Objectives To describe the clinicopathologic findings and outcome in dogs with atypical hypoadrenocorticism (Group 1) and dogs with suspected atypical hypoadrenocorticism whose post-adrenocorticotropic hormone stimulation cortisol concentrations were greater than 55 nmol/L but below the laboratory reference interval (Group 2). Methods Medical records were searched to identify dogs diagnosed with hypoadrenocorticism between January 2004 and June 2014. Dogs were excluded if their Na:K ratio was less than 27 or if they had received prior therapy that could interfere with adrenocorticotropic hormone stimulation testing. Results Forty dogs were included in Group 1 and nine dogs in Group 2. In Group 1, the most common biochemical abnormalities were hypoalbuminaemia (87%) and hypocholesterolaemia (76%). Of 35 dogs in Group 1 with follow-up biochemistry results, five (14%) developed electrolyte abnormalities at 2 to 51 months post diagnosis. Of seven dogs in Group 2 with follow-up, glucocorticoid therapy was discontinued in two dogs without return of clinical signs, four dogs were subsequently diagnosed with inflammatory bowel disease and one dog continued to have clinical signs despite glucocorticoid treatment. Clinical Significance Dogs with gastrointestinal signs and hypoalbuminaemia and, or, hypocholesterolaemia should be evaluated for atypical hypoadrenocorticism. Follow-up electrolyte monitoring is recommended because some will develop electrolyte abnormalities. Although dogs in Group 2 had a clinical presentation compatible with atypical hypoadrenocorticism, the diagnosis appears unlikely based on review of follow-up data. Dogs with equivocal adrenocorticotropic hormone stimulation results should be evaluated for other underlying diseases such as inflammatory bowel disease. The use of endogenous adrenocorticotropic hormone measurements in these dogs warrants investigation.

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SUMMARYThe effects of propranolol on the electrical behavior of ventricular muscle fibers were investigated in the anesthetized dog by simultaneously recording surface and intracellular electrograms. After administration of propranolol during sinus rhythm, the RR, PQ and QT intervals were significantly prolonged, while the QRS duration remained unchanged. During electrically driven rhythm, propranolol caused a slight but insignificant prolongation of the QT interval. There were no changes in the QRS duration. Significant delay of the interatrial and atrioventricular conduction times was observed. There were no significant changes in the intraventricular conduction time. Propranolol principally affects the sinoatrial node, the atrioventricular node and the conduction time of the atria. Effects of propranolol on the intracellular electrograms from the ventricle were as follows. The duration of the membrane action potential was significantly prolonged. No changes were observed in the amplitudes of the membrane action potential, membrane resting potential and overshoot. The maximum upstroke velocity of the membrane action potential did not change. Propranolol has a quinidine-like action as well as a beta adrenergic blocking action. Both actions contribute to the effectiveness of the drug in the treatment of cardiac arrhythmias.