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PubMed1983

Substance P and capsaicin-induced contraction of human bronchi.

Substance P induced a dose-dependent contraction of human segmental bronchi in vitro with a threshold dose of about 10(-6) M. These preparations were obtained from patients undergoing lung tumor surgery. The substance P-induced contractions were resistant to mepyramine and atropine, suggesting a direct effect on the bronchial smooth muscle. Capsaicin (10(-5) M) also induced a slowly developing strong atropine-resistant contraction of human bronchi in vitro. a rapid tachyphylaxis developed for the response to capsaicin. Both substance P and capsaicin were less potent than acetylcholine and histamine in inducing contractions of human bronchi. This finding may however be partly due to the experimental conditions and both substance P and capsaicin were comparatively much more potent in guinea-pig preparations. Transmural field stimulation of the bronchial preparations in man resulted in contractions that were largely sensitive to atropine. The presence of capsaicin-induced bronchial contractions however indicates the existence of a local non-cholinergic axon-reflex control of bronchial smooth muscle tone by substance P in man.

Acetylcholine↗
PubMed1985

Nervous control of mucin secretion into human bronchi.

Pieces of ferret trachea and human bronchi were mounted in Ussing chambers and given [35S]sulphate as a radiolabelled precursor of mucous glycoproteins (mucins). The output of 35S bound to macromolecules was studied as an index of mucin secretion. In the ferret trachea, electrical field stimulation increased the rate of mucin secretion. Tetrodotoxin (10(-7) M or 10(-6) M) abolished this effect. Pilocarpine (25 microM) stimulated the output of mucins from human bronchus. Atropine (10(-5) M) abolished this effect. Electrical field stimulation of human bronchus stimulated mucin secretion. Tetrodotoxin (10(-6) M) abolished this effect. Field stimulation in the presence of either atropine (10(-5) M) or atropine with l-propranolol (10(-5) M) and phentolamine (10(-5) M) caused no stimulation of mucin secretion rate. Some bronchi were treated with noradrenaline (10(-5) M) for 1 h to allow the adrenergic nerves to take up transmitter. Even in these, atropine prevented the effect of field stimulation. We conclude that activity in cholinergic nerves can stimulate mucin secretion in the bronchi in man. Our results provide no evidence that the adrenergic nerves or non-adrenergic, non-cholinergic nerves have a direct action on bronchial secretory cells in man.

Adult↗
PubMed1984

The larger bronchi in byssinosis: a morphometric study.

The proportions of gland, muscle and cartilage were measured in the named bronchi of 43 byssinotics, and compared with the proportions in normal subjects and chronic bronchitics. The smoking habits and symptomatology of the byssinotics were also investigated. In the byssinotics the proportions of gland, muscle and cartilage were higher than in the normal, non-smoking subject at all levels in the bronchial tree, and were similar to those in chronic bronchitics. The increase was not confined to the lobar bronchi as the results of a previous investigation had suggested. It is concluded that although exposure to cotton dust is a factor in the pathogenesis of chronic byssinosis, anatomical changes in the bronchi of Lancashire cotton workers are non-specific, and are confounded by other environmental factors. Smoking has a deleterious effect on the natural history of the disease, but no morphological difference between smokers and non-smokers was found.

Adult↗
PubMed1987

Cells containing IgA subclasses in bronchi of subjects with and without chronic obstructive lung disease.

Necropsy specimens were obtained from the lungs of 10 subjects who had no history of lung disease, 10 who had died with chronic bronchitis, and 10 with bronchiectasis. Tissue sections were stained for IgA1 or IgA2 using the immunoperoxidase technique, and the number of cells in the bronchi stained for these proteins was counted. The total number of IgA positive cells was increased in bronchitic and bronchiectatic lungs compared with those from control subjects. The number of IgA2 positive cells was similar in those with bronchitis and bronchiectasis and significantly higher than in controls. Similarly, cells containing IgA1 were increased in the lungs of subjects with chest disease but were higher in those with bronchitis than in those with bronchiectasis. The proportion of IgA2:total IgA containing cells was similar in sections from controls (mean (SD) 25 (5.0)%) and those with bronchiectasis (mean (SD) 24 (4)%), but lower in those with bronchitis (mean (SD) 19 (5.0)%). The results show that cells containing IgA1 predominate in the major bronchi but that the proportion of cells containing IgA2 is higher than in non-mucosal lymphoid tissues. Bronchitis and bronchiectasis are associated with greater numbers of cells producing IgA in the bronchi, and this is consistent with increased local production of IgA in the lung secretions of bronchitic subjects.

