Effect of medetomidine administration on bispectral index measurements in dogs during anesthesia with isoflurane

OBJECTIVE: To determine the relationship between bispectral index (BIS) and minimum alveolar concentration (MAC) multiples of isoflurane after IM injection of medetomidine or saline (0.9% NaCl) solution in anesthetized dogs. ANIMALS: 6 dogs. PROCEDURE: Each dog was anesthetized 3 times with isoflurane. First, the MAC of isoflurane for each dog was determined by use of the tail clamp method. Second, anesthetized dogs were randomly assigned to receive an IM injection of medetomidine (8 microg x kg(-1)) or an equal volume of isotonic saline (0.9% NaCl) solution 30 minutes prior to beginning BIS measurements. Last, anesthetized dogs received the remaining treatment (medetomidine or isotonic saline solution). Dogs were anesthetized at each of 4 MAC multiples of isoflurane. Ventilation was controlled and atracurium (0.2 mg/kg followed by 6 microg/kg/min as a continuous infusion, IV) administered. After a 20-minute equilibration period at each MAC multiple of isoflurane, BIS data were collected for 5 minutes and median values of BIS calculated. RESULTS: BIS significantly decreased with increasing MAC multiples of isoflurane over the range of 0.8 to 2.0 MAC. Mean (+/- SD) MAC of isoflurane was 1.3 +/- 0.2%. During isoflurane-saline anesthesia, mean BIS measurements at 0.8, 1.0, 1.5, and 2.0 MAC were 65 +/- 8, 60 +/- 7 52 +/- 3, and 31 +/- 28, respectively. During isoflurane-medetomidine anesthesia, mean BIS measurements at 0.8, 1.0, 1.5, and 2.0 MAC were 77 +/- 4, 53 +/- 7, 31 +/- 24, and 9 +/- 20, respectively. CONCLUSIONS AND CLINICAL RELEVANCE: BIS monitoring in dogs anesthetized with isoflurane has a predictive value in regard to degree of CNS depression. During isoflurane anesthesia, our results support a MAC-reducing effect of medetomidine.     

Clinical effects and pharmacokinetics of medetomidine and its enantiomers in dogs

The clinical effects and pharmacokinetics of medetomidine (MED) and its enanti-omers, dexmedetomidine (DEX) and levomedetomidine (LEVO) were compared in a group of six beagle dogs. The dogs received intravenously (i.v.) a bolus of MED (40 microg/kg), DEX (20 and 10 microg/kg), LEVO (20 and 10 microg/kg), and saline placebo in a blinded, randomized block study in six separate sessions. Sedation and analgesia were scored subjectively, and the dogs were monitored for heart rate, ECG lead II, direct blood pressure, respiratory rate, arterial blood gases, and rectal body temperature. Blood samples for drug analysis were taken. Peak sedative and analgesic effects were observed at mean (+/- SD) plasma levels of 18.5 +/- 4.7 ng/mL for MED40, 14.0 +/- 4.5 ng/mL for DEX20, and 5.5 +/- 1.3 ng/mL for DEX10. The overall level of sedation and cardiorespiratory effects did not differ between MED40, DEX20 and DEX10 during the first hour, apparently due to a ceiling effect. However, the analgesic effect of DEX20 lasted longer than the effect of the corresponding dose of racemic medetomidine, suggesting greater potency for dexmedetomidine in dogs. Levomedetomidine had no effect on cardio-vascular parameters and caused no apparent sedation or analgesia. The pharmacokinetics of dexmedetomidine and racemic medetomidine were similar, but clearance of levomedetomidine was more rapid (4.07 +/- 0.69 L/h/kg for LEVO20 and 3.52 +/- 1.03 for LEVO10) than of the other drugs (1.26 +/- 0.44 L/h/kg for MED40, 1.24 +/- 0.48 for DEX20, and 0.97 +/- 0.33 for DEX10).     

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.     

