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those airborne particles, mainly through hay feeding, airflow obstruction, neutrophilic airway inflammation, and bronchial wall remodeling occur. 3 Among the structural alterations of the bronchial wall, the remodeling of the airway smooth muscle (ASM

Open access
in American Journal of Veterinary Research

associated with heaves. 9 These bronchi models lack ASM, which is important to include because the contractile properties of ASM contribute to airway hyperresponsiveness. 10 Airway smooth muscle also has the ability to synthesize and release bioactive

Full access
in American Journal of Veterinary Research

Abstract

Objective

To determine the effect of in vivo antigen sensitization (Ascaris suum) of cats on tracheal smooth muscle (TSM) and bronchial smooth muscle (BSM) muscarinic reactivity in vitro.

Animals

Healthy domestic shorthair cats of either sex.

Procedure

Cats were sensitized and were longterm antigen (or sham) challenge exposed for 6 weeks by aerosolization with soluble Ascaris suum. Tracheal and BSM preparations were obtained and stimulated in vitro by electrical field stimulation (EFS), acetylcholine (ACh, a muscarinic agonist), and physostigmine (an AChase inhibitor). Responses were compared with responses of comparable tissues from sham antigen challenge-exposed cats.

Results

Tracheal and BSM from sensitized, compared with sham-sensitized (control), cats had greater isometric contraction (expressed as percentage of the response observed for isotonic, 63 mM KCl-elicited contraction [% KCI]) in response to endogenous (EFS) and exogenous muscarinic receptor activation (ACh). Contractions in response to EFS by TSM from control cats were 74 % KCI vs 97 %KCI for antigen-sensitized TSM (P < 0.04). Muscarinic responses were augmented comparably by in vivo sensitization; TSM from control cats contracted to 190 % KCI vs 230 % KCl (P < 0.03) for TSM from immune-sensitized cats. Physostigmine augmented responses of all tissues to ACh so that TSM from control (290 %KCI) and antigen-sensitized (257 %KCI) cats were similar. Responses of BSM from antigen-sensitized cats had similar augmentation of contractile response to EFS and ACh.

Conclusions

Long-term in vivo antigen sensitization increases numbers of muscarinic receptors on airway smooth muscle or decreases the availability or activity of AChase in cats.

Clinical Relevance

Modulation of muscarinic receptors may be useful for treatment of asthmatic cats with in vivo airway hyperreactivity. (Am J Vet Res 1997;58:672–676)

Free access
in American Journal of Veterinary Research

SUMMARY

We assessed the effect of serotonergic inhibition by cyproheptadine on the responsiveness of tracheal smooth muscle (tsm) strips and epithelium-intact third-generation bronchial rings from immune-sensitized (Ascaris suum) cats after exposure to antigen. Cats were sensitized by im administration of antigen and adjuvant twice over a 4-week period. Sensitization was confirmed in vivo by skin testing with antigen and by physiologic airway responses after exposure to nebulized antigen. Tissues were tethered isometrically to force transducers and were actively equilibrated by exposures to KCl-substituted perfusate. Maximal response after exposure to antigen (expressed as percentage of maximal contraction of each tissue to 63 mM KCl (%KCl) was 169 ± 18% KCl for sensitized tsm and 43 ± 18% KCl for sensitized tsm pretreated with cyproheptadine (P < 0.001). Similarly, maximal response to antigen was 81 ± 27% KCl for sensitized bronchial rings, compared with 16 ± 14% KCl for sensitized bronchial rings pretreated with cyproheptadine (P = 0.05 vs control). Blockade of leukotriene synthesis by 10−6 to 10−4 M A-64077, a selective 5-lipoxygenase inhibitor, had no significant effect on peak response for either tsm (193 ± 13% KCl vs 169 ± 18% KCl for sensitized untreated tsm) or bronchial rings (79 ± 20% KCl vs 81 ± 27% KCl for sensitized untreated bronchial rings). Release of serotonin from airway tissues was confirmed by the presence of serotonin in the perfusate of 8 sensitized tsm preparations after, but not before, antigen challenge. Our data indicate that airways from immune-sensitized cats have typical immediate-type hypersensitivity responses when exposed to antigen and that these responses are inhibited by serotonin-receptor blockade, but not by blockade of 5-lipoxygenase. These data implicate serotonin as an important mediator in the immediate-type hypersensitivity reaction in the immune-sensitized airways of cats and suggest a potential role for serotonin antagonists in the clinical treatment of asthma in this species.

