Effects of medetomidine premedication on propofol infusion anaesthesia in dogs

Observations of cardiovascular and respiratory parameters were made on six dogs anaesthetized on two separate occasions for 120 minutes with a propofol infusion, once without premedication and once following premedication with 10 μg kg-¹ of intramuscular medetomidine. During anaesthesia the heart rate and cardiac index tended to be lower following medetomidine premedication, while the mean arterial pressure was significantly greater (p<0.05). Although the differences were not statistically significant, the systemic vascular resistance, pulmonary vascular resistance and stroke volume index were also greater in dogs given medetomidine. The mean arterial oxygen and carbon dioxide tensions were similar under both regimens, but in 2 dogs supplementary oxygen had to be administered during anaesthesia to alleviate severe hypoxaemia on both occasions they were anaesthetized. Minute and tidal volumes of respiration tended to be greater in dogs not given medetomidine but medetomidine premedication appeared to have no effect on venous admixture. Dogs given medetomidine received intramuscular atipamezole at the end of the 120 min. propofol infusion; the mean time from induction of anaesthesia to walking without ataxia was 174. min in the unpremedicated dogs and 160 min. in the dogs given atipamezole. The mean blood propofol concentration at which the dogs walked without ataxia was higher in the unpremedicated animals (2.12 ± 0.077 μg. ml-¹ compared with 1.27 ± 0.518 μg. ml-¹ in the premedicated dogs). The oxygen delivery to the tissues was lower after medetomidine premedication (p = 0.03) and the oxygen consumption was generally lower after medetomidine premedication but the difference did not achieve statistical significance. No correlation could be demonstrated between blood propofol concentration and cardiac index, systemic or pulmonary vascular resistance indices, systolic, diastolic or mean arterial blood pressures.     

Dexmedetomidine or medetomidine premedication before propofol-desflurane anaesthesia in dogs

The objective of this study was to evaluate dexmedetomidine as a premedicant in dogs prior to propofol-desflurane anaesthesia, and to compare it with medetomidine. Six healthy dogs were anaesthetized. Each dog received intravenously (i.v.) five preanaesthetic protocols: D1 (dexmedetomidine, 1 microg/kg, i.v.), D2 (dexmedetomidine, 2 microg/kg, i.v.), M1 (medetomidine, 1 microg/kg, i.v.), M2 (medetomidine, 2 microg/kg, i.v.), or M4 (medetomidine, 4 microg/kg, i.v.). Anaesthesia was induced with propofol (2.3-3.3 mg/kg) and maintained with desflurane. The following variables were studied: heart rate (HR), mean arterial pressure, systolic arterial pressure, diastolic arterial pressure, respiratory rate (RR), arterial oxygen saturation, end-tidal CO2, end-tidal concentration of desflurane (EtDES) required for maintenance of anaesthesia and tidal volume. Arterial blood pH (pHa) and arterial blood gas tensions (PaO2, PaCO2) were measured during anaesthesia. Time to extubation, time to sternal recumbency and time to standing were also recorded. HR and RR decreased significantly during sedation in all protocols. Cardiorespiratory variables during anaesthesia were statistically similar for all protocols. EtDES was significantly different between D1 (8.1%) and D2 (7.5%), and between all doses of medetomidine. Desflurane requirements were similar for D1 and M2, and for D2 and M4 protocols. No statistical differences were observed in recovery times. The combination of dexmedetomidine, propofol and desflurane appears to be effective for induction and maintenance of general anaesthesia in healthy dogs.     

Cardiopulmonary effects of fentanyl in conscious dogs and dogs sedated with a continuous rate infusion of medetomidine

