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To characterize the magnitude, character, and time course of chronotropic and dysrhythmogenic responses of dogs with vagally mediated bradycardia to atropine sulfate.


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Seven clinically normal adult mixed-breed dogs.


Vagally mediated bradycardia was induced with morphine and fentanyl citrate. Atropine (0.02 mg/kg of body weight) was administered IV, SC, or IM. Electrocardiograms were recorded continuously for 5 minutes before and for 35 minutes after atropine administration or until a sustained parasympatholytic response was observed. Data were digitized, analyzed independently for changes in atrial and ventricular rate, and compared between different routes of administration.


All dogs developed second-degree atrioventricular (AV) block after IV administration of atropine, and 71% of dogs developed AV block after SC or IM administration. The AV block arose and resolved more rapidly with IV administration than with SC or IM administration. The AV block was principally attributable to an increase in the atrial rate prior to increases in the ventricular rate. Atropine, regardless of route of administration, potentiated baseline ventricular bradycardia in 62% of the experiments (mean heart rate decrease of 16 beats/min; decreased to < 20 beats/min in 2 dogs for ≤ 10 seconds). Duration of the bradycardic potentiation was longer with SC administration (9.1 minutes, SC, vs 1.4 minutes, IV, and 4.6 minutes, IM). Parasympatholytic rate was higher for IV than SC or IM administration (128 beats/min vs 92 beats/min and 101 beats/min). Two dogs given atropine SC failed to resolve the AV block and attain sinus rhythm.


Administration of 0.02 mg of atropine/ kg by IV, IM, and SC routes for vagally mediated bradycardia in dogs consistently induces AV block and occasional brief potentiation of ventricular bradycardia.

Clinical Relevance

Parasympathomimetic effects occur and resolve most rapidly and consistently, and the stable parasympatholytic effect is of greatest magnitude after IV administration. Thus, vagally mediated bradycardia in clinically normal dogs appears to be best abolished by IV administration of atropine.(Am J Vet Res 1996;57:337-341)

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in American Journal of Veterinary Research


Objective—To define relationships between hoofacceleration patterns of galloping horses and dynamic properties of the track.

Animals—8 Thoroughbred horses without lameness.

Procedure—Acceleration-time curves were recorded by use of accelerometers attached to each hoof as each horse galloped over the track straightaway. Four sessions were conducted for each horse, with the track surface modified by sequentially adding water before each session. These acceleration-time curves were analyzed to determine peak accelerations during the support phase of the stride. Track dynamic properties (hardness, rebound, deceleration rate, rebound rate, and penetration) were recorded with a track-testing device. Moisture content and dry density were measured from soil samples. Stepwise multiple regression was used to identify relationships between hoof-acceleration variables and track dynamic properties.

Results—Track rebound rate was most consistently related to hoof variables, especially through an inverse relationship with negative acceleration peaks for all hooves. Also, rebound rate was related to initial acceleration peak during propulsion of the hooves of the forelimb and the nonlead hind limb as well as to the second acceleration peak during propulsion of the lead hooves of the hind limb and nonlead forelimb.

Conclusions and Clinical Relevance—The inverse relationship between track rebound rate and negative acceleration peaks for all hooves reflects the most important dynamic property of a track. Any factor that reduces negative acceleration of the hooves will increase stride efficiency by allowing smoother transition from retardation to propulsion and therefore may be important in determining the safety of racing surfaces. (Am J Vet Res 2005;66:589–595)

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in American Journal of Veterinary Research