To assess the effect of administration of medetomidine alone or in combination with tramadol on tear secretion (TS) in cats as well as their reversal with atipamezole. For the purpose of the study, a total of 46 cats, representing different breeds and genders, were selected and divided into two groups using a random assignment method. Group M was administered medetomidine at a dose of 80 µg/kg intramuscularly. Group MT was given a combination of medetomidine and tramadol at doses of 80 µg/kg and 2 mg/kg intramuscularly, respectively. Tear secretion was measured using Schirmer tear test I before sedation and at 15 (T15) - 60 (T60) minutes post-sedation with 15 min intervals. At 30 minutes, all cats were given atipamezole (200 µg/kg IM). TS statistically decreased until T30 measurement in both groups (P < 0.05). The TS decreased more in MT group compared to M group at T30 measurements (P < 0.05). TS increased in both groups post-atipamezole but didn't return to initial (T0) levels by study end (T60). Premedication with tear protectors or artificial tears is advised when using MT and M group agents in cats, and atipamezole can reverse their effects post-procedure.

This study was conducted to compare the sedative and cardiovascular effects of alfaxalone and medetomidine in cats. In the study, 18 owned cats brought for X-ray, ultrasound, dental examination, ear diseases examination, and bandage change were used. The cats were randomly divided into two groups; 4 mg/kg alfaxalone was intravenously administered to one group and 0.08 mg/kg medetomidine to the other group. After the application, movement changes and sedation conditions were recorded. Sedation score, analgesia score, heart rate, respiratory rate, and side effects were also recorded. The sedation score was higher and the duration of sedation was longer in the medetomidine group, and the differences were statistically significant. As a result, it was concluded that alfaxalone and medetomidine have clinically similar sedative and analgesic efficacy, medetomidine should be preferred in applications requiring prolonged sedation in cats, and alfaxalone is more reliable in animals with cardiovascular problems.

OBJECTIVE To examine the effects of imidazoline and nonimidazoline α-adrenergic agents on aggregation of feline platelets. SAMPLE Blood samples from 12 healthy adult cats. PROCEDURES In 7 experiments, the effects of 23 imidazoline and nonimidazoline α-adrenoceptor agonists or antagonists on aggregation and antiaggregation of feline platelets were determined via a turbidimetric method. Collagen and ADP were used to initiate aggregation. RESULTS Platelet aggregation was not induced by α-adrenoceptor agonists alone. Adrenaline and noradrenaline induced a dose-dependent potentiation of ADP- or collagen-induced aggregation. Oxymetazoline and xylometazoline also induced a small potentiation of ADP-stimulated aggregation, but other α-adrenoceptor agonists did not induce potentiation. The α2-adrenoceptor antagonists and certain imidazoline α-adrenergic agents including phentolamine, yohimbine, atipamezole, clonidine, medetomidine, and dexmedetomidine inhibited adrenaline-potentiated aggregation induced by ADP or collagen in a dose-dependent manner. The imidazoline compound antazoline inhibited adrenaline-potentiated aggregation in a dose-dependent manner. Conversely, α1-adrenoceptor antagonists and nonimidazoline α-adrenergic agents including xylazine and prazosin were ineffective or less effective for inhibiting adrenaline-potentiated aggregation. Moxonidine also was ineffective for inhibiting adrenaline-potentiated aggregation induced by collagen. Medetomidine and xylazine did not reverse the inhibitory effect of atipamezole and yohimbine on adrenaline-potentiated aggregation. CONCLUSIONS AND CLINICAL RELEVANCE Adrenaline-potentiated aggregation of feline platelets may be mediated by α2-adrenoceptors, whereas imidazoline agents may inhibit in vitro platelet aggregation via imidazoline receptors. Imidazoline α-adrenergic agents may have clinical use for conditions in which there is platelet reactivity to adrenaline. Xylazine, medetomidine, and dexmedetomidine may be used clinically in cats with minimal concerns for adverse effects on platelet function.

OBJECTIVE To evaluate the effects of a medetomidine-ketamine combination on tear production of clinically normal cats by use of the Schirmer tear test (STT) 1 before and during anesthesia and after reversal of medetomidine with atipamezole. ANIMALS 40 client-owned crossbred domestic shorthair cats (23 males and 17 females; age range, 6 to 24 months). PROCEDURES A complete physical examination, CBC, and ophthalmic examination were performed on each cat. Cats with no abnormalities on physical and ophthalmic examinations were included in the study. Cats were allocated into 2 groups: a control group (n = 10 cats) anesthetized by administration of a combination of medetomidine hydrochloride (80 μg/kg) and ketamine hydrochloride (5 mg/kg), and an experimental group (30) anesthetized with the medetomidine-ketamine combination and reversal by administration of atipamezole. Tear production of both eyes of each cat was measured by use of the STT I before anesthesia, 15 minutes after the beginning of anesthesia, and 15 minutes after administration of atipamezole. RESULTS Anesthesia with a medetomidine-ketamine combination of cats with no ophthalmic disease caused a significant decrease in tear production. The STT I values returned nearly to preanesthetic values within 15 minutes after reversal with atipamezole, whereas the STT I values for the control group were still low at that point. CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that a tear substitute should be administered to eyes of cats anesthetized with a medetomidine-ketamine combination from the time of anesthetic administration until at least 15 minutes after administration of atipamezole.

