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- Author or Editor: Jeff C. H. Ko x
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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 compare the analgesic effects of intra-articularly administered saline (0.9% NaCl) solution, morphine, dexmedetomidine, and a morphine-dexmedetomidine combination in dogs undergoing stifle joint surgery for cranial cruciate ligament rupture.
Design—Randomized, controlled, clinical trial.
Animals—44 dogs with cranial cruciate ligament rupture that underwent tibial tuberosity advancement (TTA) or tibial plateau leveling osteotomy (TPLO).
Procedures—Dogs received intra-articular injections of saline solution (0.2 mL/kg [0.09 mL/lb]), morphine (0.1 mg/kg [0.045 mg/lb]), dexmedetomidine (2.5 μg/kg [1.14 μg/lb]), or a combination of morphine (0.1 mg/kg) and dexmedetomidine (2.5 μg/kg). Intra-articular injections of the stifle joint were performed after completion of the corrective osteotomy procedure, just prior to skin closure. Signs of pain were assessed every 2 hours thereafter on the basis of mean behavioral and objective pain scores. Dogs with pain scores exceeding predetermined thresholds were given hydromorphone (0.05 mg/kg [0.023 mg/lb], SC) as rescue analgesia.
Results—Time to rescue analgesia did not significantly differ between dogs that underwent TTA versus TPLO. No significant difference in time to rescue analgesia was found among dogs receiving intra-articular injections of dexmedetomidine (median, 6 hours; range, 2 to 10 hours), morphine (median, 7 hours; range, 4 to 10 hours), or saline solution (median, 5 hours; range, 4 to 10 hours). However, time to rescue analgesia for dogs receiving intra-articular injection of the morphine-dexmedetomidine combination (median, 10 hours; range, 6 to 14 hours) was significantly longer than the time to rescue analgesia for other treatment groups.
Conclusions and Clinical Relevance—Intra-articular administration of the morphine-dexmedetomidine combination provided longer-lasting postoperative analgesia, compared with either morphine or dexmedetomidine alone, in dogs undergoing TTA or TPLO. (J Am Vet Med Assoc 2014;244:1291–1297)
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.
Abstract
Objective—To evaluate renal effects of carprofen in healthy dogs following general anesthesia.
Design—Randomized clinical trial.
Animals—10 English hound dogs (6 females and 4 males).
Procedure—Dogs were randomly assigned to control (n = 5) or carprofen (5) groups. Anesthesia was induced with propofol (6 to 8 mg/kg [2.7 to 3.6 mg/lb] of body weight, IV) and maintained with isoflurane (end-tidal concentration, 2.0%). Each dog underwent two 60-minute anesthetic episodes with 1 week between episodes, and mean arterial blood pressure was maintained between 60 and 90 mm Hg during each episode. Dogs in the carprofen group received carprofen (2.2 mg/kg [1 mg/lb], PO) at 9:00 AM and 6:00 PM the day before and at 7:00 AM the day of the second anesthetic episode. Glomerular filtration rates (GFR) were determined during each anesthetic episode by use of renal scintigraphy. Serum creatinine and BUN concentrations and the urine γ-glutamyltransferase-to-creatinine concentration (urine GGT: creatinine) ratio were determined daily for 2 days before and 5 days after general anesthesia.
Results—Significant differences were not detected in BUN and serum creatinine concentrations, urine GGT:creatinine ratio, and GFR either between or within treatment groups over time.
Conclusions and Clinical Relevance—Carprofen did not significantly alter renal function in healthy dogs anesthetized with propofol and isoflurane. These results suggest that carprofen may be safe to use for preemptive perioperative analgesia, provided that normal cardiorespiratory function is maintained. (J Am Vet Med Assoc 2000;217:346–349)
Abstract
Objective—To evaluate effects of medetomidine on anesthetic dose requirements, cardiorespiratory variables, plasma cortisol concentrations, and behavioral pain scores in dogs undergoing ovariohysterectomy.
Design—Randomized, prospective study.
Animals—12 healthy Walker-type hound dogs.
Procedure—Dogs received medetomidine (40 µg/kg [18.2 µg/lb] of body weight, IM; n = 6) or saline (0.9% NaCl) solution (1 ml, IM; 6) prior to anesthesia induction with thiopental; thiopental dose needed for endotracheal intubation was compared between groups. Ovariohysterectomy was performed during halothane anesthesia. Blood samples were obtained at various times before drug administration until 300 minutes after extubation. Various physiologic measurements and end-tidal halothane concentrations were recorded.
