This study investigated the pharmacokinetic profile of and pharmacodynamic response to dexmedetomidine administered intramuscularly (IM) at a dose of 10 μg/kg in healthy cats. Nine adult cats were evaluated before and after administration of the drug, with serial collections of plasma samples. Dexmedetomidine induced deep sedation, with a rapid onset of action and a duration of one hour, reaching a peak between 20 and 30 min after administration. The half-life (T½) was 70.2 ± 48 min, with a maximum concentration (Cmax) of 2.2 ± 1.9 ng/mL and time to reach maximum concentration (Tmax) of 26.4 ± 19.8 min. The area under the curve (AUC) was 167.1 ± 149.1 ng/mL*min, with a volume of distribution (Vd) of 2159.9 ± 3237.8 mL/kg and clearance (Cl) of 25.8 ± 33.0 mL/min/kg. There was a reduction in heart rate (HR) and respiratory rate (RR) in relation to the baseline, with a slight decrease in systolic (SBP), diastolic (DBP), and mean (MAP) blood pressure in the first hour. Blood glucose increased after 60 min. Dexmedetomidine proved to be effective and safe, with rapid absorption, metabolization, and elimination, promoting good sedation with minimal adverse effects after IM administration in healthy cats.

This study aimed to determine the pharmacokinetic profile of the active dipyrone metabolites, 4-methylaminoantipyrine and 4-aminoantipyrine, following intravenous administration in dogs. Eleven mixed-breed dogs received a 25 mg·kg⁻¹ dipyrone dose and blood samples were collected at 0, 5, 15, 30 and 45 min, as well as at 1, 1.5, 2, 4, 6, 8, 10, 12, 24, 36 and 48 h. Plasma concentrations of both metabolites were analyzed by ultra-performance liquid chromatography coupled to mass spectrometry. The PKSolver 2.0 and GraphPad Prisma 10 software programs were used for pharmacokinetic and statistical analyses, applying a Principal Component Analysis for MAA and descriptive statistics for both metabolites. Two groups were noteworthy concerning MAA: slow metabolizers (SM) and normal/rapid metabolizers (NM). Significant differences were observed between half-life (T_½) and MRT_{0_inf obs} values between the MAA groups. The T_½ and MRT_{0_info obs} were 44.44 ± 11.74 and 32.62 ± 16.53 h for the SM group and 11.25 ± 5.37 and 7.44 ± 4.25 h for the NM group, respectively. The C_max of AA was 2.80 ± 1.43 µg mL⁻¹. Metabolites were detectable for 48 h in all animals for MAA and seven for AA. These findings suggest that metamizole reaches analgesia plasma concentrations associated with cyclooxygenase inhibition with few adverse effects in dogs. However, additional pharmacogenetic and pharmacotherapeutic monitoring studies are required.

Our objective was to assess the pharmacokinetic characteristics of metamizole when administered together with tramadol in a single intravenous dose to donkeys. Ten male animals received 10 mg∙kg⁻¹ of dipyrone associated with 2 mg∙kg⁻¹ of tramadol (T₂M₁₀) and 25 mg∙kg⁻¹ of dipyrone with 2 mg∙kg⁻¹ of tramadol (T₂M₂₅). Venous blood samples were taken from groups to determine the pharmacokinetics after drug administration, using initial brief intervals that were followed by extended periods until 48 h. Restlessness and ataxia were observed in two animals in the T₂M₂₅ group. Analysis revealed prolonged detectability of tramadol, 4-methylamine antipyrine, 4-aminoantipyrine (up to 24 h), and O-desmethyltramadol (up to 12 h) after administration. Although metamizole and its metabolites showed no significant pharmacokinetic changes, tramadol and O-desmethyltramadol exhibited altered profiles, likely because of competition for the active sites of CYP450 enzymes. Importantly, the co-administration of metamizole increased the bioavailability of tramadol and O-desmethyltramadol in a dose-dependent manner, highlighting their potential interactions and emphasizing the need for further dose optimization in donkey analgesic therapies. In conclusion, metamizole co-administered with tramadol interferes with metabolism and this interference can change the frequency of drug administration and its analgesic efficacy.

