A useful approach for evaluating antitussive drugs in humans is to determine the sensitivity of the cough reflex to a standard challenge. The purpose of this study was to determine if methods used to induce coughing in humans would be effective when used on awake, untrained, healthy dogs for future application in therapeutic trials involving dogs with spontaneous disease. Methods tested were: mechanically stimulating the trachea by digital compression as well as by vibration from an electric shaver, neck massager, and palm sander (11 dogs), and administering nebulized irritant (3000 micromolar capsaicin), acidic (1 M citric acid), and hypotonic (deionized water) solutions using face masks (4 dogs). The threshold for success was defined as induction of at least 2 moderate or strong coughs in at least 75% of the dogs. None of the methods tested was successful. Digital compression induced soft (n = 2) or moderate (n = 1) coughing in 3 of 11 dogs tested. Nebulization of citric acid induced 1 soft cough in 1 of 4 dogs. It was concluded that coughing cannot be successfully induced in awake, healthy dogs using methods that are successful in humans. Other strategies must be developed so that cough sensitivity can be objectively and non-invasively measured in dogs for clinical research purposes.

Objective—To compare responses of equine digital arteries (EDAs) and veins (EDVs) to human-acalcitonin gene-related peptide (hαCGRP), evaluate effect of the endothelium, and characterize receptors and sources of endogenous CGRP. Sample—Palmar digital vessels (5 to 9/experiment) from healthy adult horses killed at an abattoir. Procedures—Vessel rings were mounted under tension in organ baths containing Krebs-Henseleit solution at 30°C, with relaxation responses examined in vessels preconstricted with a thromboxane-mimetic (3 × 10(−8)M). Responses of endothelium-intact (+e) and -denuded (−e) EDAs and EDVs to hαCGRP C10−10 to 3 × 10(−7)M) were compared. Following incubation with an hαCGRP receptor antagonist (hαCGRP8–37; 1μM), responses of EDA(−e) and EDV(−e) to hαCGRP (10(−7)M) were obtained. Responses of endothelium-intact and -denuded arteries and veins to hαCGRP (3 × 10(−7)M) or capsaicin (10(−5)M) were evaluated as well as responses of endothelium-intact and -denuded EDA and EDV to hαCGRP (10(−10) to 10(−6)M) after incubation with endothelin-1 (ET-1; 10(−12)M). Results—hαCGRP resulted in nonendothelium, concentration-dependent relaxation in EDAs and EDVs, with greater responses in EDAs. Treatment with hαCGRP8–37 had minimal effect on responses to hαCGRP in either vessel type. Capsaicin induced relaxation in both vessel types. There were no differences between responses to hαCGRP for vessels pretreated with ET-1 or vehicle. Conclusions and Clinical Relevance—Both hαCGRP and capsaicin induced digital vasodilation unaffected by a functional endothelium. This suggested that endogenous CGRP likely emanates from sensory-motor nerves and may contribute to digital vasodilation.