Comparison of romifidine and medetomidine pre-medication in propofol-isoflurane anaesthetised dogs

The objective of this paper was to evaluate romifidine as a pre-medicant in dogs prior to propofol-isoflurane anaesthesia, and to compare it with medetomidine. For this, eight healthy dogs were anaesthetised. Each dog received three pre-anaesthetic protocols: R40 (romifidine, 40 microg/kg, IV), R80 (romifidine, 80 microg/kg, IV) or MED (medetomidine, 10 microg/kg, IV). Induction of anaesthesia was delivered with propofol and maintained with isoflurane. The following variables were studied before sedative administration and 10 min after sedative administration: heart rate (HR), mean arterial pressure (MAP), systolic arterial pressure (SAP) and diastolic arterial pressure (DAP) and respiratory rate (RR). During maintenance, the following variables were recorded at 5-min intervals: HR, MAP, SAD, DAP, arterial oxygen saturation (SpO(2)), end-tidal CO(2)(EtCO(2)), end-tidal concentration of isoflurane (EtISO) required for maintenance of anaesthesia and tidal volume (TV). Time to extubation, time to sternal recumbency and time to standing were also registered. HR and RR experimented a significantly decreased during sedation in all protocols respect to baseline values. Mean HR, MAP, SAP, DAP, SpO(2), EtCO(2), and TV during anaesthesia were similar for the three protocols. End tidal of isoflurane concentration was statistically similar for all protocols. Recovery time for R40 was significantly shorter than in R80 and MED. The studied combination of romifidine, propofol and isoflurane appears to be an effective drug combination for inducing and maintaining general anaesthesia in healthy dogs.     

Sedative, analgesic, and cardiovascular effects of levomedetomidine alone and in combination with dexmedetomidine in dogs

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 microg/kg), IV, as a bolus, followed by continuous infusion at a dose of 25 microg/kg/h; a high dose of levomedetomidine (80 microg/kg), IV, as a bolus, followed by continuous infusion at a dose of 200 microg/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 microg/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 were monitored. 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 of dexmedetomidine. CONCLUSIONS 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.     

Duration of nonresponse to noxious stimulation after intramuscular administration of butorphanol, medetomidine, or a butorphanol-medetomidine combination during isoflurane administration in dogs

OBJECTIVE: To assess duration of actions of butorphanol, medetomidine, and a butorphanol-medetomidine combination in dogs given subanesthetic doses of isoflurane (ISO). ANIMALS: 6 healthy dogs. PROCEDURE: Minimum alveolar concentration (MAC) values for ISO were determined. for each dog. Subsequently, 4 treatments were administered to each dog (saline [0.9% NaCl] solution, butorphanol [0.2 mg/kg of body weight], medetomidine [5.0 microg/kg], and a combination of butorphanol [0.2 mg/kg] and medetomidine [5.0 microg/kg]). All treatments were administered IM to dogs concurrent with isoflurane; treatment order was determined, using a randomized crossover design. Treatments were given at 7-day intervals. After mask induction with ISO and instrumentation with a rectal temperature probe, end-tidal CO2 and anesthetic gas concentrations were analyzed. End-tidal ISO concentration was reduced to 90% MAC for each dog. A tail clamp was applied 15 minutes later. After a positive response, 1 of the treatments was administered. Response to application of the tail clamp was assessed at 15-minute intervals until a positive response again was detected. RESULTS: Duration of nonresponse after administration of saline solution, butorphanol, medetomidine, and butorphanol-medetomidine (mean +/- SD) was 0.0+/-0.0, 1.5+/-1.5, 2.63+/-0.49, and 5.58+/-2.28 hours, respectively. Medetomidine effects were evident significantly longer than those for saline solution, whereas effects for butorphanol-medetomidine were evident significantly longer than for each agent administered alone. CONCLUSION AND CLINICAL RELEVANCE: During ISO-induced anesthesia, administration of medetomidine, but not butorphanol, provides longer and more consistent analgesia than does saline solution, and the combination of butorphanol-medetomidine appears superior to the use of medetomidine or butorphanol alone.     

Effects of intramuscular administration of low doses of medetomidine and medetomidine-butorphanol in middle-aged and old dogs.

