction via 5-HT release induced by compound 48/80. In addition, the specific mast cell-deficient (Ws/Ws) rats provide a good tool for studying the roles of mast cells in airway system.

Animals↗
PubMed1997

Brief exposure of air-filled guinea-pig isolated trachea to low levels of toluene diisocyanate (TDI) vapor in vitro increases reactivity to methacholine.

Toluene diisocyanate (TDI) causes occupational asthma characterized by inflammation and hyperreactivity of airways to irritants and bronchoconstrictor drugs. We examined the non-immune, direct effect of TDI on airway reactivity in vitro in the absence of an inflammatory response using the guinea-pig isolated, perfused trachea preparation to measure reactivity to methacholine (MCh), and fixed point ion mobility spectrometry to measure moment to moment levels of TDI vapor in air that was delivered to the tracheal mucosa. MCh was added to the mucosal modified Krebs-Henseleit (MKH) perfusing solution to generate control concentration-response curves for contractile responses. The lumen was then emptied and perfused with air or air containing 5, 20 or 70 ppb TDI vapor, after which the trachea was perfused with MKH solution and reactivity to MCh was re-examined. After only 30 min of treatment, TDI vapor concentration-dependently increased reactivity of the trachea to MCh (2.4- and 2.9-fold, respectively, for 20 and 70 ppb TDI; 5 ppb TDI and air alone had no effect). In tracheas treated in vitro with 2 microM capsaicin to deplete tachykinins, TDI caused the same (4-fold) increase in reactivity to MCh that was observed in control tracheas. However, TDI vapor (70 ppb) no longer enhanced reactivity to MCh in tracheas from which the epithelium had been removed. Our results indicate that a direct, non-immune, non-inflammatory action of TDI on respiratory epithelium leads to hyperreactivity of airways in vitro.

Air↗
PubMed1998

Bradykinin-induced responses in a coaxial bioassay system composed of rat anococcygeus muscle and guinea pig trachea.

1. Epithelium-dependent effects of bradykinin (BK) were investigated in a coaxial bioassay system which consisted of guinea pig trachea as donor organ and rat anococcygeus muscle as test tissue. 2. BK (10(-9) to 10(-5) M) produced concentration-dependent relaxations on the phenylephrine (3 x 10(-6) M)-precontracted rat anococcygeus muscle mounted alone. Relaxations decreased significantly when muscle was mounted in epithelium-intact trachea. There was also a significant difference between the relaxations obtained in the muscle within epithelium-intact and epithelium-denuded trachea (at 10(-7) to 10(-5) M concentrations). 3. Capsaicin (10(-5) M) pretreatment did not change BK (10(-9) to 10(-5) M)-induced relaxations in each preparation compared with vehicle pretreatment. Indomethacin (10(-6) M) in combination with thiorphan (10(-5) M) and atropine (10(-6) M) did not affect the BK-induced relaxations of the muscle within capsaicin-pretreated epithelium-intact or denuded trachea. 4. CGS 8515 (a specific 5-lipoxygenase inhibitor, 10(-6) M) did not change BK (10(-5) M)-induced relaxation on the muscle alone, and caused an increase of BK-induced relaxation on the muscle within epithelium-intact trachea compared with that obtained without CGS 8515. 5. Results showed that epithelial or nonepithelial factors were capable of modulating the responsiveness of rat anococcygeus muscle to BK. The decreased relaxation by BK in anococcygeus muscle did not occur by the release of cyclooxygenase products or tachykinins from tracheal epithelium, but it may have occurred by the contractile action of lipoxygenase product secreted by nonepithelial sources. In addition, BK might stimulate the secretion of an epithelium-derived inhibitory factor from the trachea.

Anal Canal↗
PubMed2004

Computed tomographic assessment of the trachea in the German shepherd dog.