Adult↗
PubMed1989

Kinetics of cellular influx and histamine release in normal human bronchi.

Inhalation of certain substances can induce bronchial inflammation followed by bronchoconstriction or bronchial hyperreactivity. We have developed a model of airway inflammation and bronchoconstriction induced by an aqueous extract of cotton bracts (CBE) in which the severity of flow rate reduction correlates with the presence of bronchoalveolar neutrophils. In the current study normal human volunteers underwent local bronchial instillation of CBE. Bronchial lavage histamine concentrations and cellular populations were determined at time intervals after local challenge. In addition, bronchial biopsies were obtained after CBE instillation, and the degree of subepithelial inflammation was quantitated. We report that lavage of bronchi locally exposed to CBE contains 1) greater histamine concentrations 4 min after challenge compared with lavage from saline-challenged bronchi and 2) concentrations of eosinophils and macrophages that are greater than control lavage 8 min after exposure. Bronchial biopsies taken after CBE instillation also demonstrated a variable degree of subepithelial granulocyte infiltration that correlated with the global bronchoconstricting response to CBE assessed on a separate day. These studies suggest that inflammation can develop rapidly in normal human bronchi and may precede significant flow rate reductions by greater than 1 h.

Biopsy↗
PubMed1991

Mechanism underlying ozone-induced in vitro hyperresponsiveness in canine bronchi.

The effects of ozone inhalation on the contractility of canine bronchi and the mechanisms underlying any changes observed were investigated. Ozone inhalation caused acetylcholine airway hyperresponsiveness in vivo. Isolated segments of bronchi (3rd to 5th order) from dogs previously exposed to ozone (or normal air) were mounted in organ baths. Contractile responses to electrical field stimulation (FS) in all tissues decreased in magnitude over time (measured at 10, 120, 210, and 300 min after mounting tissues in the organ baths); responses to 150 mM KCl did not show such a progressive decrease. Ozone inhalation produced a dramatic enhancement of FS responses, a smaller enhancement of responses to carbachol (10(-8)-10(-4) M), and no change in responses to KCl (150 mM). In the presence of 10(-5) M indomethacin, all responses were enhanced and tended to increase in magnitude over time; indomethacin also abolished the differences in responsiveness between the control and ozone-exposed tissues. In the presence of the thromboxane receptor antagonist L-670,596 (10(-8) M), the magnitudes of all FS responses showed a progressive decrease over time while KCl responses did not; again, the differences in FS responses between control and ozone-exposed tissues were decreased or made insignificant. In conclusion, ozone produced airway hyperresponsiveness in vivo and hyperresponsiveness in canine bronchi in vitro via decreased prejunctional and postjunctional inhibition (likely mediated by prostaglandin E2) and increased prejunctional excitation mediated by thromboxane A2. However, direct measurements of mediator release should be carried out to reach a firm conclusion.

Administration, Inhalation↗
PubMed1993

Effect of an inhibitor of nitric oxide synthase on neural relaxation of human bronchi.