OBJECTIVE: To determine the hemodynamic consequences of the coadministration of a continuous rate infusion (CRI) of medetomidine with a fentanyl bolus in dogs. ANIMALS: 12 healthy sexually intact male dogs weighing 30.3 -/+ 4.2 kg (mean +/- SD). PROCEDURE: Dogs received either fentanyl alone (15.0 microg/kg, i.v. bolus) or the same dose of fentanyl during an 11-hour CRI of medetomidine (1.5 microg/kg/h, i.v.). Prior to drug administration, dogs were instrumented for measurement of cardiac output, left atrial pressure, and systemic arterial blood pressures. Additionally, blood samples were collected from the pulmonary artery and left atrium for blood gas analysis. RESULTS: Medetomidine infusion reduced the cardiac index, heart rate, and O2, delivery while increasing left atrial pressure. Subsequent fentanyl administration further decreased the cardiac index. The Pao2 was not significantly different between the 2 treatment groups; however, fentanyl transiently decreased Pao2 from baseline values in dogs receiving a CRI of medetomidine. CONCLUSIONS AND CLINICAL RELEVANCE: Because of the prolonged hemodynamic changes associated with the CRI of medetomidine, its safety should be further evaluated before being clinically implemented in dogs.     

Total intravenous anaesthesia with propofol or propofol/ketamine in spontaneously breathing dogs premedicated with medetomidine

The cardiorespiratory parameters, the depth of anaesthesia and the quality of recovery were evaluated in six spontaneously breathing dogs that had been premedicated with medetomidine (40 microg/kg, supplemented with 20 microg/kg an hour later), administered with either propofol (1 mg/kg followed by 0.15 mg/kg/minute, intravenously), or with ketamine (1 mg/kg followed by 2 mg/kg/hour, intravenously) and propofol (0.5 mg/kg followed by 0.075 mg/kg/minute, intravenously). The dogs' heart rate and mean arterial blood pressure were higher and their minute volume of respiration and temperature were lower when they were anaesthetised with propofol plus ketamine, and a progressive hypercapnia leading to respiratory acidosis was more pronounced. When the dogs were anaesthetised with propofol/ketamine they recovered more quickly, but suffered some unwanted side effects. When the dogs were anaesthetised with propofol alone they recovered more slowly but uneventfully.     

Effect of medetomidine infusion on the anaesthetic requirements of desflurane in dogs

The objective of this paper was to evaluate the effect of constant rate infusion of medetomidine on the anaesthetic requirements of desflurane in dogs. For this, six healthy dogs were studied. Measurements for baseline were taken in the awake, unsedated dogs, then each dog received intravenously (i.v.) three anaesthetic protocols: M (no medetomidine infusion), M0.5 (infusion of medetomidine at 0.5 microg/kg/h, i.v.) or M1 (infusion of medetomidine at 1 microg/kg/h, i.v.). All dogs were sedated with medetomidine (2 microg/kg, i.v.) and measurements repeated in 10 min. Induction of anaesthesia was delivered with propofol (3 mg/kg, i.v.) and maintained with desflurane for 90 min to achieve a defined surgical plane of anaesthesia in all cases. After tracheal intubation infusion of medetomidine was initiated and maintained until the end of anaesthesia. Cardiovascular, respiratory, arterial pH (pHa) and arterial blood gas tensions (PaO(2), PaCO(2)) variables were measured during the procedure. End tidal desflurane concentration (EtDES) was recorded throughout anaesthesia. Time to extubation, time to sternal recumbency and time to standing were also noted. Heart rate and respiratory rate were significantly decreased during sedation in all protocols compared to baseline values. Mean heart rate, mean arterial pressure, systolic arterial pressure, diastolic arterial pressure, respiratory rate, tidal volume, arterial oxygen saturation, end-tidal CO(2), pHa, PaO(2), and PaCO(2) during anaesthesia were similar for all protocols. EtDES for M (8.6 +/- 0.8%) was statistically higher than for M0.5 (7.6 +/- 0.5%) and M1 (7.3 +/- 0.7%) protocols. Infusion of medetomidine reduces desflurane concentration required to maintain anaesthesia in dogs.     

Clinical use of a low-dose medetomidine infusion in healthy dogs undergoing ovariohysterectomy

Eight healthy dogs undergoing elective ovariohysterectomy were anesthetized with a standard protocol and received a low-dose medetomidine constant rate infusion during surgery. Cardiorespiratory parameters, including non-invasive cardiac output, were measured at various times. This protocol resulted in acceptable and stable cardiovascular performance, allowed low isoflurane concentrations, and provided smooth recoveries.     