Computed tomographic (CT) examination of the trachea was performed in 10 German shepherd dogs to determine the normal value of some tracheal measurements under general anesthesia and in sternal recumbence position. Measurements obtained from nine segments were evaluated in four groups as the cranial cervical, caudal cervical, thoracic inlet and the thoracal tracheas. The inner transverse (T) and vertical (V) diameters were measured with the aid of electronic calipers from the software of the CT scanner. The cross-sectional lumen area (CSA) was calculated by using vertical and transverse diameters. The ratio of the transverse and vertical diameters (T/V) was also calculated. There was not any significant difference between thoracic inlet and thoracic tracheas, however, the mentioned regions were found to be significantly different from both cranial and caudal cervical regions in all measurements except the ratio of T/V. The ratio of T/V between 0.92 and 1.06 gradually changed and there was not any statistical difference between subsequent regions while differences were found among further regions. The largest CSA, seen in cranial cervical trachea was as 364.62 mm2 and decreased gradually to 309.29, 245.69 and 226.50 mm2 in caudal cervical, thoracic inlet and thoracic tracheas, respectively. From the point of view of technique, CT examination of the dog trachea was very easy and it was possible to take sensitive and repeated measurements. It, however, may be accepted as expensive and that it is disadvantageous to require general anesthesia. The data presented in this study represent tracheal values in the healthy German shepherd dog under the conditions of the study.

Animals↗
PubMed1985

Microsurgical reconstruction of the trachea in rats (an experimental study).

This study was carried out to evaluate the use of 'Zenoderm' (enzyme treated procine dermis) as a patch for the repair of tracheal defects in rats, with particular reference to its application in the treatment of some cases of tracheal stenosis. Fifty-three rats were included in the study. Using microsurgical techniques, a defect was created in the cervical trachea and repaired using a suitable patch of 'Zenoderm' (two groups with different sized defects). In a further group of rats, healing of the trachea was studied after excision of a segment and end to end anastomosis. A set number of rats were sacrificed after intervals of 14, 28, 91 and 182 days when the trachea was excised and evaluated. Healing of the tracheae following end to end anastomosis was satisfactory in all cases with no evidence of stenosis. The two groups of tracheae with Zenoderm patches showed progressive stenosis at the area of the repair but there was no evidence of respiratory obstruction or distress. The Zenoderm patch and the regenerating epithelium were both evaluated by light microscopy and scanning electromicroscopy. The Zenoderm patch showed gradual absorption and was replaced by host collagen. There was gradual regeneration of epithelium which showed slow maturation from flat non-ciliated epithelium to partially cuboidal and columnar epithelium with some cilia showing early differentiation to respiratory epithelium. In conclusion, this experimental study confirmed the biocompatibility of 'Zenoderm' in rats. It provided a suitable surface for regeneration of tracheal epithelium. Replacement of the patch by the host collagen is promising but requires further study to assess its rigidity and ability to withstand pressure changes in the trachea.

Animals↗
PubMed1997

Characterization of the muscarinic receptor subtype(s) mediating contraction of the guinea-pig lung strip and inhibition of acetylcholine release in the guinea-pig trachea with the selective muscarinic receptor antagonist tripitramine.