This study examines the roles of peptides and nitric oxide (NO) as mediators of inhibitory nonadrenergic, noncholinergic (NANCi) neurons in human and guinea pig airways in vitro. Tissues were contracted with 0.3 microM methacholine (MCh) and relaxation studied before and after the addition of the peptidase alpha-chymotrypsin (alpha-CT) (2 U/ml) and NG-nitro-L-arginine methyl ester (L-NAME 0.1-1.1 mM), an inhibitor of NO synthase, the enzyme catalyzing the formation of NO. alpha-CT alone, in comparison to parallel time controls, inhibited control relaxation to electrical field stimulation (EFS) by 29.2 +/- 8.6% in guinea pig tracheae (n = 9), whereas a small augmentation of relaxation was observed in human bronchi (n = 7). L-NAME inhibited the NANCi response in both guinea pig tracheae and human bronchi: in guinea pig tracheae, maximal inhibition of the alpha-CT-insensitive relaxation was 59.3 +/- 11.5% (SE, P = 0.003) at low frequencies (4-16 Hz) and 28.6 +/- 8.9% (P = 0.08) at 32 Hz; in human bronchi, the maximal inhibition was 37.7 +/- 9.3% (P = 0.008) at 8 or 16 Hz, and 37.9 +/- 5.9% (P = 0.005) at 32 Hz. Inhibition was greater after repeated baseline EFS for 90 min before initiation of contraction with MCh and addition of L-NAME (59.8 +/- 13.9% after repeated baseline EFS, n = 4; vs. 34.9 +/- 6.2% without repeated baseline EFS, n = 9, P = 0.025). Relaxant responses to sodium nitroprusside, vasoactive intestinal peptide, and isoproterenol were not affected by L-NAME. L-Arginine (10 mM), a precursor of NO, partially reversed the effect of L-NAME.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Oxidoreductases↗
PubMed1994

Passive sensitization of human bronchi augments smooth muscle shortening velocity and capacity.

We assessed whether incubation with human serum from atopic individuals containing high concentrations of immunoglobulin E (IgE) causes augmentation of maximal contraction of human bronchial smooth muscle from non-atopic subjects in vitro. Bronchi were obtained from eight patients undergoing lung resection, and force-velocity relationships were determined for eight pairs of epithelium-intact bronchial rings of generations 6-7 using an electromagnetic lever system, which allowed isotonic shortening when load-clamps [from 0 to maximal isometric force (P0)] were applied at specific times after onset of contraction. Contractions were elicited by supramaximal electrical field stimulation (50 Hz, 10 s train duration, 25 V). Optimal length (Lo) for each tissue was determined during equilibration. After resection, tissues were sensitized passively with human sera containing high titers (> 1,000 U/ml) of IgE by incubation for 16 h at 20 degrees C. Maximal shortening velocity (Vmax) was increased for passively sensitized bronchi [0.1150 +/- 0.0240 1/2 circumferences/s (1/2Cir/s)] compared with sham-sensitized bronchi [0.0731 +/- 0.0152 1/2Cir/s, P = 0.038]. Similarly, maximal shortening (delta Lmax) was augmented in sensitized bronchial rings (11.27 +/- 1.80 %Lo) compared with sham-sensitized tissues (8.19 +/- 1.39 %Lo, P = 0.012). However, P0 did not differ between sensitized (122.5 +/- 24.4 mN/cm2) compared with sham-sensitized tissues (138.4 +/- 32.1 mN/cm2, P = 0.642). Our data are the first demonstration that Vmax and delta Lmax are augmented in sensitized but not challenged human bronchial rings after passive sensitization using human serum containing high concentrations of IgE.

Bronchi↗
PubMed1996

Evidence for functional tachykinin NK1 receptors on human isolated small bronchi.

On human small isolated bronchi (diameter < 1 mm), but not on larger bronchi (diameter 3-5 mm), substance P (SP) and specific tachykinin SP-preferring neurokinin (NK1) receptor agonists {[beta Ala4, Sar9, Met(O2)11]SP-(4-11), [Sar9, Met(O2)11]SP, [Arg6,Sar9,Met(O2)11]SP-(6-11), and septide; 10(-10) to 10(-6) M} produced a concentration-dependent contraction that occurred at low concentrations (pD2 values of 7.79-8.33) and was characterized by a low intrinsic activity [maximal effect (Emax) of 38-45% of Emax induced by 3 mM acetylcholine, in a noncumulative manner]. Comparison of cumulative and noncumulative concentration-response curves to SP and NK1 receptor agonists suggest rapid receptor desensitization. The SP (10(-8) M)-induced contraction was inhibited by tachykinin NK1 receptor antagonists (rank order of potency: SR-140333 > CP-96,345 > RP-67580) but not by the tachykinin NK2 receptor antagonist SR-48968. Indomethacin (10(-6) M) abolished the SP-induced contraction. Our results suggest that tachykinin NK1 receptors are present on human small bronchi and that their stimulation induces a prostanoid-dependent contraction. The small isolated bronchus is an interesting model of human tissue to test NK1 receptor antagonists.

