Airways Of Dogs Research Articles

Comparison of in vitro drug responses in airways of atopic dogs with and without in vivo airway hyperresponsiveness

For comparison with previous studies in greyhounds and in the Basenji-Greyhound dog model of asthma (BG), basenji dogs were studied under identical conditions with respect to airway responsiveness to inhaled methacholine, cutaneous responses to intradermal antigen injection, and the sensitivity of isolated trachealis muscle to methacholine and isoproterenol. The relaxant effect of isoproterenol was assessed in trachealis muscle precontracted with methacholine (ED 50). The basenji dogs resembled the BG dogs in that they showed multiple positive skin tests. Further, trachealis muscle showed a markedly reduced sensitivity to methacholine (pD 2 6.64 ± 0.10) (±S.E.) in vitro. However, basenji dogs resembled the greyhounds in requiring high concentrations of methacholine aerosols to produce a 2-fold increase in pulmonary resistance (1.68 mg/ml ± 1.21). Thus, there were no significant correlations between sensitivity to methacholine in vitro and airway responsiveness to methacholine in vivo; however, the reduced sensitivity to methacholine in vitro in both basenji and BG dogs may be related to the marked atopy characteristic of both groups. In vitro sensitivity to isoproterenol was correlated (r=0.82) with the concentration of methacholine needed to elicit the test contraction, but isoproterenol sensitivity in BG dogs was significantly less (p=.0027) than that predicted by the common regression line. This deficit in beta adrenergic function in trachealis muscle unrelated to atopy may be important in the in vivo airway hyperresponsiveness of BG dogs.

Deposition and Clearance of Radiolabeled Particles from Small Ciliated Airways in Beagle Dogs

ABSTRACT Clearance rates of particles from small ciliated airways were measured in five Beagle dogs to determine if clearance was virtually complete in a few days, as predicted by most models. Both 3–μm latex microspheres radiolabeled with 85Sr and 9–μm latex microspheres radiolabeled with l41Ce were used. A powder aerosol generator was developed to produce a puff of the mixed microspheres for deposition limited to selected airway segments. This aerosol was introduced through a catheter in the biopsy channel of a fiberoptic bronchoscope. The tip of the bronchoscope was located in a 6th–generation airway of the anesthetized dogs. Deposition of fluorescent particles followed by immediate sacrifice, drying of the lung, and sectioning, showed that deposition occurred predominantly in the 6th–10th generation bronchi without significant deposition in the alveolar region. Gamma–camera images of radiolabeled particles were consistent with this finding; deposition was restricted to discrete spots in the five dogs....

Editorial Is 24 Hour Lung Retention an Index of Alveolar Deposition?