OBJECTIVE: To determine effects of low doses of medetomidine administered with and without butorphanol and glycopyrrolate to middle-aged and old dogs. DESIGN: Prospective randomized clinical trial. ANIMALS: 88 healthy dogs > or = 5 years old. PROCEDURE: Dogs were assigned randomly to receive medetomidine (2, 5, or 10 micrograms/kg [0.9, 2.3, or 4.6 micrograms/lb] of body weight, i.m.) alone or with glycopyrrolate (0.01 mg/kg [0.005 mg/lb], s.c.), medetomidine (10 micrograms/kg) and butorphanol (0.2 mg/kg [0.1 mg/lb], i.m.), or medetomidine (10 micrograms/kg), butorphanol (0.2 mg/kg), and glycopyrrolate (0.01 mg/kg). Anesthesia was induced with thiopental sodium and maintained with isoflurane. Degree of sedation and analgesia were determined before and after medetomidine administration. Respiratory rate, heart rate, and mean arterial blood pressure were determined 10 and 30 minutes after medetomidine administration. Adverse effects and amounts of thiopental and isoflurane used were recorded. RESULTS: Sedation increased after medetomidine administration in 79 of 88 dogs, but decreased in 7 dogs that received 2 or 5 micrograms of medetomidine/kg. Mean postsedation analgesia score and amounts of thiopental and isoflurane used were less in dogs that received medetomidine and butorphanol, compared with other groups. Respiratory rate, heart rate, and blood pressure were not different among groups. Significantly more adverse effects developed in dogs that did not receive glycopyrrolate. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of medetomidine (10 micrograms/kg, i.m.) and butorphanol (0.2 mg/kg, i.m.) induced sedation and analgesia and reduced amounts of thiopental and isoflurane required for anesthesia in middle-aged and old dogs. Glycopyrrolate decreased frequency of medetomidine-associated adverse effects.     

Effect of medetomidine on respiration and minimum alveolar concentration in halothane- and isoflurane-anesthetized dogs

OBJECTIVE: To evaluate the effect of medetomidine on minimum alveolar concentration (MAC), respiratory rate, tidal volume, minute volume (V(M)), and maximum inspiratory occlusion pressure (IOCP(max)) in halothane- and isoflurane-anesthetized dogs. ANIMALS: 6 healthy adult dogs (3 males and 3 females). PROCEDURE: The MAC of both inhalants was determined before and 5, 30, and 60 minutes after administration of medetomidine (5 microg/kg, IV). Dogs were subsequently anesthetized by administration of halothane or isoflurane and administered saline (0.9% NaCl) solution IV or medetomidine (5 microg/kg, IV). Respiratory variables and IOCP(max) were measured at specific MAC values 15 minutes before and 5, 30, and 60 minutes after IV administration of medetomidine while dogs breathed 0% and 10% fractional inspired carbon dioxide (FICO2). Slopes of the lines for VM/FICO2 and IOCP(max)/FICO2 were then calculated. RESULTS: Administration of medetomidine decreased MAC of both inhalants. Slope of V(M)/FICO2 increased in dogs anesthetized with halothane after administration of medetomidine, compared with corresponding values in dogs anesthetized with isoflurane. Administration of medetomidine with a simultaneous decrease in inhalant concentration significantly increased the slope for V(M)/FICO2, compared with values after administration of saline solution in dogs anesthetized with halothane but not isoflurane. Values for IOCP(max) did not differ significantly between groups. CONCLUSIONS AND CLINICAL RELEVANCE: Equipotent doses of halothane and isoflurane have differing effects on respiration that are most likely attributable to differences in drug effects on central respiratory centers. Relatively low doses of medetomidine decrease the MAC of halothane and isoflurane in dogs.     

Cardiorespiratory responses and plasma cortisol concentrations in dogs treated with medetomidine before undergoing ovariohysterectomy