1. The muscarinic receptor subtypes mediating contraction of the guinea-pig lung strip and inhibition of the release of acetylcholine from cholinergic vagus nerve endings in the guinea-pig trachea in vitro have previously been characterized as M2-like, i.e. having antagonist affinity profiles that are qualitatively similar but quantitatively dissimilar compared to cardiac M2 receptors. The present study sought to establish definitely the identity of these receptor subtypes by using the selective muscarinic receptor antagonist, tripitramine. Guinea-pig atria and guinea-pig trachea (postjunctional contractile response) were included for reference. 2. It was found that tripitramine antagonized methacholine-induced contractions of the guinea-pig lung strip with pKB value of 8.76 +/- 0.05. Both the parallel shifts of the concentration-response curves and the slope of the Schild plot begin not significantly different from unity (when antagonist preincubation was for 2 h) indicated the involvement of a single population of receptors in the contractile response. From the pKB values obtained with tripitramine and a range of other selective muscarinic receptor antagonists (cf. Roffel et al., 1993), this single population of receptors can only be classified as M2-like. 3. Tripitramine antagonized methacholine-induced chronotropic and inotropic responses in guinea-pig right and left atria with apparent pKB values of 9.4-9.6. However, such values were only obtained when antagonist preincubation was relatively long and/or antagonist concentration relatively high (e.g with 1 h at 100 or 300 nM but 3 h at 30 nM). It thus appears that low concentrations of tripitramine do not readily equilibrate with M2 receptors in guinea-pig atria nor with M2-like receptors in the guinea-pig lung strip. 4. Tripitramine increased electrical field stimulation-induced cholinergic twitch contractions in guinea-pig trachea in concentrations of 0.3-100 nM, by blocking prejunctional muscarinic inhibitory autoreceptors; with higher concentrations, twitch contractions were progressively diminished, as a result of blocking postjunctional M3 receptors (apparent pKB value 6.07 +/- 0.15). The pEC20 value (-log concentration that increases twitch by 20% maximum) was 8.29 +/- 0.08, which would suggest that M4 receptors are involved in this response. 5. Oxotremorine-induced inhibition of the release of prelabelled [3H]-acetylcholine from guinea-pig trachea, under conditions where there is no auto-feedback, was blocked by tripitramine (2 h preincubation) with a pKB value of 8.56 +/- 0.06. The slope of the corresponding Schild plot was not significantly different from unity, which together with the parallel shifts of the concentration-response curves indicated the involvement of a single muscarinic receptor subtype. 6. Since the pKB value for tripitramine at prejunctional receptors in guinea-pig trachea is in between the affinities towards M2 and M4 receptors, correlation plots were constructed to compare the pKB values obtained with tripitramine and a range of other selective muscarinic receptor antagonists (cf. Kilbinger et al., 1995) to reported affinities at M1-M4 receptors. This showed rather similar distribution patterns of the data points around the line of equality in the case of M2 and M4 receptor subtypes. However, the correlation coefficient was markedly better for M2 (0.9667) than for M4 (0.5976). Since recent evidence suggests that M4 receptors are not expressed in cholinergic nerves from guinea-pig trachea, it is concluded that prejunctional muscarinic autoinhibitory receptors in this tissue exhibit an atypical M2 type character, with a pharmacological profile distinct from cardiac M2 receptors.

Acetylcholine↗
PubMed1986

DNA ethylation in hamster tissues during subchronic diethylnitrosamine administration and in the hamster trachea after acute diethylnitrosamine administration.

Formation of O6-ethylguanine (O6EG) in trachea DNA was measured 12 h after acute i.p. administration of 50, 100 and 200 mg diethylnitrosamine (DEN)/kg body wt to Syrian golden hamsters. Purine bases were fractionated by h.p.l.c., and ethylated guanines were quantified optically by fluorescence spectrophotometry. Significant levels of this promutagenic base were found after the various single doses of DEN. O6EG in trachea DNA was also measured at various times up to 48 h after an acute i.p. dose of 200 mg DEN/kg body wt. The maximum level of O6EG was detected 12 h after DEN treatment. A rapid decrease in O6EG concentration was seen in trachea DNA between 12 and 24 h, but only a negligible decrease was detected from 24 to 48 h post-treatment. The formation and accumulation of O6EG in trachea, liver, lung and kidney DNA were determined in hamsters treated subchronically with DEN, 20 mg/kg body wt, s.c. twice weekly up to 8 weeks. O6EG accumulated to significant levels in trachea and liver DNA. 7-Ethylguanine did not accumulate in the DNA of any of the organs studied during subchronic DEN exposure. The formation and persistence of O6EG in trachea DNA of DEN-treated hamsters correlated with the sensitivity of this tissue to the carcinogenic action of DEN.

Alkylation↗
PubMed1978

Sources of gram-negative bacilli colonizing the tracheae of intubated patients.

Twenty acutely ill patients requiring prolonged orotracheal intubation were studied to determine the source and progression of gram-negative bacilli colonizing the trachea. Organisms recovered from daily tracheal, hypopharyngeal, and rectal cultures were typed and speciated to identify identical strains at the three sites. All patients acquired gram-negative bacilli in the trachea by day 3 after intubation. Thirty organisms that were not recovered from the tracheal aspirate immediately following intubation were isolated for at least two days some time thereafter. Nine of the 30 colonizing bacteria were Enterobacteriaceae, and all were found in another culture site, usually the hypopharynx, before isolation from the trachea. In contrast, only four of the 21 non-Enterobacteriaceae that colonized the trachea were recovered previously from either the hypopharynx or rectum, a finding which represents a significant difference (P = 0.0002). Quantitation of isolates from the hypopharynx was of no value in predicting subsequent acquisition in the trachea, and the numbers of bacteria recovered from the first positive tracheal specimen were not predictive of subsequent persistence in the trachea.