Romifidine-ketamine anaesthesia in atropine and triflupromazine pre-medicated buffalo calves

The study was conducted on 10 buffalo calves with a weight of 98.5 +/- 3.9 kg and age 9.7 +/- 1.3 months. Ten trials of two treatments were carried out using a randomized block design. Atropine at the dose of 0.02 mg/kg bodyweight was administered in both the groups. The animals of group I received romifidine at the dose of 10 microg/kg i.v., 10 min after atropine administration, whereas, animals of group II received triflupromazine at the dose of 0.3 mg/kg i.m. and 10 min later romifidine at the dose of 10 microg/kg i.v. immediately followed by ketamine at the dose of 5 mg/kg i.v. The onset of action of romifidine in group I occurred within 2 min and the animals remained under mild sedation for 31 +/- 4.8 min. In group II, the triflupromazine-romifidine-ketamine combination induced anaesthesia for 14 +/- 2.3 min. Hypothermia, significant bradycardia and respiratory depression was noticed in both groups at different time intervals.     

The effect of medetomidine premedication upon propofol induction and infusion anaesthesia in the dog

The effect of premedication with four different intramuscular doses of medetomidine (5.0,10.0, 20.0 and 40.0 μg.kg-¹) and a saline placebo were compared in a group of six adult beagle dogs anaesthetised with propofol on five separate occasions. Anaesthesia was induced 30 minutes after premedication and maintained by intravenous injection and continuous infusion of propofol. The effects of medetomidine were reversed with atipamezole 30 minutes after anaesthetic induction. The marked synergistic effects of medetomidine with propofol were demonstrated by a dose related reduction in the induction and infusion requirements for a similar degree of anaesthesia. The effect appeared exponential in nature; lower medetomidine doses produced a disproportionately greater effect.
The maintenance of anaesthesia with propofol following a saline placebo or low doses of medetomidine proved to be difficult. Higher doses of medetomidine required less propofol for induction and infusion and allowed a more stable anaesthesia to be maintained. Propofol produced no statistically significant change in heart rate during infusion. Changes in respiratory rate were markedly group specific. A significant reduction in respiratory rate was seen in dogs given either 5 μg.kg- or 10 μ-g.kg-¹ medetomidine. No change was recorded in dogs given 20 /μg.kg-¹ medetomidine and a significant increase was seen in dogs given 40 μg.kg-¹ medetomidine. Recovery was monitored following the termination of propofol infusion after the reversal of medetomidine using atipamezole at five times the medetomidine dose. Recovery was slower for dogs given lower doses of medetomidine and consequently higher doses of propofol.     

A comparative study of medetomidine/ketamine and xylazine/ketamine anaesthesia in dogs

The anaesthetic and physiological effects of a combination of 40 micrograms medetomidine with 2.5 ketamine, 5.0 or 7.5 mg/kg administered intramuscularly were compared with the effects of a combination of 1 mg/kg xylazine and 15 mg/kg ketamine. All the combinations rapidly induced an anaesthetic state that permitted endotracheal intubation, with the absence of the pedal reflex and with good muscle relaxation, and induced bradycardia that was less pronounced as the dose of ketamine was increased. All the combinations produced a decrease in respiratory rate. Increasing the dose of ketamine combined with medetomidine resulted in a very significant prolongation of the duration of anaesthesia, the duration of muscle relaxation and the arousal time. The duration of the anaesthetic effects of 40 micrograms/kg medetomidine with 5 mg/kg ketamine was comparable to that provided by the recommended xylazine/ketamine combination but the period of muscle relaxation was significantly longer. The recovery from medetomidine/ketamine took longer than recovery from xylazine/ketamine but there were fewer side effects.     

