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Abstract

Abstract

Objective—To compare anesthetic, analgesic, and cardiorespiratory effects in dogs after IM administration of dexmedetomidine (7.5 μg/kg)–butorphanol (0.15 mg/kg)–tiletamine-zolazepam (3.0 mg/kg; DBTZ) or dexmedetomidine (15.0 μg/kg)-tramadol (3.0 mg/kg)-ketamine (3.0 mg/kg; DTrK) combinations.

Animals—6 healthy adult mixed-breed dogs.

Procedures—Each dog received DBTZ and DTrK in a randomized, crossover-design study with a 5-day interval between treatments. Cardiorespiratory variables and duration and quality of sedation-anesthesia (assessed via auditory stimulation and sedation-anesthesia scoring) and analgesia (assessed via algometry and electrical nerve stimulation) were evaluated at predetermined intervals.

Results—DBTZ or DTrK induced general anesthesia sufficient for endotracheal intubation ≤ 7 minutes after injection. Anesthetic quality and time from drug administration to standing recovery (131.5 vs 109.5 minutes after injection of DBTZ and DTrK, respectively) were similar between treatments. Duration of analgesia was significantly longer with DBTZ treatment, compared with DTrK treatment. Analgesic effects were significantly greater with DBTZ treatment than with DTrK treatment at several time points. Transient hypertension (mean arterial blood pressure > 135 mm Hg), bradycardia (heart rate < 60 beats/min), and hypoxemia (oxygen saturation < 90% via pulse oximetry) were detected during both treatments. Tidal volume decreased significantly from baseline with both treatments and was significantly lower after DBTZ administration, compared with DTrK, at several time points.

Conclusions and Clinical Relevance—DBTZ or DTrK rapidly induced short-term anesthesia and analgesia in healthy dogs. Further research is needed to assess efficacy of these drug combinations for surgical anesthesia. Supplemental 100% oxygen should be provided when DBTZ or DTrK are used.

Abstract

Objective—To determine the cardiorespiratory effects of preemptive atropine administration in dogs sedated with medetomidine.

Design—Randomized crossover trial.

Animals—12 healthy adult dogs.

Procedures—Dogs underwent 6 treatments. Each treatment consisted of administration of atropine (0.04 mg/kg [0.018 mg/lb] of body weight, IM) or saline solution (0.9% NaCl, 1 ml, IM) and administration of medetomidine (10, 20, or 40 µg/kg [4.5, 9.1, or 18.2µg/lb], IM) 10 minutes later. Treatments were administered in random order, with a minimum of 1 week between treatments. Cardiorespiratory effects before and after atropine and medetomidine administration were assessed. Duration of lateral recumbency and quality of sedation and recovery were assessed.

Results—Bradycardia (heart rate < 60 beats/min) was seen in all dogs when saline solution was administered followed by medetomidine, and the dose of medetomidine was not associated with severity or frequency of bradycardia or second-degree heart block. However, a medetomidine dose-dependent increase in mean and diastolic blood pressures was observed, regardless of whether dogs received saline solution or atropine. Preemptive atropine administration effectively prevented bradycardia and seconddegree heart block but induced pulsus alternans and hypertension. The protective effects of atropine against bradycardia lasted 50 minutes. Blood gas values were within reference limits during all treatments and were not significantly different from baseline values. Higher doses of medetomidine resulted in a longer duration of lateral recumbency.

Conclusions and Clinical Relevance—Preemptive administration of atropine in dogs sedated with medetomidine effectively prevents bradycardia for 50 minutes but induces hypertension and pulsus alternans. ( J Am Vet Med Assoc 2001;218:52–58)

Abstract

Objective—To determine sedative and cardiorespiratory effects of IM administration of medetomidine alone and in combination with butorphanol or ketamine in dogs.

Design—Randomized, crossover study.

Animals—6 healthy adult dogs.