Acinetobacter↗
PubMed1976

The contribution of extraneuronal uptake to the trachea-blood vessel selectivity of beta-adrenoceptor stimulants in vitro in guinea-pigs.

1 The potencies relative to isoprenaline of isoetharine, tertiary butyl noradrenaline, salbutamol, orciprenaline, Me 506, rimiterol, fenoterol, carbuterol and terbutaline on isolated preparations of guinea-pig trachea and blood vessels (perfused hind limb) were determined. All the compounds were selective for trachea and selectivity values, i.e. relative potency on trachea divided by relative potency on hind limb, ranged from 2.3 to 21.4. 2 Responses to isoprenaline (the reference compound), tertiary butyl noradrenaline and isoetharine were potentiated on trachea by 50 muM phenoxybenzamine (PHB) and by other inhibitors of extraneuronal uptake (ENU). Under these conditions the selectivity values of all the compounds was close to unity. 3 Selectivity values were also close to unity if they were calculated from data obtained without ENU inhibition, provided that only those compounds not potentiated by PHB on trachea were used. 4 It is proposed that the trachea-blood vessel selectivity shown by beta-adrenoceptor stimulants can be caused by the influence of ENU upon them, rather than by their ability to distinguish between two beta2-adrenoceptors. 5 The suggestion that differences exist between beta2-adrenoceptors in respiratory and vascular smooth muscle is not supported by the in vitro experiments described.

Adrenergic beta-Agonists↗
PubMed1980

Purine antagonists in the identification of adenosine-receptors in guinea-pig trachea and the role of purines in non-adrenergic inhibitory neurotransmission.

1 To test the possibility that adenosine receptors exist within the trachea of the guinea-pig, an attempt has been made to identify a compound with adenosine antagonist activity in this tissue.2 Quinidine, phentolamine, phenoxybenzamine, 2-2'-pyridylisatogen tosylate (PIT) and caffeine were tested for antagonism of spasmolytic responses to adenosine, adenosine 5'-triphosphate (ATP) and adenine on the guinea-pig isolated trachea.3 Quinidine (10 and 25 mug/ml), phentolamine (10 and 30 mug/ml) and phenoxybenzamine (10 mug/ml) had little or no effect on response to adenosine, ATP and adenine. PIT (21 mug/ml) potentiated responses to adenosine, ATP and adenine by an unexplained mechanism.4 Caffeine (25 mug/ml) partially relaxed the trachea and inhibited spasmolytic responses to both adenosine and ATP, but not to adenine, isoprenaline, aminophylline or prostaglandin E(2) (PGE(2)).5 A number of compounds related to caffeine (xanthine, hypoxanthine, theophylline and theobromine) were tested for adenosine antagonist activity. Xanthine (300 mug/ml) and hypoxanthine (300 mug/ml) did not relax the trachea or antagonize spasmolytic responses to adenosine. Both theophylline (10 mug/ml) and theobromine (30 mug/ml) partially relaxed the trachea; theophylline, but not theobromine, antagonized spasmolytic responses to adenosine.6 pA(2) values for caffeine and theophylline as antagonists of adenosine were 4.3 and 4.7 respectively. However, the slopes of the Schild plot regressions were significantly less than 1.0 for both compounds.7 Four compounds, adenine, AH 8883, M30966 and ICI 63197, which like caffeine and theophylline, have phosphodiesterase inhibitory activity were tested for adenosine antagonist activity in the trachea. Adenine and AH 8883 had no effect and M30966 and ICI 63197 caused significant potentiation.8 The effects of caffeine and theophylline were also investigated on the non-adrenergic inhibitory response to nerve stimulation (NAIR). Both caffeine (100 mug/ml, n = 4) and theophylline (30 mug/ml, n = 4) enhanced the NAIR (20 Hz) while virtually abolishing matched responses to exogenous adenosine.9 The results support the existence of adenosine receptors in the guinea-pig trachea.

Adenosine↗
PubMed1991

Epithelium-dependent potentiation of anaphylactic contractions by beta-endorphin in tracheae isolated from actively sensitized guinea-pigs.

