Hypothermia and rewarming times during general anesthesia in Hispaniolan Amazon parrots (Amazona ventralis): A comparative study between isoflurane, sevoflurane and desflurane.

OBJECTIVE: To evaluate induced hypothermia and rewarming times in Hispaniolan Amazon parrots (HAP; Amazona ventralis) anesthetized using isoflurane, sevoflurane or desflurane, and to describe selected cardiovascular and respiratory effects. STUDY DESIGN: Randomized, balanced, crossover experimental study. ANIMALS: A group of 12 adult HAP. METHODS: Parrots were premedicated with intramuscular butorphanol (0.5 mg kg-1) and anesthetized with the three inhalants with a 7 day washout period between events. Anesthesia was induced using isoflurane at 4 vol%, sevoflurane at 6 vol% or desflurane 12 vol% carried in oxygen, delivered via face mask. After orotracheal intubation, anesthesia maintenance was with end-tidal concentrations of 1.4-2% (Fe'Iso), 2.4-3% (Fe'Sevo) and 8.5-9.2% (Fe'Des). Hypothermia was defined as an esophageal temperature (BT) below 37.8 °C. External heat support was provided when BT dropped to 37.5 °C. Time for temperature decrease from 38.9 °C to 37.5 °C (T1), time to first increase in BT above 37.5 °C (T2) and time from external heat support to achieving 38.9 °C (T3) were recorded and compared via Friedman tests with post hoc Dunn's test. Heart rate, respiratory rate and end-tidal carbon dioxide, amongst other variables, were evaluated. RESULTS: All inhalants caused hypothermia (T1): isoflurane, 12 (2-37) minutes [median (range)]; sevoflurane, 12 (4-18) minutes; desflurane, 11.5 (6-24) minutes, with no significant differences between treatments (p > 0.05). T2 was significantly (p = 0.042) longer for sevoflurane than for desflurane but not isoflurane. Transient apnea was observed with all inhalants, including 25% of birds anesthetized with sevoflurane. Second-degree atrioventricular block and ventricular escape beats occurred with all inhalants with hypothermia potentially exacerbating cardiac arrhythmias. CONCLUSIONS AND CLINICAL RELEVANCE: Hypothermia rapidly developed in butorphanol-sedated HAP anesthetized using isoflurane, sevoflurane or desflurane. Sevoflurane prolonged warming time. Hypothermia may be associated with an increased likelihood of bradyarrhythmia in parrots anesthetized with inhalants.

Pharmacokinetics of intra-articular buprenorphine in horses with lipopolysaccharide-induced synovitis.

The objective of this study was to describe the pharmacokinetics of intra-articular (IA) administered buprenorphine in horses with lipopolysaccharide (LPS)-induced synovitis. Radiocarpal synovitis was induced in six healthy adult horses with the IA injection of LPS (0.5 ng/joint) on two occasions in a randomized cross-over design. Treatments (IA buprenorphine (IAB) at 5 µg/kg plus intravenous saline; and intravenous buprenorphine (IVB) at 5 µg/kg plus IA saline) were administered 4 h following LPS injection. Concentrations of buprenorphine were assessed in plasma and synovial fluid (SF) at 0.5, 2, 6, 12, and 24 h after administration. Pharmacokinetic parameters after IVB and IAB in plasma and synovial fluid were calculated using a nonlinear mixed effects model. IAB was detectable in SF of all horses at 24 h [median concentration of 6.2 (3.46-22.6) ng/mL]. IAB resulted in a median plasma concentration of 0.59 (0.42-1.68) ng/mL at 0.5 h and was detectable in all subjects for up to 6 h and in two horses for up to 12 h. IVB resulted in SF concentrations detected up to 6 h in all horses [median concentration of 0.12 (0.07-0.82) ng/mL]. Results suggest that IA buprenorphine remains present in the inflamed joint for at least 24 h and systemic absorption occurs.

Buprenorphine has a concentration-dependent cytotoxic effect on equine chondrocytes in vitro.

OBJECTIVE: To investigate the cytotoxic effects of 2 different concentrations of buprenorphine and compare them with bupivacaine and morphine on healthy equine chondrocytes in vitro. SAMPLE: Primary cultured equine articular chondrocytes from 3 healthy adult horses. PROCEDURES: Chondrocytes were exposed for 0 and 2 hours to the following treatments: media (CON; negative control); bupivacaine at 2.2 mg/mL (BUPI; positive control); morphine at 2.85 mg/mL (MOR); buprenorphine at 0.12 mg/mL (HBUPRE); or buprenorphine at 0.05 mg/mL (LBUPRE). Chondrocyte viability was assessed using live/dead staining, water-soluble tetrazolium salt-8 (WST-8) cytotoxic assay, LDH assay, and flow cytometry. All continuous variables were evaluated with a mixed ANOVA with treatment, time, and their interactions as the fixed effects and each horse as the random effect. RESULTS: Buprenorphine showed a concentration-dependent chondrotoxic effect. The viability of chondrocytes was significantly decreased with exposure to HBUPRE and BUPI compared to CON, MOR, and LBUPRE. CLINICAL RELEVANCE: Negligible chondrotoxic effects were observed in healthy cultured equine chondrocytes exposed to 0.05 mg/mL of buprenorphine, whereas higher concentrations (0.12 mg/mL) showed a marked cytotoxic effect. Based on these results, low concentrations of buprenorphine appear to be safe for intra-articular administration. Further evaluation of this dose in vivo is needed before recommending its clinical use.