OBJECTIVE: To evaluate effects of medetomidine on anesthetic dose requirements, cardiorespiratory variables, plasma cortisol concentrations, and behavioral pain scores in dogs undergoing ovariohysterectomy. DESIGN: Randomized, prospective study. ANIMALS: 12 healthy Walker-type hound dogs. PROCEDURE: Dogs received medetomidine (40 micrograms/kg [18.2 micrograms/lb] of body weight, i.m.; n = 6) or saline (0.9% NaCl) solution (1 ml, i.m.; 6) prior to anesthesia induction with thiopental; thiopental dose needed for endotracheal intubation was compared between groups. Ovariohysterectomy was performed during halothane anesthesia. Blood samples were obtained at various times before drug administration until 300 minutes after extubation. Various physiologic measurements and end-tidal halothane concentrations were recorded. RESULTS: In medetomidine-treated dogs, heart rate was significantly lower than in controls, and blood pressure did not change significantly from baseline. Plasma cortisol concentrations did not increase significantly until 60 minutes after extubation in medetomidine-treated dogs, whereas values in control dogs were increased from time of surgery until the end of the recording period. Control dogs had higher pain scores than treated dogs from extubation until the end of the recording period. CONCLUSION AND CLINICAL RELEVANCE: Administration of medetomidine reduced dose requirements for thiopental and halothane and provided postoperative analgesia up to 90 minutes after extubation. Dogs undergoing ovariohysterectomy by use of thiopental induction and halothane anesthesia benefit from analgesia induced by medetomidine administered prior to anesthesia induction. Additional analgesia is appropriate 60 minutes after extubation.     

Comparison of three doses of dexmedetomidine with medetomidine in cats following intramuscular administration

Cats ( n  = 6) were administered dexmedetomidine (DEX) and medetomidine (MED) at three different dose levels in a randomized, blinded, cross-over study. DEX was administered at 25, 50 and 75 μg/kg (D25, D50 and D75), corresponding to MED 50, 100 and 150 μg/kg (M50, M100 and M150). Sedation, analgesia and muscular relaxation were scored subjectively. Heart and respiratory rates and rectal temperature were measured. Corresponding doses of DEX and MED were compared. Effects were also compared between dose levels for each compound. At dose level 2 (D50-M100), the duration of effective clinical sedation was significantly shorter after DEX (202.5±16.0 min) than after MED (230.0±41.2 min). Proceeding from D50-M100 to D75-M150, the duration of effective clinical sedation was increased more after DEX (by 57.5±38.4 min) than after MED (by 14.2±41.9 min) Increasing from D50-M100 to D75-M150, heart rate was further decreased after DEX (by 8.1±13.4%) but not after MED. There was no statistically significant difference between corresponding doses of DEX and MED for any of the other parameters studied. Changes in sedation, analgesia and muscular relaxation were dose-dependent. It was concluded that anaesthetic effects of medetomidine in cats are probably due entirely to its d-isomer and that dexmedetomidine at 25, 50 and 75 μg/kg induces dose-dependent sedation, analgesia and muscular relaxation of clinical significance in cats.     

Intramuscular anesthesia of bonito and Pacific mackerel with ketamine and medetomidine and reversal of anesthesia with atipamezole

OBJECTIVE: To determine anesthetic effects of ketamine and medetomidine in bonitos and mackerels and whether anesthesia could be reversed with atipamezole. DESIGN: Clinical trial. ANIMALS: 43 bonitos (Sarda chiliensis) and 47 Pacific mackerels (Scomber japonica). PROCEDURE: 28 bonitos were given doses of ketamine ranging from 1 to 8 mg/kg (0.5 to 3.6 mg/lb), i.m., and doses of medetomidine ranging from 0.2 to 1.6 mg/kg (0.1 to 0.7 mg/lb), i.m. (ratio of ketamine to medetomidine, 2.5:1 to 20:1). Doses of atipamezole equal to 1 or 5 times the dose of medetomidine were used. The remaining 15 bonitos were used to determine the anesthetic effects of ketamine at a dose of 4 mg/kg (1.8 mg/lb) and medetomidine at a dose of 0.4 mg/kg (0.2 mg/lb). The mackerels were given ketamine at doses ranging from 11 to 533 mg/kg (5 to 242 mg/lb) and medetomidine at doses ranging from 0.3 to 9.1 mg/kg (0.1 to 4.1 mg/lb; ratio of ketamine to medetomidine, 3:1 to 800:1). Doses of atipamezole equal to 5 times the dose of medetomidine were used. RESULTS: I.m. administration of ketamine at a dose of 4 mg/kg and medetomidine at a dose of 0.4 mg/kg in bonitos and ketamine at a dose of 53 to 228 mg/kg (24 to 104 mg/lb) and medetomidine at a dose of 0.6 to 4.2 mg/kg (0.3 to 1.9 mg/lb) in mackerels was safe and effective. For both species, administration of atipamezole at a dose 5 times the dose of medetomidine reversed the anesthetic effects. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that a combination of ketamine and medetomidine can safely be used for anesthesia of bonitos and mackerels and that anesthetic effects can be reversed with atipamezole.     