Benzamides↗
PubMed1975

Effect of vibration on isolated dog bronchi.

Vibratory stress, induced by turbulent flow, has been shown to alter the structural properties in arteries. Since turbulent flow can exist in the lungs it seems important to know whether a similar effect can occur in bronchi. To answer that question air was passed through isolated dog bronchi. Turbulent flow was created by having, at one end, a cannula acting as a stenosis, producing vibrations or a "flitter" in the wall. A measure of the elastic properties was obtained by coupling pressure-volume data with photographs taken at different pressures. The results demonstrate a significant alteration in the structural properties, localized to ares under maximum vibration. A "yielding" in the direction of maximum stress was observed with a corresponding structural rearrangement (radius decreased, length increased). This effect and its relation to structural fatigue is discussed. The physiological significance of the results are that the bronchi become more resistant to deformation under positive pressures and less resistant to collapse under negative pressures.

Animals↗
PubMed1984

Surrounding structures affect pressure-diameter behavior of excised dog bronchi.

The effects of adjacent large blood vessels, fibroelastic membrane, and parenchyma on pressure-diameter (P-D) behavior of intrapulmonary bronchi were studied in five dog lung lobes. Central lobar airways were inflated separately by blocking all branches with beads and inflating the distal lobar air spaces via pleural capsules. After bronchial P-D curves were obtained at fixed pleural pressures (Ppl) of -30, -10, and -5 cmH2O, the P-D properties of the isolated bronchi were measured in each of four stages of dissection: 1) lobar artery and vein were left attached to the bronchus, but parenchyma was removed to within 1-2 mm of the limiting membranes; 2) all remaining parenchyma was carefully removed; 3) the large vessels were removed, leaving the bronchial fibroelastic membrane intact; and 4) the fibroelastic membrane was peeled from the bronchus. From stage 1 it was deduced that in the intact lobes, peak peribronchial parenchymal stress (Px) averaged -29.2 cmH2O at Ppl = -30 cmH2O). In stage 2 bronchial recoil was reduced only approximately 5%. The major decrease (approximately 35%) occurred in stage 3, indicating that interaction between vessels and bronchi contributed significantly to bronchial stiffness. A final decrease of approximately 10% was seen in stage 4. We conclude that Px in the intact state is similar to Ppl at a transpulmonary pressure of 30 cmH2O and that stages 1 or 2 may provide a better basis for estimating Px than the commonly employed bronchus free of vessels and tissue.

Animals↗
PubMed1997

Acetylcholine via muscarinic receptors inhibits histamine release from human isolated bronchi.

Human bronchi were incubated in organ baths to measure histamine release. The calcium ionophore A23187 (10 mumol/L; 1 min) stimulated histamine release by 148 +/- 28% (n = 11) above the prestimulation level but was ineffective in epithelium-denuded bronchi. Neither bradykinin (0.1 mumol/L) nor compound 48/80 (10 micrograms/ml) triggered the release of histamine from epithelium-intact bronchi. Acetylcholine did not affect spontaneous histamine release (about 2 nmol/g x 5 min) but inhibited A23187-evoked histamine release in an atropine-sensitive manner. Already a concentration as low as 0.1 nmol/L acetylcholine was effective, the maximal inhibition (by 89%) occurred at 100 nmol/L, whereas a concentration of 10 mumol/L acetylcholine was ineffective. Oxotremorine (1 nmol/L), a stable agonist at muscarinic receptors, suppressed stimulated histamine release completely. Physostigmine (0.1 mumol/L), an acetylcholinesterase inhibitor, reduced A23187-evoked histamine release by 58%. Antihuman IgE antibody stimulated histamine release by 127 +/- 30% (n = 6) above the prestimulation level. Acetylcholine (100 nmol/L) inhibited also the immunologically evoked histamine release by 70%. In conclusion, the present experiments provide a model to characterize mast cells that are localized in or close to the airway surface epithelium. Acetylcholine via muscarinic receptors strongly inhibits the releasability of these mucosal mast cells being among the first cells to interact with inhaled antigens and environmental agents. The inhibitory action of physostigmine indicates the involvement of endogenous, probably non-neuronal acetylcholine expressed in airway epithelial cells.