A clinical trial of propofol infusion anaesthesia in dogs

Studies were carried out on 40 dogs premedicated with acepromazine (0·05 mg. kg^-1) and atropine (0·02 mg. kg^-1) to determine the minimum infusion rate of propofol needed to maintain anaesthesia and to compare the quality of the anaesthesia with that produced by halothane/nitrous oxide/oxygen. In 30 dogs anaesthesia was induced with propofol and maintained with a continuous infusion and in the other ten dogs anaesthesia was induced with thiopentone and maintained with the inhalation agents. An infusion rate of 0·4 mg. kg^-1 min^-1 of propofol produced surgical anaesthesia in dogs breathing oxygen or oxygen-enriched air. Cardiovascular and respiratory effects were similar to those in dogs anaesthetized with halothane/nitrous oxide and with both anaesthetic regimens myocardial oxygen consumption appeared to increase with increasing duration of anaesthesia. A possible familial susceptibility resulting in a more prolonged recovery was revealed and propofol infusion was associated with a 16 per cent incidence of vomiting in the recovery period. It was concluded that in canine anaesthesia the continuous infusion of propofol to maintain anaesthesia in healthy dogs was safe but less satisfactory than the use of halothane/nitrous oxide.     

Minimal alveolar concentration of desflurane in combination with an infusion of medetomidine for the anaesthesia of ponies

The minimum alveolar concentration of desflurane when combined with a continuous infusion of medetomidine at 3.5 microg/kg/hour was measured in seven ponies. Anaesthesia was induced with medetomidine (7 microg/kg intravenously) followed by ketamine (2 mg/kg intravenously) and maintained with desflurane in oxygen. The infusion of medetomidine was started 20 minutes after the induction of anaesthesia. The electrical test stimulus was applied at the coronary band (50 V, 10 ms bursts at 5 Hz for one minute), and heart rates and rhythms, arterial blood pressures, and arterial blood gas tensions were measured at intervals, just before the application of the stimulus. The mean (sd) minimum alveolar concentration of desflurane was 5.3 (1.04) per cent (range 3.2 to 6.4 per cent), 28 per cent less than the previously published value for desflurane alone after the induction of anaesthesia with xylazine and ketamine. The cardiopulmonary parameters remained stable throughout the period of anaesthesia. The mean (sd) time taken by the ponies to stand after the administration of desflurane ceased was 16.5 (6.17) (range 5.8 to 26) minutes, and the quality of recovery was good or excellent. However, one pony died shortly after standing; a postmortem examination revealed that it had chronic left atrial dilatation.     

Opioid-sparing effect of a medetomidine constant rate infusion during thoraco-lumbar hemilaminectomy in dogs administered a ketamine infusion

ObjectiveTo evaluate the perioperative opioid-sparing effect of a medetomidine (MED) infusion compared to a saline (SAL) infusion in otherwise healthy dogs undergoing thoraco-lumbar hemilaminectomy surgery.Study designRandomized, partially blinded, clinical study.AnimalsA total of 44 client-owned adult dogs.MethodsAll dogs were administered a 1 μg kg^–1 MED loading dose, followed by a 1.7 μg kg^–1 hour^–1 constant rate infusion (CRI) intravenously or equivalent volumes of SAL. Infusions were started 10–15 minutes before surgical incision and continued throughout the surgical procedure. All dogs were administered a standardized anaesthetic and analgesic protocol (including a ketamine CRI). Multiparametric monitoring, including invasive arterial blood pressure, was performed. A trained investigator, unaware of the treatment, performed pain scores for 4 hours postoperatively. Rescue analgesia consisted of fentanyl administered intraoperatively and methadone postoperatively. Data were tested for normality and analysed with Fisher’s exact test, Mann–Whitney U-test, analysis of variance and Kaplan–Meier survival analysis. Data are shown as median (interquartile range) and p-value was set at < 0.05.ResultsThe total dose of fentanyl was significantly lower with MED 0 (0–0.8) μg kg^–1 hour^–1 compared to SAL 3 (1.8–5.3) μg kg^–1 hour^–1 (p = 0.004). In the MED group, one dog compared to 12 dogs in the SAL group required a fentanyl CRI (p = 0.001). There were no statistically significant differences between groups regarding the total dose of methadone administered.Conclusions and clinical relevanceThe addition of a low-dose medetomidine CRI to the anaesthetic protocol decreased the need for a fentanyl CRI in otherwise healthy dogs undergoing thoraco-lumbar hemilaminectomy surgery during administration of a ketamine CRI.     

