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- Author or Editor: Erja Kuusela x
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Objective—To compare 3 dose levels of medetomidine and dexmedetomidine for use as premedicants in dogs undergoing propofol-isoflurane anesthesia.
Animals—6 healthy Beagles.
Procedure—Dogs received medetomidine or dexmedetomidine intravenously at the following dose levels: 0.4 µg of medetomidine or 0.2 µg of dexmedetomidine/kg of body weight (M0.4/D0.2), 4.0 µg of medetomidine or 2.0 µg of dexmedetomidine/ kg (M4/D2), and 40 µg of medetomidine or 20 µg of dexmedetomidine/kg (M40/D20). Sedation and analgesia were scored before induction. Anesthesia was induced with propofol and maintained with isoflurane. End-tidal isoflurane concentration, heart rate, and arterial blood pressures and gases were measured.
Results—Degrees of sedation and analgesia were significantly affected by dose level but not drug. Combined mean end-tidal isoflurane concentration for all dose levels was higher in dogs that received medetomidine, compared with dexmedetomidine. Recovery time was significantly prolonged in dogs treated at the M40/D20 dose level, compared with the other dose levels. After induction, blood pressure decreased below reference range and heart rate increased in dogs treated at the M0.4/D0.2 dose level, whereas blood pressure was preserved in dogs treated at the M40/D20 dose level. However, dogs in these latter groups developed profound bradycardia and mild metabolic acidosis during anesthesia. Treatment at the M4/D2 dose level resulted in more stable cardiovascular effects, compared with the other dose levels. In addition, PaCO2 was similar among dose levels.
Conclusions and Clinical Relevance—Dexmedetomidine is at least as safe and effective as medetomidine for use as a premedicant in dogs undergoing propofol-isoflurane anesthesia. (Am J Vet Res 2001;62:1073–1080)
Objective—To determine whether a high dose of levomedetomidine had any pharmacologic activity or would antagonize the sedative and analgesic effects of dexmedetomidine in dogs.
Animals—6 healthy Beagles.
Procedure—Each dog received the following treatments on separate days: a low dose of levomedetomidine (10 µg/kg), IV, as a bolus, followed by continuous infusion at a dose of 25 µg/kg/h; a high dose of levomedetomidine (80 µg/kg), IV, as a bolus, followed by continuous infusion at a dose of 200 µg/kg/h; and a dose of isotonic saline (0.9% NaCl) solution, IV, as a bolus, followed by continuous infusion (control). For all 3 treatments, the infusion was continued for 120 minutes. After 60 minutes, a single dose of dexmedetomidine (10 µg/kg) was administered IV. Sedation and analgesia were scored subjectively, and heart rate, blood pressure, respiratory rate, arterial blood gas partial pressures, and rectal temperatures were monitored.
Results—Administration of levomedetomidine did not cause any behavioral changes. However, administration of the higher dose of levomedetomidine enhanced the bradycardia and reduced the sedative and analgesic effects associated with administration of dexmedetomidine.
Conclusion and Clinical Relevance—Results suggest that administration of dexmedetomidine alone may have some cardiovascular benefits over administration of medetomidine, which contains both dexmedetomidine and levomedetomidine. Further studies are needed to confirm the clinical importance of the effects of levomedetomidine in dogs. (Am J Vet Res 2001;62:616–621)
Objective—To detect monocarboxylate transporters (MCTs) in canine RBC membranes and to determine the distribution of lactate between plasma and RBCs.
Sample population—Blood samples obtained from 6 purpose-bred Beagles.
Procedures—Monocarboxylate transporter isoforms 1, 2, 4, 6, 7, and 8 and CD147 were evaluated in canine RBCs by use of western blot analysis. Lactate influx into RBCs was measured as incorporation of radioactive lactate.
Results—2 MCT isoforms, MCT1 and MCT7, were detected in canine RBC membranes on western blot analysis, whereas anti-MCT2, anti-MCT4, anti-MCT6, and anti-MCT8 antibodies resulted in no signal. No correlation was found between the amount of MCT1 or MCT7 and lactate transport activity, but the ancillary protein CD147 that is needed for the activity of MCT1 had a positive linear correlation with the rate of lactate influx. The apparent Michaelis constant for the lactate influx in canine RBCs was 8.8 ± 0.9mM. Results of in vitro incubation studies revealed that at lactate concentrations of 5 to 15mM, equilibrium of lactate was rapidly obtained between plasma and RBCs.
Conclusions and Clinical Relevance—These results indicated that at least half of the lactate transport in canine RBCs occurs via MCT1, whereas MCT7 may be responsible for the rest, although an additional transporter was not ruled out. For practical purposes, the rapid equilibration of lactate between plasma and RBCs indicated that blood lactate concentrations may be estimated from plasma lactate concentrations.
Objective—To identify variables and evaluate methods for assessing chronic pain in dogs.
Animals—41 dogs with canine hip dysplasia (CHD), and 24 apparently healthy dogs with no history of pain.
Procedure—2 veterinarians evaluated the dogs' locomotion and signs of pain. Owners of dogs with CHD and control dogs answered a questionnaire regarding their dogs' demeanor, behavior, and locomotion (descriptive scales) and assessed pain and locomotion (visual analog scales). Plasma concentrations of several stress-related hormones were determined, and 13 radiologic variables were assessed in affected hip joints.
Results—For many of the questions, answers provided by owners of dogs with CHD differed significantly from those of owners of control dogs. Stress hormone concentrations differed significantly between dogs with CHD and controls, but individual variation was too great for them to be of value in pain assessment. None of the radiologic variables examined correlated well with owner or veterinarian pain scores.