Anesthetic effects of ketamine or isoflurane induction prior to isoflurane anesthesia in medetomidine-premedicated dogs

Dogs were given medetomidine (10 microg/kg body weight, intramuscularly) followed in 10 minutes by either ketamine (4 mg/kg body weight, intravenously) or isoflurane mask induction and maintained on isoflurane for 30 minutes. Medetomidine induced lateral recumbency in all dogs. Endotracheal intubation was faster and smoother when dogs were given ketamine than when induced with isoflurane. Analgesia was excellent in all groups. Respiratory depression was more profound when dogs were given ketamine. Recovery quality was smooth and similar among all groups. Medetomidine-premedicated dogs could be induced with either ketamine or isoflurane and maintained on 1.3% isoflurane to achieve good analgesia with smooth recovery from anesthesia.     

Response of hypotensive dogs to dopamine hydrochloride and dobutamine hydrochloride during deep isoflurane anesthesia

OBJECTIVE: To evaluate the dose-related cardiovascular and urine output (UrO) effects of dopamine hydrochloride and dobutamine hydrochloride, administered individually and in combination at various ratios, and identify individual doses that achieve target mean arterial blood pressure (MAP; 70 mm Hg) and cardiac index (CI; 150 mL/kg/min) in dogs during deep isoflurane anesthesia. ANIMALS: 10 young clinically normal dogs. PROCEDURES: Following isoflurane equilibration at a baseline MAP of 50 mm Hg on 3 occasions, dogs randomly received IV administration of dopamine (3, 7, 10, 15, and 20 microg/kg/min), dobutamine (1, 2, 4, 6, and 8 microg/kg/min), and dopamine-dobutamine combinations (3.5:1, 3.5:4, 7:2, 14:1, and 14:4 microg/kg/min) in a crossover study. Selected cardiovascular and UrO effects were determined following 20-minute infusions at each dose. RESULTS: Dopamine caused significant dose-dependent responses and achieved target MAP and CI at 7 microg/kg/min; dobutamine at 2 microg/kg/min significantly affected only CI values. At any dose, dopamine significantly affected UrO, whereas dobutamine did not. Target MAP and CI values were achieved with a dopamine-dobutamine combination at 7:2 microg/kg/min; a dopamine-related dose response for MAP and dopamine- and dobutamine-related dose responses for CI were identified. Changes in UrO were associated with dopamine only. CONCLUSIONS AND CLINICAL RELEVANCE: In isoflurane-anesthetized dogs, a guideline dose for dopamine of 7 microg/kg/min is suggested; dobutamine alone did not improve MAP. Data regarding cardiovascular and UrO effects indicated that the combination of dopamine and dobutamine did not provide greater benefit than use of dopamine alone in dogs.     

Romifidine, medetomidine or xylazine before propofol-halothane-N2O anesthesia in dogs.