1. It has been shown that opioid peptides modulate airway function. In the present study, the effect of beta-endorphin on antigen-induced contractions of isolated tracheal rings from actively sensitized guinea-pigs has been studied. 2. beta-Endorphin had a concentration-dependent bimodal effect on anaphylactic contractions of the trachea. Low concentrations of beta-endorphin (10(-10) and 10(-8) M) significantly potentiated anaphylactic contractions, whereas higher concentrations (10(-7) and 10(-6) M) significantly suppressed anaphylactic contractions of guinea-pig trachea. 3. beta-Endorphin in concentrations of 10(-8) M and 10(-7) M did not affect the responsiveness of the tracheal rings to histamine or leukotriene D4. This indicates that beta-endorphin does not influence the responsiveness of tracheal smooth muscle to anaphylactic mediators. 4. In the presence of the non-selective opioid receptor antagonist naloxone, 10(-8) M beta-endorphin still potentiated the anaphylactic contractions of the trachea. In addition, an equimolar concentration of des-Tyr1-beta-endorphin, a fragment of beta-endorphin without opioid-like activity, also potentiated anaphylactic contractions. The potentiation of anaphylactic contraction by 10(-8) M beta-endorphin is not therefore mediated by classical opioid-receptors. 5. In the presence of naloxone, 10(-7) M, beta-endorphin did not suppress anaphylactic contractions of the trachea. Thus, the suppression of anaphylactic contraction is mediated via a classical opioid-receptor. 6. In epithelium-denuded trachea, both 10(-8) and 10(-7) M beta-endorphin suppressed the anaphylactic contractions, whereas 10(-8) and 10(-7) M des-Tyr1-beta-endorphin did not affect anaphylactic contractions. It is concluded that the potentiation of the anaphylactic contraction in intact trachea is epithelium-dependent whereas the suppression of the anaphylactic contraction is epithelium-independent.

Anaphylaxis↗
PubMed1994

Beta-adrenoceptors mediate inhibition of [3H]-acetylcholine release from the isolated rat and guinea-pig trachea: role of the airway mucosa and prostaglandins.

1. Rat or guinea pig isolated tracheae were labelled with [3H]-choline to measure evoked tritium outflow, which reflects neuronal release of [3H]-acetylcholine. Tritium outflow was evoked either by electrical stimulation of the extrinsic vagal nerve (rat tracheae) or by 27 mM potassium (guinea pig tracheae). 2. In rat tracheae isoprenaline (0.01, 0.1 microM) inhibited evoked [3H]-acetylcholine release, whereas beta 2-adrenoceptor-selective agonists (fenoterol, formoterol, salbutamol) were ineffective. 3. The inhibitory effect of isoprenaline was abolished under the following conditions: (i) presence of propranolol (1 microM) or of the beta 1-selective antagonist CGP 20712 A (0.1 microM); (ii) removal of the mucosa at the start of the experiments; (iii) blockade of cyclooxygenase activity by 3 microM indomethacin. 4. In rat isolated tracheae prelabelled with [3H]-arachidonic acid, isoprenaline (0.1 microM) but not formoterol (0.01 microM) enhanced the outflow of [3H]-prostaglandins (PGD2, PGE2). This effect was blocked by 0.1 microM CGP 20712 A. 5. In guinea pig tracheae electrical stimulation of the extrinsic vagal nerve did not cause a constant release of [3H]-acetylcholine, but 27 mM potassium elicited a reproducible release of [3H]-acetylcholine. In this species both isoprenaline (0.1 microM) and formoterol (0.01 microM) inhibited evoked [3H]-acetylcholine release. Inhibition was abolished under the following conditions: (i) presence of propranolol (1 microM) or of the beta 2-selective antagonist ICI 118551 (0.3 microM); (ii) removal of the mucosa at the start of the experiments; (iii) blockade of cyclooxygenase activity by 3 microM indomethacin. 6. In conclusion, the present experiments have demonstrated that activation of beta-adrenoceptors localized in the mucosa mediates inhibition of [3H]-acetylcholine release from the neuroeffector junctions of the pulmonary, parasympathetic nerves most probably by the liberation of inhibitory prostaglandins from the airway mucosa. The adrenoceptor subtype involved differs in rat (beta 1 subtype) and guinea pig (beta 2 subtype) airways.

Acetylcholine↗
PubMed1996

Influence of regional differences in ETA and ETB receptor subtype proportions on endothelin-1-induced contractions in porcine isolated trachea and bronchus.