Journal of Aerosol MedicineVol. 1, No. 1 Editorial Is 24 Hour Lung Retention an Index of Alveolar Deposition?WM. MICHAEL FOSTERWM. MICHAEL FOSTERSearch for more papers by this authorPublished Online:4 Feb 2009https://doi.org/10.1089/jam.1988.1.1AboutSectionsPDF/EPUB Permissions & CitationsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail FiguresReferencesRelatedDetailsCited byMucociliary FunctionRemoval of sedimentation decreases relative deposition of coarse particles in the lung peripheryJournal of Applied Physiology, Vol. 115, No. 4Nanoparticle-Lung Interactions and Their Potential Consequences for Human Health4 January 2013Deposition, Imaging, and Clearance: What Remains to be Done? Gerhard Scheuch, William Bennett, Lars Borgström, Andy Clark, Richard Dalby, Myrna Dolovich, John Fleming, Peter Gehr, Igor Gonda, Chris O'Callaghan, Glyn Taylor, and Steve Newman6 December 2010 | Journal of Aerosol Medicine and Pulmonary Drug Delivery, Vol. 23, No. S2Particulate Dosimetry in the Respiratory Tract28 March 2013Mucociliary and long-term particle clearance in the airways of healthy nonsmoker subjectsJournal of Applied Physiology, Vol. 97, No. 6Simulation of the regional manifestation of asthmaJournal of Pharmaceutical Sciences, Vol. 93, No. 5Risk assessment dosimetry model for inhaled particulate matter: II. Laboratory surrogates (rat)Toxicology Letters, Vol. 138, No. 1-2Clearance of Particles Deposited in the Lungs23 August 2013An Empirical Dosimetry Model of Aerodynamic Particle Deposition in the Rat Respiratory Tract27 September 2008 | Inhalation Toxicology, Vol. 8, No. 6Implications of Airway Retention for Radiation Doses from Inhaled Radionuclides M.R. BAILEY, M.-D. DORRIAN, and A. BIRCHALL4 February 2009 | Journal of Aerosol Medicine, Vol. 8, No. 4Annexe E. clearance of particles from the respiratory tract16 November 2016 | Annals of the ICRP, Vol. 24, No. 1-3Deposition of Sulfate Acid Aerosols in the Developing Human Lung27 September 2008 | Inhalation Toxicology, Vol. 5, No. 1Extrapolation Modeling of Aerosol Deposition in Human and Laboratory Rat Lungs27 September 2008 | Inhalation Toxicology, Vol. 4, No. 4Influence of Inhaled Atropine on Lung Mucociliary Function in HumansAmerican Review of Respiratory Disease, Vol. 144, No. 5Histological and Stereological Analysis of Particle Retention in the Conducting Airways of Hamster Lungs MARIANNE GEISER, VINZENZ IM HOF, PETER GEHR, and LUIS M. CRUZ-ORIVE19 March 2009 | Journal of Aerosol Medicine, Vol. 3, No. 2Stereological estimation of particle retention and clearance in the intrapulmonary conducting airways of the hamster lungsJournal of Aerosol Science, Vol. 21, No. 3Deposition and Clearance of Radiolabeled Particles from Small Ciliated Airways in Beagle Dogs R.K. WOLFF, H. TILLQUIST, B.A. MUGGENBURG, J.R. HARKEMA, and J.L. MAUDERLY27 July 2010 | Journal of Aerosol Medicine, Vol. 2, No. 3 Volume 1Issue 1Jan 1988 To cite this article:WM. MICHAEL FOSTER.Editorial Is 24 Hour Lung Retention an Index of Alveolar Deposition?.Journal of Aerosol Medicine.Jan 1988.1-9.http://doi.org/10.1089/jam.1988.1.1Published in Volume: 1 Issue 1: February 4, 2009PDF download

Sensor for measuring surface fluid conductivity in vivo

Thin-film microelectronic technology was used to fabricate a miniature, flexible sensor that can be placed directly onto the surface of the airway to measure the electrical conductance of the fluids present. Gold was deposited on glass, oxidized silicon, and polyimide substrates. The parallel gold electrodes were etched into an interdigitated configuration that increased the effective sensing area without increasing the sensor size. A temperature-sensitive resistor was added to make calculations possible to account for the effect of temperature on fluid conductivity. Fluid conductivity was measured and from this information osmolarity was calculated. Physiologic evaluation of the device and corroboration of the calculations was obtained by placing the sensor in the airway of mongrel dogs and simultaneously collecting surface fluids for atomic absorption spectroscopy and freezing-point-depression analysis. Osmolarity calculations made from the sensor data were consistently about 25% lower than clinical laboratory osmolarity analysis. In vitro tests of the sensor included calibration in multiple dilute salt solutions, temperature sensitivity assessment, and evaluation of the effects of solution concentration on electrical conductance.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>

Comparative distribution of cholinomimetic and parasympathetic contractile responses in the major diameter airways of dogs

The distribution of cholinomimetic and parasympathetic contractile responses in the major diameter airways and the simultaneous change in lung resistance was examined in 10 mongrel dogs in vivo. The airways of animals anesthetized with chloralose-urethane were insufflated with tantalum, and responses in airway generations 0 (trachea) through 5 were assessed as the change in airway diameter (dDaw) at functional residual capacity (FRC). All animals had beta-adrenergic blockade with propranolol to block reflex sympathetic effects resulting from hypotension. Sequential dose-response curves to 10(-10) to 10(-7) mol/kg iv methacholine (MCh; n = 5) were elicited; in separate studies, stimulus-response curves were generated (1-20 Hz; n = 5) at 7 min intervals. Tantalum bronchograms were obtained at each point on the stimulus/dose-response curve for each animal. Maximal parasympathetic stimulation caused a 28.8 +/- 4.35% dDaw in trachea, a 37.2 +/- 2.33% dDaw in generation 1 airways and a 42.4 +/- 3.63% dDaw in generation 5 airways. In contrast, cholinomimetic stimulation caused substantially less narrowing of trachea (dDaw = 8.04 +/- 2.60%; P less than 0.001 vs cholinomimetic stimulation) and generation 1 airways (21.6 +/- 2.06%; P less than 0.001) and substantially less change in airway resistance (981 +/- 107% for MCh vs 1634 +/- 173% P less than 0.01) when diameter changes in generation 5 airways were comparable (45.6 +/- 7.38% vs 42.4 +/- 3.63%; P = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Muscarinic cholinergic inhibition of adenylate cyclase in airway smooth muscle.