Acetylcholine↗
PubMed1991

Tachykinin receptors and noncholinergic bronchoconstriction in the guinea-pig isolated bronchi.

The aim of the study was to assess which type(s) of tachykinin receptor mediate the noncholinergic bronchoconstriction produced by activation (electrical field stimulation) of capsaicin-sensitive primary afferents in epithellum-denuded guinea-pig isolated bronchi. Experiments with natural and synthetic tachykinin agonists indicated the presence of both NK-1 and NK-2 receptors at this level. Experiments with the putative NK-1 (L668, 169) or NK-2 (MEN 10,207, MEN 10,376, L659,877, and R396) selective antagonists against NK-1 and NK-2 selective agonists further supported this conclusion. All the tachykinin antagonists tested reduced the noncholinergic bronchoconstriction to field stimulation with the order of potency MEN 10,207 = MEN 10,376 greater than L659,877 greater than L668,169 congruent to R396. In the presence of peptidase inhibitors, the activity of MEN 10,376 toward the noncholinergic bronchoconstriction was slightly reduced, whereas that of L668,169 was increased. These findings demonstrate that both NK-1 and NK-2 receptors mediate the noncholinergic constriction produced by endogenous tachykinins in guinea-pig bronchi and that the relative contribution of NK-2 receptors is greater than that of NK-1. These findings implicate a major role for neurokinin A rather than for substance P as an endogenous bronchoconstrictor in the guinea-pig isolated bronchi. In the presence of peptidase inhibitors, the relative contribution of NK-1 receptors is increased.

Animals↗
PubMed2004

Allergen exposure of mouse airways evokes remodeling of both bronchi and large pulmonary vessels.

Remodeling of airway structures is a well-documented feature of allergic airway inflammation. To investigate whether bronchial remodeling is associated with remodeling of adjacent pulmonary vessels, sensitized mice were subjected to repeated ovalbumin inhalations, and bronchi and pulmonary vessels were subjected to histologic analysis. Allergen challenges induced peribronchial as well as perivascular eosinophilia. Remodeling of systemic airway microcirculation, as studied in tracheal whole-mount preparations, revealed an allergen-induced increase in both the diameter and length of the airway microvessels. Immunostaining for alpha-smooth muscle actin disclosed an increase in smooth muscle mass in both bronchi and large pulmonary vessels. Both bronchi and pulmonary vessels also displayed increased expression of procollagen I and procollagen III. Staining for proliferating cell nuclear antigen revealed increased proliferation of bronchial epithelial and smooth muscle cells as well as pulmonary vascular endothelial and smooth muscle cells. We conclude that central features of remodeling that take place in allergen-exposed airways are present also in the pulmonary vessels. The significance of this finding with respect to occurrence in disease, pathophysiologic importance, and involved mechanisms warrants further investigation.

Animals↗
PubMed1995

IgE-induced passive sensitization of human isolated bronchi and lung mast cells.

Passive sensitization of human isolated lung with serum from atopic asthmatic patients provides an opportunity to study the link between airway hyper-responsiveness and the allergic process. To directly demonstrate the role of immunoglobulin E (IgE) in the effect of the atopic serum, we have compared the effect of passively sensitizing both human bronchi and isolated lung mast cells with either serum from atopic asthmatic patients or human monoclonal IgE. Peripheral bronchi ( < 5 mm in internal diameter) were dissected out from human lung obtained at thoractomy and isometric contraction was studied in response to a variety of immunological stimuli according to the sensitization protocol. Mast cells were also isolated from human lung and histamine release was measured under similar experimental conditions. A contractile response was elicited by either the specific antigen or anti-IgE (0.6-600 ng.mL-1) but not anti-immunoglobulin G (IgG) 0.2-20 micrograms.mL-1) in airways sensitized with atopic serum (total IgE concentration of approximately 1,000 international units (IU).mL-1). The maximal contractile response to anti-IgE was 75 +/- 22% of the response to 1 mM acetylcholine. Similarly, anti-IgE released histamine from isolated lung mast cells sensitized with atopic serum up to 22.4 +/- 2% of total histamine measured within mast cells. When isolated airways or mast cells were sensitized with human monoclonal IgE (1,000 IU.mL-1), response to anti-IgE in terms of contractile response or histamine release, respectively, were not significantly different from those obtained following passive sensitization with atopic serum. Finally, the bronchial contractile response to anti-IgE depended not only on the concentration of anti-IgE but also on that of IgE (300-2,000 IU.mL-1) used to sensitize the airways. These results indicate that the effect of antigen or anti-IgE in peripheral bronchi passively sensitized with atopic serum is mimicked when sensitization is carried out directly with human monoclonal IgE.