1. Quantitative autoradiographic studies were conducted to determine the distributions and densities of ETA and ETB binding site subtypes in porcine tracheal and bronchial smooth muscle. In addition, the roles of ETA and ETB receptors in endothelin-1-mediated contraction of these tissues were assessed. 2. Quantitative autoradiographic studies revealed that both ETA and ETB binding sites for [125I]-endothelin-1 were present in both bronchial and tracheal airway smooth muscle. However, the proportions of these sites were markedly different at these two levels within the respiratory tract. In tracheal smooth muscle, the proportions of ETA and ETB sites were 30 +/- 1% and 70 +/- 1% respectively, whereas in bronchial smooth muscle, these proportions were virtually reversed, being 73 +/- 2% and 32 +/- 8% respectively. 3. Endothelin-1 induced concentration-dependent contraction of porcine tracheal and bronchial airway smooth muscle. Endothelin-1 had similar potency (concentration producing 30% of the maximum carbachol contraction, Cmax) in trachea (22 nM; 95% confidence limits (c.l.), 9-55 nM; n = 9) and bronchus (22 nM; c.l., 9-55 nM; n = 6). Endothelin-1 also produced comparable maximal contractions in trachea (59 +/- 5% Cmax; n = 9) and bronchus (65 +/- 4% Cmax, n = 6). 4. In trachea, endothelin-1 induced contractions were not significantly inhibited by either the ETA receptor-selective antagonist, BQ-123 (3 microM) or the ETB receptor-selective antagonist, BQ-788 (1 microM). However, in the combined presence of BQ-123 and BQ-788, the concentration-effect curve to endothelin-1 was shifted to the right by 3.7 fold (n = 8; P = 0.01). 5. In bronchus, concentration-effect curves to endothelin-1 were shifted to the right by BQ-123 (3 microM; 4.3 fold; P < 0.05), but not by BQ-788 (1 microM). In the presence of both antagonists, concentration-effect curves to endothelin-1 were shifted by at least 6.7 fold (n = 6; P = 0.01). 6. Sarafotoxin S6c induced contraction in both tissue types, although the maximum contraction was greater in trachea (53 +/- 7% Cmax; n = 6) than in bronchus (21 +/- 5% Cmax; n = 6). BQ-788 (1 microM) markedly reduced sarafotoxin S6c potency in both trachea and bronchus (e.g. by 50 fold in trachea; c.l., 14-180; n = 6; P < 0.05). 7. These data demonstrate that the proportions of functional endothelin receptor subtypes mediating contraction of airway smooth muscle to endothelin-1, vary significantly at different levels in the porcine respiratory tract.

Animals↗
PubMed1978

Resection of thyroid carcinoma infiltrating the trachea.

We have treated surgically 11 patients with thyroid carcinoma that had infiltrated into the trachea. Three patients had primary tumours, and eight had recurrent tumours after previous operations. Sleeve resection of trachea was performed where thyroid carcinoma had proliferated; the trachea was reconstructed by end-to-end anastomosis. In two patients 10 rings of the trachea were resected. In three patients the anterior half of the cricoid cartilage was resected along with the cervical trachea. In one patient tracheoplasty was performed using partial extracorporeal circulation because severe tracheal stenosis prevented endotracheal intubation. Two of the 11 patients died from the surgery and one from disseminated metastases. One patient who had undergone tracheal resection for thyroid carcinoma three years and five months previously had a recurrence of the tumour in the trachea adjacent to the anastomosis, and a second tracheal resection was performed. In three patients postoperative laryngeal stenosis occurred. Five patients are alive and well two years and one month to four years and seven months after their operations. The histological pattern of the tumour was papillary adenocarcinoma in all 11 patients.

Adenocarcinoma, Papillary↗
PubMed1983

Parathyroid hormone (PTH) fragments relax the guinea-pig trachea in vitro.

