Effect of tepoxalin on renal function and hepatic enzymes in dogs exposed to hypotension with isoflurane.

OBJECTIVE: To evaluate the possible renal and hepatic toxicity of tepoxalin in dogs exposed to hypotension during isoflurane anesthesia. STUDY DESIGN: Prospective, randomized experimental study. ANIMALS: Twenty adult mixed-breed dogs, weighing 18.8 ± 2.8 kg. METHODS: The animals received 10 mg kg(-1) tepoxalin orally 2 hours before the anesthetic procedure (PRE; n = 6), or 30 minutes after anesthesia (POST; n = 6), along with a control group (CON; n = 8), which were only anesthetized. The PRE and POST groups also received the same dose of tepoxalin for 5 days post-procedure. All dogs were anesthetized with propofol and maintained with isoflurane and the end-tidal isoflurane (Fe'Iso) was increased until mean arterial pressure decreased to 50-60 mmHg. These pressures were maintained for 60 minutes. Heart rate, arterial pressures and Fe'Iso were recorded at 0, 10 and every 10 minutes up to 60 minutes of hypotension. Blood gases, pH, electrolytes and bleeding time were analyzed before and at 30 and 60 minutes of hypotension. Renal and hepatic changes were quantified by serum and urinary biochemistry and creatinine clearance. RESULTS: Serum concentrations of alanine amino transferase (ALT), alkaline phosphatase (ALP) and γ-glutamyl transferase (GGT), blood urea nitrogen (BUN) and creatinine (Cr), and urinary output, urinary Cr, Cr clearance, and GGT:Cr ratio remained stable throughout the evaluations. During the anesthetic procedure there were no important variations in the physiological parameters. No side effects were observed in any of the groups. CONCLUSIONS AND CLINICAL RELEVANCE: Tepoxalin did not cause significant effects on renal function or cause hepatic injury in healthy dogs exposed to hypotension with isoflurane, when administered pre- or postanesthetic and continued for five consecutive days.

Evaluation of analgesic and physiologic effects of epidural morphine administered at a thoracic or lumbar level in dogs undergoing thoracotomy.

OBJECTIVE: To evaluate the analgesic and physiological effects of epidural morphine administered at the sixth and seventh lumbar or the fifth and sixth thoracic vertebrae in dogs undergoing thoracotomy. STUDY DESIGN: Prospective, randomized, blinded trial. ANIMALS: Fourteen mixed-breed dogs, weighing 8.6 ± 1.4 kg. METHODS: The animals received acepromazine (0.1 mg kg⁻¹) IM and anesthesia was induced with propofol (4 mg kg)⁻¹ IV. The lumbosacral space was punctured and an epidural catheter was inserted up to the region between the sixth and seventh lumbar vertebrae (L, n = 6) or up to the fifth or sixth intercostal space (T, n = 8). The dogs were allowed to recover and after radiographic confirmation of correct catheter position, anesthesia was reinduced with propofol IV and maintained with 1.7% isoflurane. Following stabilization of monitored parameters, animals received morphine (0.1 mg kg⁻¹) diluted in 0.9% NaCl to a final volume of 0.25 mL kg⁻¹ via the epidural catheter, and after 40 minutes, thoracotomy was initiated. Heart rate and rhythm, systolic, mean and diastolic arterial pressures, respiratory rate, arterial hemoglobin oxygen saturation, partial pressure of expired CO2 and body temperature were measured immediately before the epidural administration of morphine (0 minute) and every 10 minutes during the anesthetic period. The Melbourne pain scale and the visual analog scale were used to assess postoperative pain. The evaluation began 3 hours after the epidural administration of morphine and occurred each hour until rescue analgesia. RESULTS: There were no important variations in the physiological parameters during the anesthetic period. The post-operative analgesic period differed between the groups, being longer in T (9.9 01.6 hours) compared with L (5.8 ± 0.8 hours). CONCLUSIONS: The use of morphine, at a volume of 0.25 mL kg 0.1, administered epidurally over the thoracic vertebrae provided longer lasting analgesia than when deposited over the lumbar vertebrae.

Afundamento costal estabilizado com suporte externo de metilmetacrilato em um felino / Ditching costal stabilized with external support of methylmethacrylate in a feline

O tórax instável ou afundamento costal acontece quando há fraturas múltiplas de pelo menos duas costelas consecutivas (CROWE et al., 2005). Nesse caso, durante a inspiração, o segmento fraturado, ao invés de expandir com o restante da caixa torácica, tende a penetrar no tórax. Subsequentemente, no momento da expiração, o conjunto instável tende a expansão (CROWE et al., 2005, FOSSUM, 2008). O tratamento inicial consiste em tornar o tórax estável, com uma pinça backhaus (AGUIAR, 2011). Posteriormente faz-se necessária a imobilização externa, que permitirá a adequada expansão torácica, sendo mantida por alguns dias até a estabilização do paciente. Para o tratamento cirúrgico recomenda-se a reconstrução anatômica das costelas fraturadas (CUNHA et al., 2009). O objetivo desse trabalho é demonstrar o tratamento da instabilidade costal com metilmetacrilato em felino, descrita por Coutinho et al. (2012).

Total intravenous anesthesia with propofol and S(+)-ketamine in rabbits.

OBJECTIVE: To evaluate total intravenous anesthesia with propofol alone or in combination with S(+)-ketamine in rabbits undergoing surgery. STUDY DESIGN: Prospective, randomized, blinded trial. ANIMALS: Nine 6-month-old New Zealand white rabbits, weighing 2.5-3 kg. METHODS: Animals received acepromazine (0.1 mg kg(-1)) and buprenorphine (20 microg kg(-1)) IM, and anesthesia was induced with propofol (2 mg kg(-1)) and S(+)-ketamine (1 mg kg(-1)) IV. Rabbits received two of three treatments: propofol (0.8 mg kg(-1) minute(-1)) (control treatment, P), propofol (0.8 mg kg(-1) minute(-1)) + S(+)-ketamine (100 microg kg(-1) minute(-1)) (PK100) or propofol (0.8 mg kg(-1) minute(-1)) + S(+)-ketamine (200 microg kg(-1) minute(-1)) (PK200). All animals received 100% O(2) during anesthesia. Heart rate, mean arterial pressure, hemoglobin oxygen saturation and respiratory rate were measured every 5 minutes for 60 minutes. Blood-gas parameters were measured at zero time and 60 minutes. Additional propofol injections, if necessary, and recovery time were recorded. RESULTS: An increase in heart rate was observed in P and PK200 up to 10 minutes after induction of anesthesia. Blood pressure decreased from baseline values during the first 10 minutes in P and PK200, and during the first 15 minutes and between 45 and 55 minutes in PK100. A reduction in respiratory rate was observed after 5 minutes in all treatments. Respiratory acidosis was observed in all treatments. Six (2.8) [median (interquartile range)] further propofol injections were necessary in P, which differed statistically from PK100 [1 (0.2)] and PK200 [2 (0.6)]. Recovery time was shorter in P compared with PK100 and PK200, being [7.5 minutes (4.11)], [17.5 minutes (10.30)], and [12 minutes (10.30)], respectively. CONCLUSIONS AND CLINICAL RELEVANCE: S(+)-ketamine potentiates propofol-induced anesthesia in rabbits, providing better maintenance of heart rate. All of these techniques were accompanied by clinically significant respiratory depression.