The objective of this paper was to evaluate romifidine as a premedicant in dogs prior to propofol-halothane-N2O anesthesia, and to compare it with the other alpha2-agonists (medetomidine and xylazine). For this, ten healthy dogs were anesthetized. Each dog received 3 preanesthetic protocols: atropine (10 microg/kg BW, IM), and as a sedative, romifidine (ROM; 40 microg/kg BW, IM), xylazine (XYL; 1 microg/kg, IM), or medetomidine (MED; 20 microg/kg BW, IM). Induction of anesthesia was delivered with propofol 15 min later and maintained with halothane and N2O for one hour in all cases. The following variables were registered before preanesthesia, 10 min after the administration of preanesthesia, and at 5-minute intervals during maintenance: PR, RR, rectal temperature (RT), MAP, SAP, and DAP. During maintenance, arterial oxygen saturation (SpO2), end-tidal CO2 (EtCO2) and percentage of halothane necessary for maintaining anesthesia (%HAL) were also recorded. Induction dose of propofol (DOSE), time to extubation (TE), time to sternal recumbency (TSR) and time to standing (TS) were also registered. The statistical analysis was carried out during the anesthetic period. ANOVA for repeat measures revealed no differences between the 3 groups for PR and RR; however, MAP, SAP and DAP were higher in the MED group; SpO2 was lower in MED and EtCO2 was lower in ROM; %HAL was higher in XYL. No statistical differences were observed in DOSE, TE, TSR or TS. Percentage of halothane was lower in romifidine and medetomidine than in xylazine premedicated dogs also anesthetized with propofol. All the cardiorespiratory variables measured were within normal limits. The studied combination of romifidine, atropine, propofol, halothane and N2O appears to be a safe and effective drug combination for inducing and maintaining general anesthesia in healthy dogs.     

Cardiovascular effects of medetomidine, detomidine and xylazine in horses

The cardiovascular effects of medetomidine, detomidine, and xylazine in horses were studied. Fifteen horses, whose right carotid arteries had previously been surgically raised to a subcutaneous position during general anesthesia were used. Five horses each were given the following 8 treatments: an intravenous injection of 4 doses of medetomidine (3, 5, 7.5, and 10 microg/kg), 3 doses of detomidine (10, 20, and 40 microg/kg), and one dose of xylazine (1 mg/kg). Heart rate decreased, but not statistically significant. Atrio-ventricular block was observed following all treatments and prolonged with detomidine. Cardiac index (CI) and stroke volume (SV) were decreased with all treatments. The CI decreased to about 50% of baseline values for 5 min after 7.5 and 10 microg/kg medetomidine and 1 mg/kg xylazine, for 20 min after 20 microg/kg detomidine, and for 50 min after 40 microg/kg detomidine. All treatments produced an initial hypertension within 2 min of drug administration followed by a significant decrease in arterial blood pressure (ABP) in horses administered 3 to 7.5 microg/kg medetomidine and 1 mg/kg xylazine. Hypertension was significantly prolonged in 20 and 40 microg/kg detomidine. The hypotensive phase was not observed in 10 microg/kg medetomidine or detomidine. The changes in ABP were associated with an increase in peripheral vascular resistance. Respiratory rate was decreased for 40 to 120 min in 5, 7.5, and 10 microg/kg medetomidine and detomidine. The partial pressure of arterial oxygen decreased significantly in 10 microg/kg medetomidine and detomidine, while the partial pressure of arterial carbon dioxide did not change significantly. Medetomidine induced dose-dependent cardiovascular depression similar to detomidine. The cardiovascular effects of medetomidine and xylazine were not as prolonged as that of detomidine. KEY WORDS: cardiovascular effect, detomidine, equine, medetomidine, xylazine.     

Changes in the minimum alveolar concentration of isoflurane and some cardiopulmonary measurements during three continuous infusion rates of dexmedetomidine in dogs

