Background: Antioxidants located in both the hydrophilic and lipophilic compartments of plasma act as a defence system against reactive oxygen species (ROS). Excessive production of ROS during anaesthesia affects the antioxidant capacity of plasma and may result in oxidative stress. The aim of this study was to evaluate the antioxidant capacity of lipid- (ACL) and water-soluble (ACW) antioxidants in client-owned dogs diagnosed with periodontal disease and early-stage myxomatous mitral valve degeneration (MMVD) and anaesthetised for a dental procedure with propofol and sevoflurane or with propofol only. Results: Dogs with MMVD were anaesthetised with propofol and sevoflurane (MMVD/PS, n = 8) or with propofol only (MMVD/P, n = 10). Dogs with no evidence of MMVD (PS, n = 12) were anaesthetised with propofol and sevoflurane. Blood samples for determination of ACL and ACW were collected before and 5 min, 60 min and 6 h after induction to anaesthesia. In MMVD/PS dogs, ACL was significantly higher at all sampling times when compared to PS dogs. Compared to basal values, only anaesthesia maintained with propofol significantly increased ACL at 60 min in dogs with MMVD. In MMVD/P dogs, ACW increased after induction to anaesthesia and remained elevated up to 6 h after anaesthesia. Compared to basal values, anaesthesia maintained with sevoflurane significantly increased ACW only at 60 min in both dogs with and without MMVD. The only difference between propofol and propofol/sevoflurane anaesthesia in dogs with MMVD was significantly higher ACW at 60 min after induction to anaesthesia in the propofol group. Conclusions: Regarding antioxidant capacity, propofol could be a better choice than sevoflurane for anaesthesia of dogs with early-stage MMVD, although further studies are necessary to clarify the advantage of this antioxidant capacity.

To evaluate the sedative and cardiovascular effects of premedication with acepromazine, methadone and dexmedetomidine or acepromazine and methadone in sevoflurane-anaesthetized dogs. A randomized, blinded, prospective clinical study. A total of 38 client-owned healthy dogs scheduled for elective surgery. Dogs were randomly assigned to intramuscular premedication with acepromazine (0.01 mg kg^-1), methadone (0.3 mg kg^-1) and dexmedetomidine (1.5 μg kg^-1) (Ace/D group) or with acepromazine (0.01 mg kg^-1) and methadone (0.3 mg kg^-1) (Ace group). The anaesthetist who performed the observations and anaesthesia was blinded to the group. Sedation was scored at 5, 10 and 15 minutes after premedication and postoperatively every hour until discharge, starting 30 minutes after extubation. Anaesthesia was induced with propofol and maintained with sevoflurane in oxygen and air. Body temperature, heart rate (HR), respiratory rate (f_R), direct arterial blood pressure, end-tidal sevoflurane, end-tidal carbon dioxide (Pe´CO₂) and oxygen saturation were recorded at 5 minute intervals. The normality of data distribution was assessed with the Shapiro-Wilk test. The Mann-Whitney U test was used for comparison between groups, and effect size was calculated in cases of statistical significance (p < 0.05). Dogs in the Ace/D group had significantly higher sedation scores 10 minutes after premedication (p = 0.02). The propofol induction doses were significantly lower in the Ace/D group (p = 0.001). During anaesthesia, dogs in the Ace/D group had significantly higher Pe´CO₂ values (p = 0.03), but no significant differences in blood pressure, HR and f_R were observed between the groups. Significantly fewer dogs in the Ace/D group required rescue analgesia with fentanyl (p = 0.04) during surgery (three in Ace/D and nine in Ace group). Low-dose dexmedetomidine improved preoperative sedation and intraoperative analgesia and reduced the induction dose of propofol in dogs premedicated with acepromazine and methadone.

Electrochemotherapy (ECT) is a short, minimally invasive procedure that causes mild to moderate pain. In humans, ECT can often be performed under sedation and local anesthesia, whereas general anesthesia is generally preferred in veterinary medicine. Anesthesia of dogs and cats undergoing ECT can be challenging because of altered clinical status, paraneoplastic syndromes, and concurrent chronic comorbidities. Recent evidence suggests that anesthetic and analgesic agents, particularly opioids, may modulate antitumor immune responses and potentially influence oncological outcomes, although the clinical relevance of these effects requires further investigation. Effective peri-procedural pain management is essential for patient recovery and welfare, and opioid-free or opioid-sparing strategies incorporating locoregional anesthesia may reduce opioid requirements while providing effective analgesia. The growing clinical evidence supporting the efficacy of ECT in veterinary oncology highlights the need for updated patient-tailored anesthetic and analgesic protocols. Moreover, it supports the potential of ECT as a useful research model for investigating tumor–anesthesia interactions, with translational relevance to human oncology. This mini-review summarizes current practices and practical considerations in veterinary onco-anesthesia and identifies priorities for future research.

Cannabidiol (CBD) is increasingly used as an adjunct treatment for chronic pain in dogs, but information on repeated‐dose pharmacokinetics and potential interactions with commonly used analgesics remains limited. This study evaluated the pharmacokinetics of buccally administered CBD, its major metabolites, and orally administered carprofen in dogs, and assessed potential pharmacokinetic changes during co‐administration. Twenty‐five dogs with osteoarthritis received CBD (2 mg/kg), carprofen (2 mg/kg), or both drugs twice daily for 4 weeks. Plasma samples were collected during the first 12 h after the initial dose and at two and 4 weeks of treatment. Cannabidiol, 7‐hydroxy‐cannabidiol (7‐OH‐CBD), 7‐carboxy‐cannabidiol (7‐COOH‐CBD), and carprofen concentrations were quantified using LC‐MS/MS. Pharmacokinetic parameters were estimated using non‐compartmental and compartmental analyses. Cannabidiol was rapidly absorbed but showed substantial interindividual variability. CBD exposure was higher during co‐administration with carprofen, but differences in C _max and AUC _last were not significant. Repeated dosing resulted in increasing 2‐h post‐dose CBD concentrations over time. Among metabolites, 7‐COOH‐CBD showed greater exposure and persistence than 7‐OH‐CBD. Carprofen pharmacokinetics were consistent with previous reports, with higher but non‐significant C _max and AUC _last during co‐administration with CBD. These findings warrant further investigation of potential pharmacokinetic interactions between CBD and carprofen.