Procedure—Dogs were given medetomidine alone (30 µg/kg [13.6 µg/lb] of body weight, IM), a combination of medetomidine (30 µg/kg, IM) and butorphanol (0.2 mg/kg [0.09 mg/lb], IM), or a combination of medetomidine (30 µg/kg, IM) and ketamine (3 mg/kg [1.36 mg/lb], IM). Treatments were administered in random order with a minimum of 1 week between treatments. Glycopyrrolate was given at the same time. Atipamezole (150 µg/kg [68 µg/lb], IM) was given 40 minutes after administration of medetomidine.

Results—All but 1 dog (given medetomidine alone) assumed lateral recumbency within 6 minutes after drug administration. Endotracheal intubation was significantly more difficult when dogs were given medetomidine alone than when given medetomidine and butorphanol. At all evaluation times, percentages of dogs with positive responses to tail clamping or to needle pricks in the cervical region, shoulder region, abdominal region, or hindquarters were not significantly different among drug treatments. The PaCO₂ was significantly higher and the arterial pH and PaO₂ were significantly lower when dogs were given medetomidine and butorphanol or medetomidine and ketamine than when they were given medetomidine alone. Recovery quality following atipamezole administration was unsatisfactory in 1 dog when given medetomidine and ketamine.

Conclusion and Clinical Relevance—Results suggested that a combination of medetomidine with butorphanol or ketamine resulted in more reliable and uniform sedation in dogs than did medetomidine alone. (J Am Vet Med Assoc 2000;216:1578–1583)

Abstract

OBJECTIVE To assess the isoflurane-sparing effect of a transdermal formulation of fentanyl solution (TFS) and subsequent naloxone administration in dogs.

DESIGN Experiment.

ANIMALS 6 healthy mixed-breed dogs.

PROCEDURES Minimum alveolar concentration (MAC) of isoflurane was determined in each dog with a tail clamp method (baseline). Two weeks later, dogs were treated with TFS (2.7 mg/kg [1.23 mg/lb]), and the MAC of isoflurane was determined 4 and 24 hours later. After the 4-hour MAC assessment, saline (0.9% NaCl) solution was immediately administered IV and MAC was reassessed. After the 24-hour MAC assessment, naloxone hydrochloride (0.02 mg/kg [0.01 mg/lb], IV) was immediately administered and MAC was reassessed. Heart rate, respiratory rate, arterial blood pressure, end-tidal partial pressure of CO₂, and oxygen saturation as measured by pulse oximetry were recorded for each MAC assessment.

RESULTS Mean ± SD MAC of isoflurane at 4 and 24 hours after TFS application was 45.4 ± 4.0% and 45.5 ± 4.5% lower than at baseline, respectively. Following naloxone administration, only a minimal reduction in MAC was identified (mean percentage decrease from baseline of 13.1 ± 2.2%, compared with 43.8 ± 5.6% for saline solution). Mean heart rate was significantly higher after naloxone administration (113.2 ± 22.2 beats/min) than after saline solution administration (76.7 ± 20.0 beats/min). No significant differences in other variables were identified among treatments.

CONCLUSIONS AND CLINICAL RELEVANCE The isoflurane-sparing effects of TFS in healthy dogs were consistent and sustained between 4 and 24 hours after application, and these effects should be taken into consideration when anesthetizing or reanesthetizing TFS-treated dogs.

Abstract

Objective—To investigate hemodynamic effects of acepromazine and dexmedetomidine premedication in dogs undergoing general anesthesia induced with propofol and maintained with isoflurane in oxygen and assess the influence of these drugs on oxygen-carrying capacity and PCV.

Design—Prospective, randomized crossover study.

Animals—6 healthy adult dogs.

Procedures—Dogs received acepromazine (0.05 mg/kg [0.023 mg/lb]) or dexmedetomidine (15.0 μg/kg [6.82 μg/lb]) IM. Fifteen minutes later, anesthesia was induced with propofol and maintained at end-tidal isoflurane concentration of 1.28% (1 minimum alveolar concentration) for 30 minutes. Hemodynamic variables were recorded at predetermined times. The experiment was repeated 48 hours later with the alternate premedication. Results were analyzed by repeated-measures ANOVA with a mixed-models procedure.