This study aimed to determine the pharmacokinetic profile of two active metabolites of metamizole (dipyrone), N-methyl-4-aminoanthypyrine and 4-aminoanthypyrine, after intravenous administration in cats. Eight healthy mixed-breed cats were intravenously administered metamizole (25 mg/kg). Blood samples were collected at predetermined time points for up to 48 h after administration. Information on behavioral changes in the animals and adverse effects was collected. Plasma aliquots were processed and analyzed using the ultra-performance liquid chromatography tandem mass spectrometry technique. Salivation was identified as an adverse clinical sign. The mean maximal plasma concentrations of N-methyl-4-aminoanthypyrine and 4-aminoanthypyrine were 29.31 ± 24.57 μg/mL and 1.69 ± 0.36 μg/mL, with half-lives of around 4.98 and 14 hr, respectively. The area under the plasma concentration curve values were 28.54 ± 11.33 and 49.54 ± 11.38 h*µg/mL for N-methyl-4-aminoanthypyrine and 4-aminoanthypyrine, respectively. The plasma concentration of N-methyl-4-aminoanthypyrine was detectable for up to 24 h and was smaller than 4-aminoanthypyrine. 4-aminoanthypyrine was detectable for more than 48 h. Results suggest that metamizole is converted into active metabolites in cats, similar to findings in humans. A validated UPLC-MS/MS method was used to characterize the pharmacokinetics of N-methyl-4-aminoanthypyrine and 4-aminoanthypyrine. Further PK/PD and safety studies should be performed before defining the dose or administration intervals for clinical use.

Mammary carcinomas are common malignant tumors encompassing the main diagnostic mammary gland tumor cause in female dogs and cats. Few reports in wild animals are, however, available. In this context, this study aimed to characterize the clinical and histological aspects of a mammary tubular carcinoma case in a guinea pig (Cavia porcellus). A four-year-old non-spayed female guinea pig was seen at a veterinary clinic in the municipality of Natal, Rio Grande do Norte, Brazil. Upon clinical examination, the animal was active, with a normal body condition, weighing 660 grams, hydrated, and presenting normal-colored mucous membranes. Increased left breast volume was observed, about 3.5 cm in diameter, non-adherent and with an ulcerated surface located medially to the mammary papilla, about 1.8 cm in diameter. The observed clinical findings indicated a presumptive neoplastic lesion diagnosis. A unilateral mastectomy was performed (left breast) and breast tissue fragments were histologically evaluated, confirming the tubular mammary carcinoma diagnosis. The surgical procedure and post-surgical treatment recommended in this report were proven efficient. Knowledge of diseases that affect non-conventional pets, such as the tubular mammary carcinoma reported herein, is paramount in improving the quality of life of these animals.

Tramadol exposure after low oral doses is variable in dogs, and the estimation of the terminal phase can be difficult when late concentrations plateau or rebound. This study characterized tramadol and O‐desmethyltramadol (M1) after a single oral dose of 2 mg/kg in 10 healthy female mixed‐breed dogs. Plasma was collected from 0 to 48 h and analysed by liquid chromatography‐tandem mass spectrometry (LC‐MS/MS). Non‐compartmental analysis was performed for each animal. The terminal slope was evaluated using at least three quantifiable post‐peak observations, and λz was not forced when a coherent log‐linear decline was absent. Mean maximum observed concentration ( C _max ) and area under the concentration–time curve from time zero to the last quantifiable concentration (AUC0–last) for tramadol were 434.53 ± 337.68 ng/mL and 1748.40 ± 1370.05 h·ng/mL, respectively; median time to maximum observed concentration ( T _max ) was 1.5 h (range, 0.5–2.0 h). For M1, mean C _max and AUC0–last were 6.53 ± 3.26 ng/mL and 34.86 ± 28.55 h·ng/mL, respectively; median T _max was 1.0 h (0.5–2.0 h). A terminal phase was retained in seven of 10 profiles for each analyte. In these profiles, mean terminal half‐life was 15.53 ± 10.69 h for tramadol and 12.65 ± 11.55 h for M1. Three analyte profiles lacked a defensible terminal phase. We excluded quantitative pharmacokinetic analysis of M2 and M5 because authentic analytical standards were unavailable. Oral tramadol at 2 mg/kg was rapidly absorbed, but systemic exposure varied markedly among dogs. Based on the retained terminal half‐life estimates, a 12‐h dosing interval may be pharmacokinetically plausible for future multiple‐dose studies but should not be considered a validated clinical recommendation.