Conclusions and Clinical Relevance—Chronic pain could be assessed in dogs with CHD through completion of the study questionnaire by a person familiar with the pet (eg, owner) after receiving appropriate education in its use. Eleven variables were identified as being potentially useful in assessment of chronic pain in dogs. (J Am Vet Med Assoc 2003;222: 1552–1558)
Objective—To compare the effects of pretreatment with dexamethasone, physical stress (exercise), or both on sedation and plasma hormone and glucose concentrations in dogs treated with dexmedetomidine (DEX).
Animals—6 healthy purpose-bred Beagles.
Procedure—Dogs received 4 treatments each in a randomized order prior to IV administration of DEX (5 µg/kg). Pretreatments were as follows: (1) IV administration of saline (0.9% NaCl) solution and no exercise (control group); (2) IV administration of dexamethasone (0.05 mg/kg) and no exercise (DM group); (3) IV administration of saline solution and exercise (EX group; 15 minutes of trotting on a treadmill at a speed of 2 m/s); and 4) IV administration of dexamethasone and exercise (DM+EX group).
Results—Following DEX administration, all dogs had similar times to recumbency and sedation index values, irrespective of pretreatment with dexamethasone or exercise. Plasma catecholamine concentrations decreased after DEX administration. Compared with control group dogs, plasma cortisol concentrations were higher in EX-group dogs prior to DEX administration and lower in DM- and DM+EX-group dogs following DEX administration. Administration of DEX decreased plasma cortisol concentration in EX-group dogs only. Plasma glucose concentration was not influenced by exercise or dexamethasone administration but was lower than baseline concentrations at 30 minutes after DEX administration and returned to baseline values by 90 minutes. Heart and respiratory rates and rectal temperature increased during exercise. After DEX administration, these values decreased below baseline values. The decrease in heart rate was of shorter duration in dogs that underwent pretreatment with dexamethasone, exercise, or both than in control group dogs
Conclusions and Clinical Relevance—Pretreatment with dexamethasone, moderate physical stress (exercise), or both did not influence sedation or cause adverse effects in healthy dogs treated with DEX. (Am J Vet Res 2005;66:260–265)
Objective—To compare the perioperative stress response in dogs administered medetomidine or acepromazine as part of the preanesthetic medication.
Animals—42 client-owned dogs that underwent elective ovariohysterectomy.
Procedure—Each dog was randomly allocated to receive medetomidine and butorphanol tartrate (20 µg/kg and 0.2 mg/kg, respectively, IM) or acepromazine maleate and butorphanol (0.05 and 0.2 mg/kg, respectively, IM) for preanesthetic medication. Approximately 80 minutes later, anesthesia was induced by administration of propofol and maintained by use of isoflurane in oxygen. Each dog was also given carprofen before surgery and buprenorphine after surgery. Plasma concentrations of epinephrine, norepinephrine, cortisol, and β-endorphin were measured at various stages during the perioperative period. In addition, cardiovascular and clinical variables were monitored.
Results—Concentrations of epinephrine, norepinephrine, and cortisol were significantly lower for dogs administered medetomidine. Concentrations of β-endorphin did not differ between the 2 groups. Heart rate was significantly lower and mean arterial blood pressure significantly higher in dogs administered medetomidine, compared with values for dogs administered acepromazine.
Conclusions and Clinical Relevance—Results indicate that for preanesthetic medications, medetomidine may offer some advantages over acepromazine with respect to the ability to decrease perioperative concentrations of stress-related hormones. In particular, the ability to provide stable plasma catecholamine concentrations may help to attenuate perioperative activation of the sympathetic nervous system. (Am J Vet Res 2002;63:969–975)
OBJECTIVE To compare cardiovascular effects of premedication with medetomidine alone and with each of 3 doses of MK-467 or after glycopyrrolate in dogs subsequently anesthetized with isoflurane.
ANIMALS 8 healthy purpose-bred 5-year-old Beagles.
PROCEDURES In a randomized crossover study, each dog received 5 premedication protocols (medetomidine [10 μg/kg, IV] alone [MED] and in combination with MK-467 at doses of 50 [MMK50], 100 [MMK100], and 150 [MMK150] μg/kg and 15 minutes after glycopyrrolate [10 μg/kg, SC; MGP]), with at least 14 days between treatments. Twenty minutes after medetomidine administration, anesthesia was induced with ketamine (0.5 mg/kg, IV) and midazolam (0.1 mg/kg, IV) increments given to effect and maintained with isoflurane (1.2%) for 50 minutes. Cardiovascular variables were recorded, and blood samples for determination of plasma dexmedetomidine, levomedetomidine, and MK-467 concentrations were collected at predetermined times. Variables were compared among the 5 treatments.
RESULTS The mean arterial pressure and systemic vascular resistance index increased following the MED treatment, and those increases were augmented and obtunded following the MGP and MMK150 treatments, respectively. Mean cardiac index for the MMK100 and MMK150 treatments was significantly greater than that for the MGP treatment. The area under the time-concentration curve to the last sampling point for dexmedetomidine for the MMK150 treatment was significantly lower than that for the MED treatment.
CONCLUSIONS AND CLINICAL RELEVANCE Results indicated concurrent administration of MK-467 with medetomidine alleviated medetomidine-induced hemodynamic changes in a dose-dependent manner prior to isoflurane anesthesia. Following MK-467 administration to healthy dogs, mean arterial pressure was sustained at acceptable levels during isoflurane anesthesia.