Results—Bradycardia, hypertension, and significant cardiac output (CO) reduction developed after dexmedetomidine premedication but improved during isoflurane anesthesia. Hypotension developed after acepromazine administration and persisted throughout the isoflurane maintenance period, but CO was maintained throughout the anesthetic period when dogs received this treatment. Oxygen delivery and consumption were not different between treatments at most time points, whereas arterial oxygen content was lower with acepromazine premedication owing to lower PCV during isoflurane anesthesia.

Conclusions and Clinical Relevance—Acepromazine exacerbated hypotension, but CO did not change in dogs anesthetized with propofol and isoflurane. Dexmedetomidine reduced CO but prevented propofol-isoflurane–induced hypotension. In general, oxygen-carrying capacity and PCV were higher in dexmedetomidine-treated than in acepromazine-treated dogs anesthetized with propofol and isoflurane.

Abstract

Objective—To compare efficacy and cardiorespiratory effects of dexmedetomidine and ketamine in combination with butorphanol, hydromorphone, or buprenorphine (with or without reversal by atipamezole) in dogs undergoing castration.

Design—Prospective, randomized, split-plot, blinded study.

Animals—30 healthy client-owned sexually intact male dogs.

Procedures—Dogs (n = 10 dogs/group) were assigned to receive dexmedetomidine (15 μg/kg [6.82 μg/lb]) and ketamine (3 mg/kg [1.36 mg/lb]) with butorphanol (0.2 mg/kg [0.09 mg/lb]; DKBut), the same dosages of dexmedetomidine and ketamine with hydromorphone (0.05 mg/kg [0.023 mg/lb]; DKH), or the same dosages of dexmedetomidine and ketamine with buprenorphine (40 μg/kg [18.18 μg/lb]; DKBup). All drugs were administered as a single IM injection for induction and maintenance of anesthesia for castration. At conclusion of the surgery, 5 dogs in each treatment group received atipamezole (150 μg/kg [68.18 μg/lb], IM), and the remainder received saline (0.9% NaCl) solution IM. Cardiorespiratory variables and quality of anesthesia were assessed. Supplemental isoflurane was administered to the dogs when anesthesia was considered inadequate during surgery.

Results—All drug combinations rapidly induced anesthesia. Dogs were intubated within 10 minutes after injection. Supplemental isoflurane was needed during surgery in 1, 3, and 4 dogs in the DKBup, DKBut, and DKH groups, respectively. Dogs that received atipamezole had a significantly shorter recovery time. Some dogs in each group had bradycardia and hypoxemia with hypertension.

Conclusions and Clinical Relevance—DKBup was the most suitable injectable anesthetic combination used. Recovery was shortened by IM administration of atipamezole. There were minimal adverse effects in all groups.

Abstract

Objective—To compare the efficacy of preoperative administration of buprenorphine (via oral transmucosal [OTM] and IV routes) for postoperative analgesia in dogs undergoing ovariohysterectomy.

Design—Prospective, randomized, blinded study.

Animals—18 dogs undergoing routine ovariohysterectomy.

Procedures—Dogs were allocated to 3 groups (6 dogs/group) and were assigned to receive buprenorphine (20 μg/kg [9.09 μg/lb], IV; a low dose [20 μg/kg] via OTM administration [LOTM]; or a high dose [120 μg/kg [54.54 μg/lb] via OTM administration [HOTM]) immediately before anesthetic induction with propofol and maintenance with isoflurane for ovariohysterectomy. Postoperative pain was assessed by use of a dynamic interactive pain scale. Dogs were provided rescue analgesia when postoperative pain exceeded a predetermined threshold. Blood samples were collected, and liquid chromatography-electrospray ionization-tandem mass spectrometry was used to determine plasma concentrations of buprenorphine and its metabolites. Data were analyzed with an ANOVA.

Results—Body weight, surgical duration, propofol dose, isoflurane concentration, and cardiorespiratory variables did not differ significantly among treatment groups. Number of dogs requiring rescue analgesia did not differ significantly for the HOTM (1/6), IV (3/6), and LOTM (5/6) treatments. Similarly, mean ± SEM duration of analgesia did not differ significantly for the HOTM (20.3 ± 3.7 hours), IV (16.0 ± 3.8 hours), and LOTM (7.3 ± 3.3 hours) treatments. Plasma buprenorphine concentration was ≤ 0.60 ng/mL in 7 of 9 dogs requiring rescue analgesia.

