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.     

Disposition of propofol after medetomidine premedication in beagle dogs

Propofol by infusion was administered to 6 adult beagle dogs on 2 separate occasions. The dogs received either no premedication or 20 μg/kg im medetomidine 15 min before induction of anaesthesia, with propofol given at 7 mg/kg/min to permit tracheal intubation. After tracheal intubation the infusion rate was maintained for 120 min at 0.4 mg/kg/min in the non-premedicated, and 0.2 mg/kg/min in the premedicated dogs. The latter group received atipamezole 50 μg/kg im immediately at the end of the infusion. After induction of anaesthesia, a 7F balloon catheter designed for thermal dilution measurement of cardiac output was inserted via the right jugular vein. Blood propofol concentrations were measured by HPLC with fluorescence detection and kinetic variables calculated using non-compartmental moment analysis. The induction dose of propofol was 7.00 (sem 0.55) mg/kg in non-premedicated compared with 3.09 (0.25) mg/kg in premedicated dogs. There were differences in systemic clearance and mean residence time (MRT_iv); 47.5 (6.2) ml/kg/min vs 29.0 (4.4) ml/kg/min (non-premedicated vs premedicated) and 132.3 (5.2) min vs 152.4 (3.1) min (P < 0.02 and P < 0.001, respectively). Cardiorespiratory effects were similar in the 2 groups although heart rate was lower in the premedicated dogs. Venous admixture was high (20–45%) but similar in the 2 groups.     

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.     

Propofol infusion anaesthesia in dogs pre-medicated with medetomidine

Ten laboratory beagles pre-medicated with medetomidine (40 μg/kg bodyweight [bwt]) were anaesthetised using a rapid injection of propofol, followed by propofol infusion. A loading dose of 4 mg/kg bwt of propofol was administered intravenously (iv) as a bolus and, immediately after, a 60 min iv propofol infusion (150 μg/kg bwt/min) was initiated. After a transient increase, mean arterial blood pressure decreased significantly below the pre-propofol level. However, the lowest values recorded (115 ± 11 mmHg) remained within the physiological limits. Heart rate increased significantly (from 41 ± 7.3 to 58 ± 11 beats/min) after initiation of the propofol infusion. No significant changes were seen in respiratory frequency; pO₂ decreased transiently; minimum values (10 ± 2.3 kPa) recorded 5 mins after initiation of the propofol infusion differed significantly from the starting level. pCO₂ increased significantly and the highest values recorded were 6.1 ± 0.35 kPa. Accordingly, pH decreased reaching the lowest level (pH 7.29) 15 mins after initiation of the propofol infusion. The analgesic effect of the present combination was not studied, but the absence of the palpebral and pedal reflexes suggested a surgical stage of anaesthesia. Therefore, propofol infusion in beagles pre-medicated with medetomidine proved to be a promising anaesthetic regimen but, if used clinically, oxygen-enriched inspired air should be used.     

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.     

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.     

A comparison of propofol infusion and propofol/isoflurane anaesthesia in dexmedetomidine premedicated dogs

The effects of propofol infusion were compared with propofol/isoflurane anaesthesia in six beagles premedicated with 10 microg/kg intramuscular (i.m.) dexmedetomidine. The suitability of a cold pressor test (CPT) as a stress stimulus in dogs was also studied. Each dog received isoflurane (end tidal 1.0%, induction with propofol) with and without CPT; propofol (200 microg/kg/min, induction with propofol) with and without CPT; premedication alone with and without CPT in a randomized block study in six separate sessions. Heart rate and arterial blood pressures and gases were monitored. Plasma catecholamine, beta-endorphin and cortisol concentrations were measured. Recovery profile was observed. Blood pressures stayed within normal reference range but the dogs were bradycardic (mean heart rate < 70 bpm). PaCO2 concentration during anaesthesia was higher in the propofol group (mean > 57 mmHg) when compared with isoflurane (mean < 52 mmHg). Recovery times were longer with propofol than when compared with the other treatments. The mean extubation times were 8 +/- 3.4 and 23 +/- 6.3 min after propofol/isoflurane and propofol anaesthesia, respectively. The endocrine stress response was similar in all treatments except for lower adrenaline level after propofol infusion at the end of the recovery period. Cold pressor test produced variable responses and was not a reliable stress stimulus in the present study. Propofol/isoflurane anaesthesia was considered more useful than propofol infusion because of milder degree of respiratory depression and faster recovery.     

Effects of diazepam or lidocaine premedication on propofol induction and cardiovascular parameters in dogs

The effects of diazepam or lidocaine on the propofol induction dose and certain cardiovascular parameters were documented in this randomized, blinded study. Dogs received 0.9% saline (0.1 mL/kg intravenously [i.v.]), lidocaine (2 mg/kg i.v.), or diazepam (0.25 mg/kg i.v.) prior to propofol i.v. until loss of jaw tone was achieved (up to a maximum of 8 mg/kg). Propofol was followed by 0.3 mg/kg atracurium i.v. Direct arterial blood pressures and heart rates were recorded before premedication, induction, and intubation. No statistically significant differences were found among the groups for cardiovascular measurements or for the propofol dose required for intubation.     

Cardiac troponin I in dogs anaesthetized with propofol and sevoflurane: the influence of medetomidine premedication and inspired oxygen fraction

Objective

To investigate changes in serum cardiac troponin I (cTnI) concentrations in dogs in which medetomidine was used for sedation or for premedication prior to anaesthesia with propofol and sevoflurane.

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.     

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.     

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.     

Effects of midazolam-butorphanol, acepromazine-butorphanol and medetomidine on an induction dose of propofol and their compatibility in dogs

The effects of acepromazine-butorphanol (AB), midazolam-butorphanol (MB) and medetomidine (Med) on the induction dose of propofol and their compatibility with propofol were evaluated in client-owned dogs. All premedications induced good to excellent sedation and the induction dose of propofol was considerably reduced. Of the tested premedicants, Med induced the deepest sedation and the most potent dose-sparing effect. Induction of anesthesia was excellent to good in all dogs except for one dog premedicated with MB. Most dogs premedicated with AB or MB showed temporary apnea. Although other adverse effects such as bradycardia or hypotension may also occur, premedication with MB, AB or Med is a valuable technique for the induction of anesthesia with propofol in dogs in a clinical setting.