The goal of our study was to test for an inhibitory effect of acetylcholine on adenylate cyclase activity in canine trachealis muscle. Therefore, cells were dispersed from the muscle enzymatically and lysed, and adenylate cyclase activity was assayed in a membrane suspension isolated from the lysates. Maximal beta-adrenergic stimulation, in the presence of GTP (10(-4) M), increased the activity of adenylate cyclase twofold above the activity induced by GTP alone. In the presence of GTP, acetylcholine (10(-4) M) decreased activity from 97 +/- 21 to 55 +/- 13 pmol cyclic AMP X min-1 X mg protein-1 (means +/- SE; n = 5; P less than 0.05); in the presence of GTP plus isoproterenol (10(-4) M), the acetylcholine-induced decreases were from 163 +/- 29 to 101 +/- 15 pmol cyclic AMP X min-1 X mg protein-1 (P less than 0.05). These decreases were dose dependent and they were altered by a series of cholinergic agents in a pattern consistent with a muscarinic effect. Our results suggest that one biochemical effect of vagal stimulation in the central airways of dogs may be attenuated adenylate cyclase activity in the smooth muscle.

Effects of anatomical and pharmacological vagal nerve blockade on the action of vasoactive substances in the airway and circulatory system in anesthetized dogs

Effects of anatomical and pharmacological vagal nerve blockade on the action of vasoactive substances in the airway and circulatory system in anesthetized dogs

Dry air-induced constriction in lung periphery: a canine model of exercise-induced asthma.

We studied the effects of the flow of dry air on collateral tone in the lung periphery. A bronchoscope was wedged in sublobar segments of anesthetized dogs, and measurements of collateral resistance (Rcs) were recorded before and after flow was increased from 200 to 2,000 ml/min for a 5-min period. Five minutes after exposure was completed, Rcs increased by an average of 117 +/- 25.2% (SE) over control. Maximum Rcs occurred 5 min after the challenge was concluded and required 48 +/- 10.5 min to return to base line. When flow rate was held constant and exposure period varied, Rcs increased with increased stimulus duration. With exposure times held constant, the response of the collateral system was positively associated with changes in stimulus strength (flow rate). No refractory period was observed with repetitive challenges. Finally, when dry air (delivered at 22 degrees C) and conditioned air (i.e., delivered at 28 degrees C; relative humidity = 80%) challenges were alternated in the same wedged segment, dry air produced a mean increase in Rcs of 93.2%, whereas challenge with warm moist air increased Rcs only 33.5%. Regardless of which challenge was presented first, dry air consistently produced a greater constrictor response. This response is similar to that observed in cold air- and exercise-induced asthma and indicates that the lung periphery in dogs, like larger airways in asthmatic subjects, has the potential to increase tone when exposed to dry air. Peripheral airways in dogs thus constitute a model that can be used for the investigation of exercise-induced asthma.

Location of flow-limiting segments via airway catheters near residual volume in humans.

Previous studies have demonstrated sites of flow limitation in the central airways of dogs and humans. At low lung volumes, however, during a forced expiration, it is not clear whether flow-limiting segments (FLS) move into the lung periphery. Using intrabronchial lateral pressure catheters, we located FLS in human subjects at all lung volumes between functional residual capacity (FRC) and residual volume (RV). Three individuals with severe intracranial hemorrhage maintained on ventilators were studied. Partial maximal flow-volume curves were generated from 1 liter above FRC to RV by lowering downstream pressure and using the interrupter technique. Sites of FLS were defined as the most downstream points where lateral pressure did not change with driving pressure. FLS were found in all subjects in the central airways. In one subject, FLS moved from segmental bronchi to the first subsegmental bronchus as RV was approached but not beyond. In the other two subjects, FLS remained fixed in location at all measured lung volumes. At constant volume, multiple FLS were located, all in parallel, e.g., fixed in left upper, left lower, and right middle lobar bronchi. In conclusion, sites of flow limitation remain in the central airways as lung volume approaches RV. FLS may move peripherally within the central airways but not beyond proximal subsegmental bronchi.