Synthetic bovine parathyroid hormone fragment containing the N-terminal 1-34 amino acids (bPTH-(1-34) ) relaxed the guinea-pig trachea constricted with histamine in vitro. Peptides with bovine and human sequences purchased from Peninsula Laboratories and Beckman Bioproducts produced similar effects. Substitution of methionine in positions 8 and 18 by norleucine did not affect this property of bPTH-(1-34). However, when the methionines were oxidized by treating the peptide with hydrogen peroxide, the peptide could no longer produce relaxation in the trachea. Oxidation of the methionine-replaced analog did not affect the action of the peptide on the trachea. It seems that the methionines per se are not necessary, but once oxidized the conformation of the molecule may be sufficiently altered to affect its ability to relax the trachea. While propranolol can block the relaxing action of isoproterenol, this blocking agent produces no inhibition of the bPTH-(1-34) effect. This action of PTH on the trachea may be related to cAMP because isobutyryl-methylxanthine, a phosphodiesterase inhibitor, potentiates and imidazole, a phosphodiesterase stimulator, inhibits the trachea relaxing action of bPTH-(1-34).

1-Methyl-3-isobutylxanthine↗
PubMed1983

Bioelectric properties and ion transport of excised rabbit trachea.

Bioelectric properties and 22Na+ and 36Cl- isotopic flows across rabbit trachea, an airway epithelium without submucosal glands, were measured in vitro. One hundred twenty-two excised tracheas exhibited a mean transepithelial electric potential difference (PD) of 12 mV (lumen negative), a conductance (G) of 8.5 mS X cm-2, and a short-circuit current (Isc) of 90 microA X cm-2. G remained stable for more than 3 h, but Isc and PD fell slowly (10%/h). G was inversely correlated with PD, but Isc and G were not correlated. Na+ was absorbed under both open-circuit (1.7 mueq. cm-2 X h-1) and short-circuit (2.2 mueq X cm-2 X h-1) conditions. Net Na+ transport accounted for 70% of Isc of the short-circuited trachea. Net Cl- flow in the absorptive direction approximated that of Na+ under open-circuit conditions (1.6 mueq X cm-2 X h-1). Under short-circuit conditions the small net flow of Cl- in the direction of secretion (0.4 mueq X cm-2 X h-1) was not significant. Both unidirectional Cl- fluxes were correlated with G; [14C]-mannitol permeability and Na+ flows were weakly or not correlated with G. We found no evidence of net HCO-3 or proton transport. Acetylcholine (10(-4) M), phenylephrine (10(-5) M), or isoproterenol (10(-5) M) induced no change in bioelectric properties or ion flows. We conclude that the rabbit trachea is primarily a Na+ absorbing epithelium. The absence of a correlation between mannitol permeability and G suggests that much of the Cl- conductance is transcellular. Whereas insensitivity of rabbit trachea to cholinergic and alpha-adrenergic agents is compatible with the absence of glands, the lack of response to beta-adrenergic agonists denotes a species difference (compared with canine trachea) in airway-surface epithelial cell function.

Acetazolamide↗
PubMed1992

CD4+ T-lymphocytes and interleukin-5 mediate antigen-induced eosinophil infiltration into the mouse trachea.

In order to determine the role of CD4+ and CD8+ T-cells and of interleukin-5 (IL-5) in causing antigen-induced eosinophil infiltration into the site of airway late-phase reaction, we examined the effect of the in vivo depletion of CD4+ and CD8+ T-cells on the eosinophil infiltration of the trachea induced by antigen inhalation in mice. We also studied the effect of anti-murine IL-5 monoclonal antibody (mAb) on the antigen-induced eosinophil infiltration in the trachea. The eosinophil infiltration into the trachea of ovalbumin (OVA)-sensitized BALB/c mice began to increase 9 h after OVA inhalation and persisted for more than 48 h. The in vivo depletion of CD4+ T-cells by pretreatment with anti-L3T4 mAb significantly decreased the eosinophil infiltration induced by OVA inhalation in the trachea of sensitized mice. However, the in vivo depletion of CD8+ T-cells by pretreatment with anti-Lyt-2 mAb had no significant effect on OVA-induced eosinophil infiltration in the trachea. Pretreatment with anti-murine IL-5 mAb also decreased OVA-induced eosinophil infiltration in the trachea. In contrast, neither disodium cromoglycate nor a selective antagonist for platelet-activating factor CV-6209 decreased OVA-induced airway eosinophilia in the mouse. Our results provide direct evidence that CD4+ but not CD8+ T-cells mediate antigen-induced eosinophil recruitment in the airways and that IL-5 mediates this eosinophil recruitment.

Administration, Inhalation↗