The effects of 2 different continuous rate infusions (CRIs) of medetomidine over an 8-hour period on sedation score, selected cardiopulmonary parameters, and serum levels of medetomidine were evaluated in 6 healthy, conscious dogs using a crossover study design. The treatment groups were: CONTROL = saline bolus followed by saline CRI; MED1 = 2 μg/kg body weight (BW) medetomidine loading dose followed by 1 μg/kg BW per hour CRI; and MED2 = 4 μg/kg BW medetomidine loading dose followed by 2 μg/kg BW per hour CRI. Sedation score (SS), heart rate (HR), respiratory rate (RR), temperature (TEMP), systolic arterial pressure (SAP), mean arterial pressure (MAP), and diastolic arterial pressure (DAP), arterial and mixed venous blood gas analyses, lactate, and plasma levels of medetomidine were evaluated at baseline, at various intervals during the infusion, and 2 h after terminating the infusion. Statistical analysis involved a repeated measures linear model. Both infusion rates of medetomidine-induced dose-dependent increases in SS and dose-dependent decreases in HR, SAP, MAP, and DAP were measured. Respiratory rate (RR), TEMP, central venous pH, central venous oxygen tension, and oxygen extraction ratio also decreased significantly in the MED2 group at certain time points. Arterial oxygen and carbon dioxide tensions were not significantly affected by either infusion rate. In healthy dogs, both infusion rates of medetomidine-induced clinically relevant sedative effects, accompanied by typical alpha2 agonist-induced hemodynamic effects, which plateaued during the infusion and subsequently returned to baseline. While additional studies in unhealthy animals are required, the results presented here suggest that medetomidine infusions at the doses studied may be useful in canine patients requiring sedation for extended periods.

Objective: To evaluate effects of racemic ketamine and S-ketamine in gazelles. Animals: 21 male gazelles (10 Rheem gazelles [Gazella subgutturosa marica] and 11 Subgutturosa gazelles [Gazella subgutturosa subgutturosa]), 6 to 67 months old and weighing (mean±SD) 19 ± 3 kg. Procedures: In a randomized, blinded crossover study, a combination of medetomidine (80 μg/kg) with racemic ketamine (5 mg/kg) or S-ketamine (3 mg/kg) was administered IM. Heart rate, blood pressure, respiratory rate, rectal temperature, and oxygen saturation (determined by means of pulse oximetry) were measured. An evaluator timed and scored induction of, maintenance of, and recovery from anesthesia. Medetomidine was reversed with atipamezole. The alternate combination was used after a 4-day interval. Comparisons between groups were performed with Wilcoxon signed rank and paired t tests. Results: Anesthesia induction was poor in 2 gazelles receiving S-ketamine, but other phases of anesthesia were uneventful. A dominant male required an additional dose of S-ketamine (0.75 mg/kg, IM). After administration of atipamezole, gazelles were uncoordinated for a significantly shorter period with S-ketamine than with racemic ketamine. Recovery quality was poor in 3 gazelles with racemic ketamine. No significant differences between treatments were found for any other variables. Time from drug administration to antagonism was similar between racemic ketamine (44.5 to 53.0 minutes) and S-ketamine (44.0 to 50.0 minutes). Conclusions and Clinical Relevance: Administration of S-ketamine at a dose 60% that of racemic ketamine resulted in poorer induction of anesthesia, an analogous degree of sedation, and better recovery from anesthesia in gazelles with unremarkable alterations in physiologic variables, compared with racemic ketamine.

The isoflurane-sparing effect of the alpha 2-adrenergic agonist medetomidine (30 micrograms/kg of body weight, IV) was tested in 7 dogs, using a blinded, randomized-block study design. The baseline minimal alveolar concentration (MAC) of isoflurane was 1.18 vol% (95% confidence interval [0.97,1.39]). Medetomidine significantly (P < 0.003) reduced isoflurane MAC by 47.2%. Atipamezole (0.3 mg/kg, IV), an alpha 2-adrenergic antagonist, completely reversed the effect of medetomidine on isoflurane MAC. Atipamezole alone did not significantly alter isoflurane MAC. After medetomidine administration, marked bradycardia developed in all dogs and persisted for more than 2 hours. Mean arterial blood pressure increased acutely, but later decreased, and hypotension persisted for more than 2 hours. Atipamezole reversed the bradycardic and hypotensive effects of medetomidine. Results of this study indicate that medetomidine may be useful in clinical cases in which isoflurane MAC-reduction is desirable and that atipamezole might be used to reverse desirable and undesirable effects of medetomidine during isoflurane anesthesia.