Acute effects of cigarette smoke inhalation on peripheral airways in dogs.

We studied the acute effects of the inhalation of cigarette smoke on the central and peripheral airways of 35 open-chested and tracheotomized dogs by the direct measurement of central (Rc) and peripheral (Rp) airway resistances. Rc was calculated by dividing the pressure difference between a tracheal catheter and a retrograde catheter by mouth flow, and Rp was obtained by dividing the pressure difference between the retrograde catheter and a pleural capsule by mouth flow. The pleural capsule was attached to the pleural surface for alveolar pressure measurement. Rc and Rp were measured by the 2-Hz forced oscillation method. With lung inhalation of the smoke of two-thirds of one cigarette in vagi intact dogs, Rp increased to 239% of the control value and Rc increased to 112%. After bilateral vagotomy, Rp increased to 143% and Rc increased to 104%. Propranolol did not influence the results. Hexamethonium and atropine both blocked these responses when vagi were intact. When the upper trachea, larynx, and nasopharynx, which were completely blocked by vagotomy, were exposed to the smoke of two-thirds of a cigarette, Rp increased to 155% and Rc increased to 144%. We thus conclude that cigarette smoke causes a major increase in Rp, mainly via the vagal reflex and partially via the stimulation of parasympathetic ganglia (probably nicotine), and a minor increase in Rc via vagal reflex.

Reflex depression of cardiovascular function during lung inflation.

These experiments were intended 1) to determine the cardiovascular reflex response initiated by lung inflation and 2) to determine the autonomic neural mechanisms that mediate the reflex responses. To test only the reflex effects of lung inflation and eliminate the associated mechanical effects thereof, we isolated the left airway and left pulmonary artery of dogs and performed static inflations of the left lung. Left lung inflation (LLI) to 30 cmH2O caused left ventricular systolic pressure, heart rate, and hindlimb vascular resistance to fall 20, 31, and 15%, respectively. When the hearts were paced to eliminate Bowditch effects, LLI caused left ventricular contractility, which was measured as dP/dt at 30 mmHg developed pressure and as the maximal rate of shortening of the contractile element, to fall 23 and 20%, respectively, and cardiac output (stroke volume) to fall 31%. Transection of the left cervical vagus nerve, interrupting most afferent and some efferent pathways from the left lung, virtually eliminated subsequent cardiovascular responses to LLI. Hindlimb vasodilation was mediated by alpha-adrenergic activity, and the fall in left ventricular contractile state was caused by a reduction in beta-adrenergic activity. The reflex bradycardia was mediated by increased cholinergic and decreased beta-adrenergic activity. These data establish that reflex mechanisms exist whereby expansion of the lung can reflexly modulate heart rate, ventricular contractility, systemic vasomotor tone, cardiac output, and stroke volume independent of the direct mechanical influence of lung expansion on these circulatory phenomena.

Prostaglandin F 2α increases responsiveness of pulmonary airways in dogs

We studied the effect of prostaglandin F 2α (PGF 2α) on the responsiveness of pulmonary airways in dogs. Airway responsiveness was assessed by determining the bronchoconstrictor response to increasing concentrations of acetylcholine aerosol delivered to the airways. In each of five dogs, we determined responsiveness during treatment with physiologic saline, histamine, or PGF 2α aerosols. The doses of histamine and PGF 2α were determined by establishing the largest dose of each which could be given to the dog without causing bronchoconstriction (subthreshold doses). We found that airway responsiveness was not significantly different during histamine treatment than after saline, however, responsiveness increased during treatment with PGF 2α. In addition, the hyperresponsiveness induced by PGF 2α was prevented by pretreatment with the ganglion blocking drug hexamethonium (5 mg/kg given intravenously). The results show that PGF 2α specifically increases the responsiveness of pulmonary airways in doses that do not cause bronchoncostriction, and suggest that the hyperresponsiveness involves a neural mechanism such as increased responsiveness of airway sensory nerves.