Results—In medetomidine-treated dogs, heart rate was significantly lower than in controls, and blood pressure did not change significantly from baseline. Plasma cortisol concentrations did not increase significantly until 60 minutes after extubation in medetomidine-treated dogs, whereas values in control dogs were increased from time of surgery until the end of the recording period. Control dogs had higher pain scores than treated dogs from extubation until the end of the recording period.
Conclusion and Clinical Relevance—Administration of medetomidine reduced dose requirements for thiopental and halothane and provided postoperative analgesia up to 90 minutes after extubation. Dogs undergoing ovariohysterectomy by use of thiopental induction and halothane anesthesia benefit from analgesia induced by medetomidine administered prior to anesthesia induction. Additional analgesia is appropriate 60 minutes after extubation. (J Am Vet Med Assoc 2000;217:509–514)
Abstract
Objective—To compare the anesthetic index of sevoflurane with that of isoflurane in unpremedicated dogs.
Design—Randomized complete-block crossover design.
Animals—8 healthy adult dogs.
Procedure—Anesthesia was induced by administering sevoflurane or isoflurane through a face mask. Time to intubation was recorded. After induction of anesthesia, minimal alveolar concentration (MAC) was determined with a tail clamp method while dogs were mechanically ventilated. Apneic concentration was determined while dogs were breathing spontaneously by increasing the anesthetic concentration until dogs became apneic. Anesthetic index was calculated as apneic concentration divided by MAC.
Results—Anesthetic index of sevoflurane (mean ± SEM, 3.45 ± 0.22) was significantly higher than that of isoflurane (2.61 ± 0.14). No clinically important differences in heart rate; systolic, mean, and diastolic blood pressures; oxygen saturation; and respiratory rate were detected when dogs were anesthetized with sevoflurane versus isoflurane. There was a significant linear trend toward lower values for end-tidal partial pressure of carbon dioxide during anesthesia with sevoflurane, compared with isoflurane, at increasing equipotent anesthetic doses.
Conclusions and Clinical Relevance—Results suggest that sevoflurane has a higher anesthetic index in dogs than isoflurane. Sevoflurane and isoflurane caused similar dose-related cardiovascular depression, but although both agents caused dose-related respiratory depression, sevoflurane caused less respiratory depression at higher equipotent anesthetic doses. (J Am Vet Med Assoc 2004;225:700–704)
Abstract
Objective—To evaluate the effects of butorphanol and carprofen, alone and in combination, on the minimal alveolar concentration (MAC) of isoflurane in dogs.
Design—Randomized complete-block crossover study.
Animals—6 healthy adult dogs.
Procedure—Minimal alveolar concentration of isoflurane was determined following administration of carprofen alone, butorphanol alone, carprofen and butorphanol, and neither drug (control). Anesthesia was induced with isoflurane in oxygen, and MAC was determined by use of a tail clamp method. Three hours prior to induction of anesthesia, dogs were fed a small amount of canned food without any drugs (control) or with carprofen (2.2 mg/kg of body weight [1 mg/lb]). Following initial determination of MAC, butorphanol (0.4 mg/kg [0.18 mg/lb], IV) was administered, and MAC was determined again. Heart rate, respiratory rate, indirect arterial blood pressure, endtidal partial pressure of CO2, and saturation of hemoglobin with oxygen were recorded at the time MAC was determined.
Results—Mean ± SD MAC of isoflurane following administration of butorphanol alone (1.03 ± 0.22%) or carprofen and butorphanol (0.90 ± 0.21%) were significantly less than the control MAC (1.28 ± 0.14%), but MAC after administration of carprofen alone (1.20 ± 0.13%) was not significantly different from the control value. The effects of carprofen and butorphanol on the MAC of isoflurane were additive. There were not any significant differences among treatments in regard to cardiorespiratory data.
Conclusion and Clinical Relevance—Results suggest that administration of butorphanol alone or in combination with carprofen significantly reduces the MAC of isoflurane in dogs; however, the effects of butorphanol and carprofen are additive, not synergistic. (J Am Vet Med Assoc 2000;217:1025–1028)