Adult↗
PubMed1998

Influence of external pH on ciliary beat frequency in human bronchi and bronchioles.

Ciliated respiratory epithelial cells have to tolerate variations in local pH caused by the respiratory cycle and potential ventilation-perfusion mismatches. We showed previously that peripheral bronchiolar cilia beat at a lower frequency than bronchial cilia, and have now investigated whether they show differences in tolerance to changes in pH. Using the image analysis system applied in the previous study, we compared variations in the ciliary beat frequencies (CBF) of bronchi and bronchioles sampled from human lung resections at various pH in vitro. Application of nonparametric tests (the variance of samples was not similar) indicated that CBF was not significantly modified when pH was varied between 7.5 and 10.5 for bronchi, and between 5.5 and 10.5 for bronchioles. Reversible and significantly lower CBF were observed below pH 7.0 for bronchi and below pH 5.0 for bronchioles. Extreme pH values such as 11.0 or 3.0 were lethal within a few minutes. Thus, respiratory ciliary beating is able to tolerate external pH variations between 3.5 and 10.5 without permanent impairment. In addition we found that alkaline pH values are more favourable than acidic ones and that bronchiolar ciliated cells are more tolerant to acidic pH than bronchial cells.

Bronchi↗
PubMed1997

Ciliary beat frequency in human bronchi and bronchioles.

STUDY OBJECTIVE: This study aimed to determine the differences between ciliary beat frequencies of respiratory ciliated cells from peripheral bronchioles and from proximal bronchi in humans. DESIGN: Measurements were made from resected lungs. Ciliated cells were harvested by brushing the mucosa of each site immediately after surgery. Brushings with a cytology brush were performed on normal areas of the resected cartilaginous bronchus for proximal samplings and through a peripheral bronchiole close to the visceral pleura for peripheral samplings. For each site, at least 12 different measurements were made at 22 degrees C using an image analysis system. RESULTS: A highly significant difference between proximal bronchi (mean, 7.1 Hz; SD, 1.29) and peripheral bronchioles (mean, 4.6 Hz; SD, 1.39) (p < 0.0001) was found. CONCLUSION: Thus, cilia from peripheral bronchioles beat at a 35% lower beat frequency than cilia from proximal bronchi.

Aged↗
PubMed2001

Estimation of fibrous aerosol deposition in upper bronchi based on experimental data with model bifurcation.

Lung deposition of fibrous aerosol was studied by using a model of the lung bifurcation with dimensions based on the symmetric model A of Weibel. The fibrous aerosols were introduced to the model under steady inspiratory flow conditions. Glass fibers depositing in the daughter tubes and these escaping from them were observed under a scanning electron microscope (SEM). The deposited fractions were calculated for each length and diameter using a bivariate lognormal distribution. In this study the authors propose empirical equations to estimate total deposited fractions of fibrous aerosol at upper bronchi. The dimensionless relationship among deposited fractions Fd, Stokes number St for randomly-oriented fibers and interception parameter I were used to estimate the deposited fraction at arbitrary position in the upper bronchi. The calculation procedure for Fd(St,I) consists of two steps: the determination of the four deposited fractions, Fdn for each In (n=1-4) followed by interpolation or extrapolation from Fdn to find the deposited fraction Fd at a given I. With this procedure, it is possible to determine the deposited fraction Fd in the range of 2 x 10(-3)<St<5 x 10(-2) and 5 x 10(-4)<I<5 x 10(-2). Penetration from the trachea to the 10th generation of lung bifurcation was calculated for several cases of fiber diameter, length and flow rate. In the case corresponding to an inspiration of 500 cm3 air at a constant rate for 2 s, more than half of the fibers with a length of 100 microm and diameter of 3 microm are deposited at upper bronchi but more than 90% of fibers of the same length and 1 microm in diameter pass through the region.

Aerosols↗