Airway constrictor effects of leukotriene D 4 in dogs with hyperreactive airways

Leukotriene D 4 (5 μg/ml) aerosol constricts airways of dogs with nonspecific airway hyperreactivity but not of mongrel dogs which lack nonspecific airway hyperreactivity. R L increased 200 + 25% and C dyn decreased to 77 ± 5% of the pre-challenge value. LTD 4 (10 μg/ml) produced no further increase. Atropine (0.2 mg/kg) prevented the increase in R L and decrease in C dyn, suggesting that part of the effect of LTD 4 on airways is neurally mediated.

Characterization of tracheal mast cell reactions in vivo. Inhibition by a beta-adrenergic agonist.

In 12 anesthetized dogs, we tested the effects of pharmacologic beta-adrenergic stimulation on the severity of tracheal mast cell reactions in vivo (Am Rev Respir Dis 1979; 119:62). In control dogs, tracheal arterial injections of compound 48/80 produced arteriovenous differences in histamine concentrations across the trachea (35 +/- 15 ng/ml), but not the lung; this finding suggested selective degranulation of tracheal mast cells. Tracheal arteriovenous histamine differences correlated (r = 0.70) with tracheal contractions (12 +/- 4 g/cm) induced by compound 48/80 in these animals. In other dogs, injections of isoproterenol (10 micrograms/kg) before compound 48/80 prevented the development of both tracheal arteriovenous differences and contractions. We concluded that pharmacologic beta-adrenergic stimulation inhibited degranulation of tracheal mast cells. The preparation appears suitable for examining the effects of endogenous stimuli on the severity of mast cell reactions in the central airways of anesthetized dogs.

Basenji-greyhound dog model of asthma: pulmonary responses after beta-adrenergic blockade.

To understand the mechanism underlying bronchial hyperreactivity in the Basenji-Greyhound (BG) dog, the effects of propranolol (2 mg/kg) and hexamethonium (5 mg/kg) on base-line pulmonary mechanics and on the bronchial response to aerosol challenges of citric acid and methacholine were studied in five BG dogs. Both propranolol and hexamethonium increased base-line pulmonary resistance (RL) from 0.69 +/- 0.05 (means +/- SE) cmH2O.l-1.s to 1.67 +/- 0.10 (P less than 0.05) and 2.22 +/- 0.45 cmH2O.1-1.s (P less than 0.05) and decreased dynamic compliance (Cdyn) from 190 +/- 10 ml/cmH2O to 154 +/- 9 (P less than 0.05) and 140 +/- 9 (P less than 0.05) ml/cmH2O, respectively. Both propranolol and hexamethonium potentiated the pulmonary response to 10% citric acid given for 5 min (P less than 0.05). RL postchallenge was 4.4 +/- 0.23, 8.1 +/- 0.81, and 7.8 +/- 0.31 cmH2O.l-1.s, and Cdyn was 78 +/- 5, 58 +/- 6, and 51 +/- 3 ml/cmH2O in untreated, propranolol-pretreated, and hexamethonium-pretreated animals. In untreated BG dogs, methacholine (0.075 mg/ml) increased RL from 0.94 +/- 0.25 to 2.2 +/- 0.21 cmH2O.l-1.s (234%) and decreased Cdyn from 223 +/- 39 to 141 +/- 14 ml/cmH2O (63%). In the same animals pretreated with propranolol, methacholine (0.075 mg/ml) increased RL from 1.9 +/- 0.66 to 4.8 +/- 1.37 cmH2O.l-1.s (253%) and decreased Cdyn from 144 +/- 35 to 81 +/- 15 ml/cmH2O (56%). We conclude that propranolol produces airway constriction in BG dogs, as in asthmatic humans and that the effects of propranolol on airways in BG dogs are not due to parasympathetic or alpha-adrenergic predominance.

Series distribution of airway collapsibility in dogs

We studied the series distribution of collapsibility in four different-sized airways in dogs. The trachea and the extrapulmonary main bronchi in situ were isolated from the rest of the lungs by glued beads of 6-12 mm OD. In excised dog lungs, the intrapulmonary large and small bronchi were isolated from the rest of the lung by glued beads of 1-9 mm OD. Pressure-volume relationships were measured directly in the trachea and in the extrapulmonary bronchi; those of the intrapulmonary bronchi were derived from orthogonal bronchograms. Airway collapsibility, defined as the slope of the pressure-volume curve, was found to increase in all airways as transpulmonary pressure (PL) decreased. At PL 30 cmH2O there was little difference of airway collapsibility among the different sized airways; but, as PL decreased, the peripheral airways became more collapsible than the central airways. It is concluded that the tissues surrounding the trachea provided as much or more stiffness than did the lung tissues that surrounded the intrapulmonary airways. The larger collapsibility in the peripheral airways. The larger collapsibility in the peripheral airways relative to that of the central airways at lower PL may account for the peripheral migration of the flow-limiting segment during forced expiration.

