Background: α2-adrenergic agonists stand out for their intense acting in the respiratory and hemodynamic parameters, which
sometimes aggravates the already compromised patient. Clonidine is widely used in humans due to its sedation, minimal
hemodynamic and respiratory changes and for analgesia. In veterinary medicine, clonidine has been studied recently specially
for epidural analgesia. The study aimed to evaluate the physiological changes and the sedative effect of the intramuscular
administration of clonidine in dogs, once there are no reports of intramuscularly use of clonidine.
Materials, Methods & Results: Six adult healthy mongrel dogs (5 females and 1 male) were used, after hematological
evaluation (complete hemogram) with an average weight of 12 ± 2.5 kg. The animals were randomly divided into four groups
with a minimum interval of 10 days, where: control group (GC) received 5 mL of saline IM with the other three groups
receiving different doses of clonidine, 5 μg/kg (CLO5), 15 ìg/kg (CLO15) and 30 μg/kg (CLO30) intramuscularly. Heart and
respiratory rate, oxygen saturation, systolic arterial pressure, rectal temperature and sedation by analogical descriptive scale
were evaluated before administration (baseline), after 5 and 15 min and at 15 min intervals for a period of 90 min. For each
group, all parametric variables were analyzed by use of a 1-way ANOVA for repeated measures, followed by a Dunnet test to
compare all sample collection times with baseline data (0 min). For comparisons among groups, for each time, 1-way ANOVA
was performed, followed by a Tukey test. Score sedation non parametrical variable were analyzed by Friedman test, followed
by Dunn’s. Differences were considered significant at P < 0.05. The results showed that clonidine caused a reduction in heart
rate 5 min after administration lasting for 90 min with the three doses studied, with a reduction in systolic arterial pressure but
with no signs of hypotension. There were respiratory reduction, but between normal values and decreased rectal temperature
was observed, with no changes in oxygen saturation. Sedation scores were higher with the higher doses of clonidine.
Discussion: The cardiovascular and respiratory effects of administration of α2-adrenergic agonists are characteristic, noting
reduction in heart rate which is due mostly to decrease in sympathetic nervous system tonus, which was observed in all treated
groups where a significant reduction in heart rate in a gradual manner and tending to be dose dependent since lower values
were observed with higher doses, reaching bradycardia (HR <60 bpm) in group CLO30. Another common alteration of α2-
adrenergic agonists are the changes in blood pressure, such as hypertension and subsequent hypotension and respiratory
depression, frames not observed in this study. Reduction in body temperature is especially due to decrease in muscular activity
as well interfering with thermoregulatory mechanisms. Another factor that may contribute is the room temperature, which
remained close to 25oC. Intramuscular administration of clonidine caused light and mild sedation with the studies doses and
cardiorrespiratory changes should be used in healthy animals. Further studies should be conducted with associations of other
pharmacological class to promote a more pronounced level of sedation.
