Microscopic anatomy of the horizontal part of the external ear canal was evaluated in 24 dogs. Sixteen dogs were from breeds known to have a predisposition to otitis externa. The remaining 8 dogs were from breeds that do not have a predisposition to otitis externa. Dogs were separated into groups according to predisposition to otitis externa: group 1--predisposed dogs without otic inflammation, group 2--predisposed dogs with otic inflammation, and group 3--nonpredisposed dogs without otic inflammation. Qualitative microscopic evaluation of distribution of hair follicles revealed hair within proximal, middle, and distal regions of the horizontal ear canal in all breeds. The degree of keratinization was directly proportional to the presence of otic inflammation and was excessive in group-2 dogs. Quality of sebaceous glands within the horizontal ear canal was similar among dogs with and without otitis externa, whereas the quantity of apocrine tubular glands was significantly increased (P < 0.05) in dogs with otitis. Quantity of apocrine tubular glands was also greater in group-1 dogs than in group-3 dogs. Thickness of the soft tissue in the external ear canal increased in direct proportion to the progression of disease and was greatest in the proximal region of the affected ear canal. Soft tissue located caudally between nonopposing ends of the annular cartilage, within the proximal region of the horizontal ear canal, contained few glands and hair follicles in dogs without otitis externa. In dogs with otitis externa, this region was infiltrated by distended apocrine tubular glands.

Pharmacokinetics and toxicity of a single dose of doxorubicin, at dosages of 30 mg/m2 of body surface area and 1 mg/kg of body weight, were compared in 17 dogs. Effects of doxorubicin on complete blood cell count, platelet count, and the dogs' clinical condition were evaluated for 14 days. Cluster analysis, on the basis of clinical signs of doxorubicin toxicosis at the 30-mg/m2 dosage, revealed that 6 of 7 small dogs (less than or equal to 10 kg) became ill, whereas 7 of 10 large dogs (> 10 kg) remained clinically normal. Small dogs that received doxorubicin at a dosage of 30 mg/m2 had higher peak plasma concentrations, greater area under the curve for plasma drug concentration vs time, longer drug elimination half-lives, greater volumes of distribution, and more clinical signs of toxicosis than had large dogs (P less than or equal to 0.05). Five of 9 small dogs that received doxorubicin at a dosage of 30 mg/m2 developed severe myelosuppression (< 1 X 103 granulocytes/microliter). In contrast to the toxicoses with body surface area-based dosing, myelosuppression was not induced in small dogs that received doxorubicin at a dosage of 1 mg/kg. In small and large dogs given doxorubicin at a dosage of 1 mg/kg, pharmacokinetic characteristics and clinical signs of toxicosis were similar. Mean WBC counts and granulocyte counts for all dogs were lower on day 7 with 30 mg of doxorubicin/ m2 (n = 17), compared with that for 1 mg of doxorubicin/kg (n = 14; P S 0.01). This study indicated that a body weight-based (milligram per kilogram) dosing regimen may result in more uniform therapeutic and toxic responses in dogs. Limited toxicosis was observed in dogs weighing > 10 kg treated with doxorubicin with either dosing scheme; however, differences in pharmacokinetic profiles suggested that 1 mg/kg may be an inappropriately low dosage.

A significant (P less than 0.0001) positive correlation was demonstrated between left ventricular internal chamber dimension in diastole or systole and body weight, body surface area, cycle length, and the square root of cycle length. On the basis of adjusted coefficients of determination, multiple regression analysis, using body weight or body surface area and cycle length or the square root of cycle length, was superior to separate simple regression with these variables in accounting for variations in left ventricular internal chamber dimensions. Shortening fraction had a significant (P less than 0.0001) negative correlation and left ventricular free wall measurements had a significant (P less than 0.0001) positive correlation to body weight and body surface area. For these echocardiographic variables, correlation to the square root of cycle length was insignificant (P greater than 0.05), and a multiple regression model was not helpful in developing confidence intervals. Septal wall measurements were not correlated with body weight, body surface area, cycle length, or the square root of cycle length.