A model of reflex tracheal constriction in the dog.

1 A tracheal pouch with its nerve and blood supply intact has been prepared in situ in dogs. 2 Mechanical stimulation of the upper airways in dogs anaesthetized with chloralose induced a consistent increase in pouch pressure which was abolished by bilateral vagal section. 3 The response of the pouch following mechanical stimulation of the airways was abolished by intravenous pentobarbitone, atropine, administered systemically or when present in the pouch, and tetracaine, applied to the stimulus area or when present in the pouch. 4 Salbutamol had no inhibitory effects on the response regardless of its route of administration. 5 These results suggest that the increase in pouch pressure following mechanical stimulation of the upper airways is mediated by a vagal reflex arc. 6 The technique may distinguish between drugs the site of action of which is at the afferent or efferent end of this reflex arc.

Reflex effects of left heart and pulmonary vascular distension on airways of dogs.

Two types of experiments were performed in anesthetized dogs on cardiopulmonary bypass to see if pulmonary vascular congestion and left heart distension would induce reflex bronchoconstriction. First we distended the isolated left heart and lung vessels with blood while ventilating the lungs and measuring airflow, tidal volume, and transpulmonary pressures. Congestion reduced dynamic compliance and increased inspiratory resistance. Vagotomy increased compliance and decreased resistance but did not alter the effects of congestion. Then we measured changes in tracheal wall tension while we separately distended the pulmonary vessels and left heart. Left heart distension increased tracheal tension, whereas pulmonary congestion increased tension in some dogs but decreased it in others. All effects were eliminated by vagotomy. We concluded that although left heart distension and pulmonary vascular congestion may reflexly increase airway tone, pulmonary congestion may at some times reflexly reduce tone. None of these reflex changes, however, appear to be important in the modest (approximately 20%) changes in airflow dynamics observed during combined left heart and pulmonary vascular distension.

Arterial plasma histamine concentration for airway obstruction due to different areas of the bronchial system. IV. Communication (author's transl)

The separate inhalation of A.E. aerosol in the upper and the peripheral parts of the airways in allergic dogs is followed by an increase of the histamine concentration in the arterial plasma. The correlation between the plasma histamine concentration and dynamic elastance and the correlation between dynamic elastance and arterial oxygen pressure is very similar following the challenge of the upper and the peripheral parts of the airways. The results argue for reflex bronchoconstriction also by challenge of the more peripheral airways. The results are in accord with the idea that the answer of Edyn depends on a product of local histamine concentration and the area in which the histamine is released. The number of sensory receptors per surface area which is suspected to be greater in the upper part of the airways may also be important.

Histochemical and biochemical evaluation of complex carbohydrates in respiratory tissue of a canine model of allergic asthma

Ascaris hypersensitive dogs were chronically exposed to aerosols of this antigen under conditions designed to provide reproducible, pharmacologically manipulatable, pulmonary pathophysiology. As a partial characterization of this model the activities of several glycosyltransferases present in the respiratory tissue of these animals were investigated. In most cases, no significant difference from the levels found in respiratory tissues of unchallenged dogs was observed. The observation that in a few instances the activities of the UDP-Gal: mucin galactosyltransferase was significantly higher in the challenged dogs suggests that the tissue may have been operating at a near maximal capacity with respect to the synthesis of glycoproteins, and was, perhaps, approaching the point of initiating an increase in its synthetic capacity. Airways of ascaris-challenged dogs displayed little histochemical evidence of hypersecretion except in occasional tracheal glands filled with sulfomucin. However, the tracheal and bronchial glands of the experimental dogs revealed an increased prevalence of luminal casts that consisted of sulfated complex carbohydrate which partially filled some of the somewhat dilated acinar and ductal lumens. Abundant mast cells were present around peripheral vessels and bronchi, and into alveolar septae in lungs of the experimental dogs.