OBJECTIVE To determine the temporal effects on tear flow measurements obtained by use of a Schirmer tear test (STT) I after IM administration of various doses of medetomidine or xylazine to healthy dogs. ANIMALS 5 healthy purpose-bred male Beagles. PROCEDURES Each dog received IM injections of 2.0 mL of physiologic saline (0.9% NaCl) solution (control treatment); 0.1% medetomidine hydrochloride (5, 10, 20, and 40 μg/kg), and 2.0% xylazine hydrochloride (0.5, 1.0, 2.0, and 4.0 mg/kg). Treatments were injected into the semimembranosus muscles; there was at least a 1-week interval between successive injections. Order of treatments was determined via a randomized Latin square crossover design. The STT I was performed on both eyes before (baseline) and 0.25, 0.50, 0.75, 1, 2, 3, 4, 5, 6, 7, 8, and 24 hours after each injection.RESULTS STT I values decreased significantly within 45 minutes after injection of medetomidine or xylazine, which was followed by gradual recovery. The lowest mean STT I value was < 10 mm/min for all sedation treatments, except when dogs received 5 μg of medetomidine/kg. Linear regression of the area under the curve for the 8 hours after administration yielded significant effects for all sedation treatments. CONCLUSIONS AND CLINICAL RELEVANCE IM administration of medetomidine or xylazine to dogs reduced tear flow in a dose-related manner. Artificial tear solution or ophthalmic ointment should be used to protect the ocular surface when these drugs are administered to dogs.

Objective: To establish a safe anesthetic protocol with little effect on blood biochemical values and IV glucose tolerance test (IVGTT) results in Japanese black bears (Ursus thibetanus japonicus). Animals: 16 captive female Japanese black bears (5 to 17 years of age). Procedures: Bears were randomly assigned to 4 treatment groups (4 bears/group) in which various treatment combinations were administered via blow dart: tiletamine HCl and zolazepam HCl (9 mg/kg) alone (TZ), TZ (6 mg/kg) and acepromazine maleate (0.1 mg/kg), TZ (6 mg/kg) and butorphanol tartrate (0.3 mg/kg), or TZ (3 mg/kg) and medetomidine HCl (40 μg/kg). Glucose injection for the IVGTT was started 130 minutes after TZ administration. Blood samples were obtained before, at, and intermittently after glucose injection for measurement of biochemical variables as well as plasma glucose and serum insulin concentrations during the IVGTT. Rectal temperature, pulse rate, and respiratory rate were assessed every 15 minutes during the experiment. Results: Induction and maintenance of anesthesia were safely achieved with little adverse effect on cardiopulmonary function when each of the 4 anesthetic regimens was used, although mild hypothermia was induced. No difference was evident between treatment groups in blood biochemical values. Blood glucose and insulin concentration profiles during the IVGTT were similar among the bears given TZ, with or without acepromazine or butorphanol, but hyperglycemia and hypoinsulinemia developed in bears given TZ with medetomidine. Conclusions and Clinical Relevance: All 4 anesthetic regimens yielded chemical restraint without affecting clinical and biochemical values in bears, but medetomidine appeared to affect IVGTT results. For this reason, medetomidine should not be used when anesthetizing bears for IVGTTs.

Objective—To characterize the electroencephalogram (EEG) in young cats. Animals—23 clinically normal cats. Procedures—Cats were sedated with medetomidine hydrochloride and butorphanol tartrate at 2, 4, 6, 8, 12, 16, 20, and 24 weeks of age, and an EEG was recorded at each time point. Recordings were visually inspected for electrical continuity, interhemispheric synchrony, amplitude and frequency of background electrical activity, and frequency of transient activity. Computer-aided analysis was used to perform frequency spectral analysis and to calculate absolute and relative power of the background activity at each age. Results—Electrical continuity was evident in cats ≥ 4 weeks old, and interhemispheric synchrony was evident in cats at all ages evaluated. Analysis of amplitude of background activity and absolute power revealed significant elevations in 6-week-old cats, compared with results for 2-, 20-, and 24-week-old cats. No association between age and relative power or frequency was identified. Transient activity, which consisted of sleep spindles and K complexes, was evident at all ages, but spike and spike-and-wave discharges were observed in cats at 2 weeks of age. Conclusions and Clinical Relevance—Medetomidine and butorphanol were administered in accordance with a sedation protocol that allowed investigators to repeatedly obtain EEG data from cats. Age was an important consideration when interpreting EEG data. These data on EEG development in clinically normal cats may be used for comparison in future studies conducted to examine EEGs in young cats with diseases that affect the cerebral cortex.