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
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
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
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
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
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
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
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:
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
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
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
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 the effects of pretreatment
with dexamethasone, physical stress (exercise), or
both on sedation and plasma hormone and glucose
concentrations in dogs treated with dexmedetomidine
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)
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.