Propofol anaesthesia in cats

Propofol was administered to 49 cats to induce anaesthesia. The mean dose required was 6.8 mg/kg and this was not affected by prior administration of acepromazine maleate. In 27 cases, propofol was also used as the principal maintenance agent (mean dose rate 0.51 mg/kg/minute). Inductions were very smooth and problem free. Intubation was easily achieved in 15 cats with the aid of local desensitisation by lignocaine spray or neuromuscular relaxation by suxamethonium. Heart rate did not vary significantly during induction or maintenance of anaesthesia but respiratory rates did fall significantly. Recovery from anaesthesia was remarkably smooth in all cases and there was no significant difference in recovery times between the cats in which halothane was the principal maintenance agent and cats which received propofol alone. Side effects were seen during recovery in eight cats and included retching, sneezing and pawing of the face.     

Minimum infusion rate of alfaxalone for total intravenous anaesthesia after sedation with acepromazine or medetomidine in cats undergoing ovariohysterectomy

ObjectiveTo determine the induction doses, then minimum infusion rates of alfaxalone for total intravenous anaesthesia (TIVA), and subsequent, cardiopulmonary effects, recovery characteristics and alfaxalone plasma concentrations in cats undergoing ovariohysterectomy after premedication with butorphanol-acepromazine or butorphanol-medetomidine.Study designProspective randomized blinded clinical study.AnimalsTwenty-eight healthy cats.MethodsCats undergoing ovariohysterectomy were assigned into two groups: together with butorphanol [0.2 mg kg^?1 intramuscularly (IM)], group AA (n = 14) received acepromazine (0.1 mg kg^?1 IM) and group MA (n = 14) medetomidine (20 μg kg^?1 IM). Anaesthesia was induced with alfaxalone to effect [0.2 mg kg^?1 intravenously (IV) every 20 seconds], initially maintained with 8 mg kg^?1 hour^?1 alfaxalone IV and infusion adjusted (±0.5 mg kg^?1 hour^?1) every five minutes according to alterations in heart rate (HR), respiratory rate (f_R), Doppler blood pressure (DBP) and presence of palpebral reflex. Additional alfaxalone boli were administered IV if cats moved/swallowed (0.5 mg kg^?1) or if f_R >40 breaths minute^?1 (0.25 mg kg^?1). Venous blood samples were obtained to determine plasma alfaxalone concentrations. Meloxicam (0.2 mg kg^?1 IV) was administered postoperatively. Data were analysed using linear mixed models, Chi-squared, Fishers exact and t-tests.ResultsAlfaxalone anaesthesia induction dose (mean ± SD), was lower in group MA (1.87 ± 0.5; group AA: 2.57 ± 0.41 mg kg^?1). No cats became apnoeic. Intraoperative bolus requirements and TIVA rates (group AA: 11.62 ± 1.37, group MA: 10.76 ± 0.96 mg kg^?1 hour^?1) did not differ significantly between groups. Plasma concentrations ranged between 0.69 and 10.76 μg mL^?1. In group MA, f_R, end-tidal carbon dioxide, temperature and DBP were significantly higher and HR lower.Conclusion and clinical relevanceAlfaxalone TIVA in cats after medetomidine or acepromazine sedation provided suitable anaesthesia with no need for ventilatory support. After these premedications, the authors recommend initial alfaxalone TIVA rates of 10 mg kg^?1 hour^?1.     

Effects of 2 different medetomidine infusion rates on selected neurohormonal and metabolic parameters in dogs

The effects of 2 different 8-hour continuous rate infusions (CRIs) of medetomidine on epinephrine, norepinephrine, cortisol, glucose, and insulin levels were investigated in 6 healthy dogs. Each dog received both treatments and a control as follows: MED1 = 2 μg/kg bodyweight (BW) loading dose followed by 1 μg/kg BW per hour CRI; MED2 = 4 μg/kg BW loading dose followed by 2 μg/kg BW per hour CRI; and CONTROL = saline bolus followed by a saline CRI. Both infusion rates of medetomidine decreased norepinephrine levels throughout the infusion compared to CONTROL. While norepinephrine levels tended to be lower with the MED2 treatment compared to the MED1, this difference was not significant. No differences in epinephrine, cortisol, glucose, or insulin were documented among any of the treatments at any time point. At the low doses used in this study, both CRIs of medetomidine decreased norepinephrine levels over the 8-hour infusion period, while no effects were observed on epinephrine, cortisol, glucose, and insulin.     