Free access
in American Journal of Veterinary Research

Summary

Immunohistochemical methods were used to determine the distribution of pulmonary nerves containing either an enzymatic marker of adrenergic nerves, dopamine β hydroxylase, or the putative neurotransmitter neuropeptide Y in 7 equids with healthy lungs. Nerves immunoreactive for these substances were found on airway smooth muscle in nearly all the samples of healthy equine lung examined. These nerves were generally more numerous in the larger airways but could be detected even in noncartilaginous bronchioles. Pulmonary and bronchial vessels also contained numerous immunoreactive nerves. On the basis of these findings, we suggest that dopamine β-hydroxylase- and neuropeptide Y-immunoreactive nerves may be involved in the regulation of airway and vascular diameter in equids.

Free access
in American Journal of Veterinary Research

SUMMARY

During acute bouts of recurrent airway obstruction (heaves) in horses, neutrophils that are capable of increased production of reactive oxygen species accumulate in the airways. In the study reported here, the effect of hydrogen peroxide (H2O2; 1 µM to 0.1M), one of these reactive oxygen species products, on the responses of isolated trachealis muscle of horses was determined. Before and after incubation with H2O2, contractile responses to acetylcholine, electrical field stimulation (efs), 127 mM KCl, and relaxation responses to isoproterenol and activation of the nonadrenergic noncholinergic inhibitory response (iNANC) were evaluated. Beginning at 1 mM, H2O2 contracted trachealis muscle in a concentration-dependent manner. This contraction was unaffected by atropine (1 µM), tetrodotoxin (1 µM), or 1 µM meclofenamate. Contraction of trachealis muscle in response to H2O2 is, therefore, not attributable to release of prostaglandins, acetylcholine, or other neurotransmitters. Above a concentration of 0.1 mM, H2O2 depressed the responses to efs, acetylcholine, and KCl in a concentration-dependent manner. At 0.1M, H2O2 decreased the maximal responses to efs, acetylcholine, and KCl by 62.7 ± 7.2, 60.58 ± 6.12, and 37.8 ± 9.54%, respectively. In the presence of meclofenamate (1 µM), partial but significant protection against 1 to 100 mM H2O2 was observed. In tracheal strips contracted with 0.3 µM methacholine, H2O2 had no effect on the isoproterenol concentration-response curve. Up to a concentration of 100 mM, H2O2 had no effect on iNANC response. However, in the presence of 100 mM H2O2, this response was abolished in 2 of 4 horses. We conclude that high concentrations of H2O2 affected the responses of airway smooth muscle by actions on neurotransmission, muscarinic receptors, and downstream from receptors; some of the H2O2 effects were in part mediated by cyclooxygenase products; and H2O2 had no effect on β-adrenergic or iNANC-induced relaxation.

Free access
in American Journal of Veterinary Research

hypo-responsive to the contractile agonists acetylcholine and 5-hydroxytryptamine. Also known as serotonin, 5-hydroxytryptamine is a mediator released from mast cells that is well known to cause airway smooth muscle constriction in many species

Full access
in American Journal of Veterinary Research

. Because of the entrapped air, SPAOPD-affected lungs did not collapse when the thoracic cavity was opened. Airway obstruction is primarily caused by 3 factors (constriction of airway smooth muscle; thickening of airway walls as a result of smooth muscle

Full access
in American Journal of Veterinary Research

). Airway smooth muscle hyperplasia was also observed, possibly as a consequence of chronic respiratory stress. Chronic and severe obliterating endarteritis of the pulmonary artery was detected, with hyperplasia of the endothelial cells from the intima layer

Full access
in Journal of the American Veterinary Medical Association