Ketamine-medetomidine compared to tiletamine-zolazepam-medetomidine for immobilisation of semi-captive cheetahs (Acinonyx jubatus).

ABSTRACT: The immobilisation time and cardiopulmonary effects of ketamine-medetomidine (KM) and tiletamine-zolazepam-medetomidine (TZM) were compared in semi-captive cheetahs (Acinonyx jubatus). Seven healthy adult cheetahs were included in a randomised prospective crossover study. Each cheetah was immobilised on two occasions by remote injection, once with a combination of ketamine (4.93 ± 0.75 mg/kg) and medetomidine (0.038 ± 0.003 mg/kg) (KM) and once with tiletamine-zolazepam (1.16 ± 0.12 mg/kg) and medetomidine (0.039 ± 0.002 mg/kg) (TZM). Time to safe approach, characterised by absent responses to an ear flick and tail tug, was recorded as the immobilisation time. Following immobilisation, cardiopulmonary parameters were recorded, and an arterial blood gas sample analysed. Data is reported as mean ± SD and compared using a general linear mixed model (p < 0.05). Immobilisation times were no different between combinations, 11.4 ± 5.7 minutes for KM and 13.2 ± 4.6 minutes for TZM (p = 0.528). Systolic blood pressure was 218 ± 22 mmHg for KM and 210 ± 28 mmHg for TZM (p = 0.594). There was moderate hypoxaemia with both combinations with arterial oxygen partial pressure of 58.4 ± 6.6 mmHg for KM and 61.3 ± 4.2 mmHg for TZM (p = 0.368). Haematocrit was higher with KM (40.7 ± 2.5) than TZM (35.8 ± 2.8, p = 0.007). There were differences in electrolytes, with TZM resulting in higher serum potassium (4.3 ± 0.2 mmol/L, p < 0.001) and glucose (11.8 ± 2.9 mmol/L, p = 0.039) than KM. Both combinations provided acceptable immobilisation for field use, although severe hypertension was a consistent finding. Supplementation with oxygen is recommended with both combinations.

Systemic blockage of nitric oxide synthase by L-NAME increases left ventricular systolic pressure, which is not augmented further by Intralipid®.

Intravenous lipid emulsions (LEs) are effective in the treatment of toxicity associated with various drugs such as local anesthetics and other lipid soluble agents. The goals of this study were to examine the effect of LE on left ventricular hemodynamic variables and systemic blood pressure in an in vivo rat model, and to determine the associated cellular mechanism with a particular focus on nitric oxide. Two LEs (Intralipid(®) 20% and Lipofundin(®) MCT/LCT 20%) or normal saline were administered intravenously in an in vivo rat model following induction of anesthesia by intramuscular injection of tiletamine/zolazepam and xylazine. Left ventricular systolic pressure (LVSP), blood pressure, heart rate, maximum rate of intraventricular pressure increase, and maximum rate of intraventricular pressure decrease were measured before and after intravenous administration of various doses of LEs or normal saline to an in vivo rat with or without pretreatment with the non-specific nitric oxide synthase inhibitor N(ω)-nitro-L-arginine-methyl ester (L-NAME). Administration of Intralipid(®) (3 and 10 ml/kg) increased LVSP and decreased heart rate. Pretreatment with L-NAME (10 mg/kg) increased LSVP and decreased heart rate, whereas subsequent treatment with Intralipid(®) did not significantly alter LVSP. Intralipid(®) (10 ml/kg) increased mean blood pressure and decreased heart rate. The increase in LVSP induced by Lipofundin(®) MCT/LCT was greater than that induced by Intralipid(®). Intralipid(®) (1%) did not significantly alter nitric oxide donor sodium nitroprusside-induced relaxation in endothelium-denuded rat aorta. Taken together, systemic blockage of nitric oxide synthase by L-NAME increases LVSP, which is not augmented further by intralipid(®).

Physiologic evaluation of capture and anesthesia with medetomidine-zolazepam-tiletamine in brown bears (Ursus arctos).

Physiologic variables during anesthesia with medetomidine-zolazepam-tiletamine were evaluated in 52 free-ranging brown bears (Ursus arctos) darted from a helicopter and in six captive brown bears darted at a zoo. During anesthesia, rectal temperature, respiratory rate, heart rate, and pulse oximetry derived hemoglobin oxygen saturation were recorded. Arterial blood samples were collected and immediately analyzed for evaluation of pulmonary gas exchange, acid-base status, and selected hematologic and plasma variables. At the end of anesthesia, atipamezole was administered intramuscularly at five times the medetomidine dose. Capture-induced hyperthermia and lactic acidemia were documented in free-ranging bears. Hypoxemia during anesthesia was documented in both free-ranging and captive bears. In free-ranging bears, rectal temperature, heart rate, lactate, hematocrit, and hemoglobin decreased significantly during anesthesia, whereas partial pressure of arterial carbon dioxide, pH, potassium, and glucose increased. Yearlings had a significantly higher heart rate, pH, base excess, bicarbonate, and glucose, and had a significantly lower rectal temperature, sodium, hematocrit, and hemoglobin when compared with subadult and adult brown bears. In conclusion, alterations in pulmonary gas exchange and acid-base status in brown bears during anesthesia with medetomidine-zolazepam-tiletamine with the doses and capture methods used in this study were identified. Oxygen supplementation is recommended to counteract hypoxemia during anesthesia.

Anesthetic and nephrotoxic effects of Telazol in New Zealand white rabbits.

Telazol was evaluated as an anesthetic for rabbits. Two groups of five rabbits each were injected intramuscularly with 32 or 64 mg/kg of Telazol, and the depth and duration of anesthesia period monitored. At both doses, the righting reflex was lost within 2 minutes postinjection. Animals in both groups responded to noxious stimuli for the duration of the anesthesia. Hematology and urinalyses were performed daily for 7 days postinjection. Hematologic parameters remained unchanged in both groups. In the high-dose group, blood urea nitrogen and serum creatinine levels increased 1 day postinjection and continued steadily throughout the week. Elevations in urine protein and the presence of casts correlated with this increase. In the low-dose group, blood urea nitrogen and creatinine levels increased and protein was present in the urine of four of five rabbits beginning approximately 5 days postinjection. Histologically, severe renal tubular necrosis was evident 7 days postinjection in all high-dose rabbits and in three rabbits in the low-dose group. Our results indicate that Telazol does not produce analgesia in rabbits and is nephrotoxic at both 32 and 64 mg/kg. We conclude that Telazol is contraindicated for use in rabbits.