Effects of vatinoxan in dogs premedicated with medetomidine and butorphanol followed by sevoflurane anaesthesia: a randomized clinical study

ObjectiveTo investigate effects of vatinoxan in dogs, when administered as intravenous (IV) premedication with medetomidine and butorphanol before anaesthesia for surgical castration.Study designA randomized, controlled, blinded, clinical trial.AnimalsA total of 28 client-owned dogs.MethodsDogs were premedicated with medetomidine (0.125 mg m^?2) and butorphanol (0.2 mg kg^?1) (group MB; n = 14), or medetomidine (0.25 mg m^?2), butorphanol (0.2 mg kg^?1) and vatinoxan (5 mg m^?2) (group MB-VATI; n = 14). Anaesthesia was induced 15 minutes later with propofol and maintained with sevoflurane in oxygen (targeting 1.3%). Before surgical incision, lidocaine (2 mg kg^?1) was injected intratesticularly. At the end of the procedure, meloxicam (0.2 mg kg^?1) was administered IV. The level of sedation, the qualities of induction, intubation and recovery, and Glasgow Composite Pain Scale short form (GCPS-SF) were assessed. Heart rate (HR), respiratory rate (f_R), mean arterial pressure (MAP), end-tidal concentration of sevoflurane (Fe′Sevo) and carbon dioxide (Pe′CO₂) were recorded. Blood samples were collected at 10 and 30 minutes after premedication for plasma medetomidine and butorphanol concentrations.ResultsAt the beginning of surgery, HR was 61 ± 16 and 93 ± 23 beats minute^?1 (p = 0.001), and MAP was 78 ± 7 and 56 ± 7 mmHg (p = 0.001) in MB and MB-VATI groups, respectively. No differences were detected in f_R, Pe′CO₂, Fe′Sevo, the level of sedation, the qualities of induction, intubation and recovery, or in GCPS-SF. Plasma medetomidine concentrations were higher in group MB-VATI than in MB at 10 minutes (p = 0.002) and 30 minutes (p = 0.0001). Plasma butorphanol concentrations were not different between groups.Conclusions and clinical relevanceIn group MB, HR was significantly lower than in group MB-VATI. Hypotension detected in group MB-VATI during sevoflurane anaesthesia was clinically the most significant difference between groups.     

Cerebral state monitoring in Beagle dogs sedated with medetomidine

OBJECTIVE: To provide experience of monitoring the level of hypnosis with the Cerebral State Monitor (CSM), a device extracting a single numerical variable between 0 and 100 from the electroencephalogram in dogs sedated with medetomidine during dental scale removal. STUDY DESIGN: Prospective observational study. Animals Nine female Beagle dogs weighing 13.3 +/- 1.3 kg. METHODS: Cerebral state index (CSI) and burst suppression ratio (BSR) were recorded from sub-dermal needle electrodes in dogs sedated after subcutaneous injection of 114 +/- 11 microg kg(-1) medetomidine. Ten minutes after injection CSI monitoring began, and after 5 minutes, dental scale removal with an ultrasonic probe was started. After approximately 30 minutes, the effects of medetomidine were antagonized with atipamezole. RESULTS: The CSI had a median value of 43 (range 40-56) in undisturbed sedated dogs. During dental scale removal, CSI increased to a median value of 99 (range 92-100). The BSR in undisturbed sedated dogs ranged from 2 to 15, but fell to zero during dental scale removal. CONCLUSIONS: Stimulation during dental scale removal might be expected to reduce the level of sedation and hypnosis in dogs to which medetomidine had been administered. The concurrent increase in CSI and decrease in BSR suggested that a higher CSI was associated with arousal from sedation and a reduction in the depth of hypnosis. More studies are needed to validate CSI in order to better understand the functioning of this monitor. CLINICAL RELEVANCE: The CSM shows promise for monitoring the degree of sedation and hypnosis during anaesthesia, and after adequate validation, could contribute to the refinement of anaesthetic techniques in animals.     

Effects of 2 different infusion rates of medetomidine on sedation score,cardiopulmonary parameters,and serum levels of medetomidine in healthy dogs

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.