Conclusions and Clinical Relevance—Buprenorphine (HOTM) given immediately before anesthetic induction can be an alternative for postoperative pain management in dogs undergoing ovariohysterectomy.

Abstract

Objective—To compare the efficacy and cardiorespiratory effects of dexmedetomidine-ketamine in combination with butorphanol, hydromorphone, or buprenorphine with or without reversal by atipamezole in cats undergoing castration.

Design—Prospective, randomized, split-plot, blinded study.

Animals—30 healthy male cats.

Procedures—Cats were assigned to receive dexmedetomidine (25 μg/kg [11.4 μg/lb]) and ketamine (3 mg/kg [1.4 mg/lb]) with butorphanol (0.2 mg/kg [0.09 mg/lb]; DKBut; n = 10), hydromorphone (0.05 mg/kg [0.023 mg/lb]; DKH; 10), or buprenorphine (30 μg/kg [13.6 μg/lb]; DKBup; 10). Drugs were administered as a single IM injection. Supplemental isoflurane was administered to cats if the level of anesthesia was inadequate for surgery. At the conclusion of surgery, half the cats (5 cats in each treatment group) received atipamezole (250 μg/kg [113.6 μg/lb], IM) and the remainder received saline (0.9% NaCl) solution IM. All cats received meloxicam (0.2 mg/kg, SC) immediately prior to the conclusion of surgery.

Results—All drug combinations induced lateral recumbency, and intubation was achievable in 13 of 30 (43%) cats at 10 minutes after injection. Supplemental isoflurane was needed for the surgery in 1 of 10 of the DKBut-, 2 of 10 of the DKH-, and 7 of 10 of the DKBup-treated cats. Cats that received atipamezole had a significantly shorter recovery time.

Conclusions and Clinical Relevance—DKBut and DKH combinations were suitable injectable anesthetic protocols for castration in cats commencing at 10 minutes after injection, but cats receiving DKBup may require additional time or anesthetics for adequate anesthesia.

Abstract

Objective—To compare the effect of oral administration of tramadol alone and with IV administration of butorphanol or hydromorphone on the minimum alveolar concentration (MAC) of sevoflurane in cats.

Design—Crossover study.

Animals—8 healthy 3-year-old cats.

Procedures—Cats were anesthetized with sevoflurane in 100% oxygen. A standard tail clamp method was used to determine the MAC of sevoflurane following administration of tramadol (8.6 to 11.6 mg/kg [3.6 to 5.3 mg/lb], PO, 5 minutes before induction of anesthesia), butorphanol (0.4 mg/kg [0.18 mg/lb], IV, 30 minutes after induction), hydromorphone (0.1 mg/kg [0.04 mg/lb], IV, 30 minutes after induction), saline (0.9% NaCl) solution (0.05 mL/kg [0.023 mL/lb], IV, 30 minutes after induction), or tramadol with butorphanol or with hydromorphone (same doses and routes of administration). Naloxone (0.02 mg/kg [0.009 mg/lb], IV) was used to reverse the effects of treatments, and MACs were redetermined.

Results—Mean ± SEM MACs for sevoflurane after administration of tramadol (1.48 ± 0.20%), butorphanol (1.20 ± 0.16%), hydromorphone (1.76 ± 0.15%), tramadol and butorphanol (1.48 ± 0.20%), and tramadol and hydromorphone (1.85 ± 0.20%) were significantly less than those after administration of saline solution (2.45 ± 0.22%). Naloxone reversed the reductions in MACs.

Conclusions and Clinical Relevance—Administration of tramadol, butorphanol, or hydromorphone reduced the MAC of sevoflurane in cats, compared with that in cats treated with saline solution. The reductions detected were likely mediated by effects of the drugs on opioid receptors. An additional reduction in MAC was not detected when tramadol was administered with butorphanol or hydromorphone.