OBJECTIVE: To measure the change in the minimum alveolar concentration of isoflurane associated with three constant rate infusions of dexmedetomidine. STUDY DESIGN: Prospective, randomized, and blinded experimental trial. Animals Six healthy 6-year-old Beagles weighing between 13.0 and 17.7 kg. METHODS: The dogs received each of four treatments; saline or dexmedetomidine at 0.1, 0.5 or 3 microg kg(-1) loading dose given intravenously (IV) over 6 minutes followed by infusions at 0.1, 0.5 or 3 microg kg(-1) hour(-1), respectively. There were 2 weeks between treatments. The dogs were mask-induced with and maintained on isoflurane in oxygen. Acetated Ringer's (5 mL kg(-1) hour(-1)) and saline or dexmedetomidine (each at 0.5 mL kg(-1) hour(-1)) were given IV. Pulse rate, blood pressure, samples for the measurement of blood gases, pH, lactate, packed cell volume (PCV), total protein (TP) and dexmedetomidine concentrations were obtained from an arterial catheter. Sixty minutes after induction minimum alveolar concentration (MAC) was determined by intermittently applying supramaximal electrical stimuli to the thoracic and pelvic limbs. Cardiopulmonary measurements and arterial blood samples were collected before each set of stimuli. Statistical analyses were conducted with analysis of variance or mixed models according to the experimental design. RESULTS: There was a significant decrease in the MAC of isoflurane associated with 0.5 and 3 microg kg(-1) hour(-1) but not with 0.1 mg kg(-1)hour(-1). Serum concentrations of dexmedetomidine were not measurable at the 0.1 mg kg(-1) hour(-1) and averaged 0.198 +/- 0.081 and 1.903 +/-0.621 ng mL(-1) for the 0.5 and 3 microg kg(-1) hour(-1) infusion rates, respectively. Heart rate decreased with increasing doses of dexmedetomidine while blood pressure increased. Packed cell volume increased at 3 microg kg(-1) hour(-1) but not with other doses. CONCLUSIONS AND CLINICAL RELEVANCE: Dexmedetomidine infusions decrease the intra-operative requirement for isoflurane and may be useful in managing dogs undergoing surgery, where the provision of analgesia and limitation of the stress response is desirable.     

Cardiorespiratory effects of desflurane in dogs given romifidine or medetomidine before induction of anesthesia with propofol

The objective of this study was to evaluate the use of desflurane after induction of anesthesia with propofol in dogs sedated with romifidine or medetomidine. Each of 8 healthy dogs received intravenously, in random order, 3 preanesthetic protocols: romifidine, 40 microg/kg of body weight (BW) (R40); romifidine, 80 microg/kg BW (R80); and medetomidine, 10 microg/kg BW (MED). Cardiovascular and respiratory variables were recorded during the procedure. Time to extubation, time to sternal recumbency, and time to standing were also recorded. Heart rate and respiratory rate decreased significantly during sedation from baseline values, but there were no differences between the means for the 3 preanesthetic protocols. Mean values for heart rate, mean arterial blood pressure, systolic arterial pressure, diastolic arterial pressure, respiratory rate, tidal volume, arterial oxygen saturation, end-tidal CO2 level, pH, and arterial blood gas values during anesthesia were similar for the 3 protocols. The mean end-tidal desflurane concentration was significantly lower with the R80 protocol than with the R40 protocol. The mean time to extubation was significantly shorter with the R40 protocol than with the R80 and MED protocols.     

Comparison of neurologic responses to the use of medetomidine as a sole agent or preanesthetic in laboratory beagles.

Different dose regimens of medetomidine (a potent alpha 2-adrenergic agonist), adding up to a combined dose of 80 micrograms/kg, were administered to laboratory beagles to determine physiologic responses including neurologic. The study was intended to determine EEG responses where sufficient sedative and analgesic effects are reached with medetomidine and in contrast its effects when used with ketamine or halothane. Cardiopulmonary responses were very similar in each dose regimen, showing the characteristic properties of single doses of 80 micrograms/kg of medetomidine. Effective sedative and analgesic duration seemed to be a function of when the largest dose was administered. Adequate additional sedative and analgesic could be gained from injections at doses of half of the initial one. The potent sedative and analgesic effects of medetomidine confirmed by neurologic evaluation supports its potential use as a premedication to general anesthesia in dogs. In this study, 2 different doses of medetomidine were also tested as premedication to both ketamine HCI and halothane anesthesia. Neorologic responses were determined at the same time cardiopulmonary parameters, anesthetic quality, and dose requirements were recorded. Medetomidine was found to have favorable qualities in conjunction with these anesthetics. Cardiopulmonary parameters remained satisfactory in both groups as preanesthetic medication prior to halothane, but no additional benefits could be seen from doses of 40 micrograms/kg medetomidine compared to 20 micrograms/kg, except a significant 30% reduction in halothane requirement. The positive chronotropic and inotropic properties of ketamine restored the medetomidine-induced bradycardia and produced a short anesthetic period of 15 to 30 min depending on the dose of medetomidine. The quality of anesthesia was better when 40 micrograms/kg medetomidine was used, but recovery was quicker with 20 micrograms/kg medetomidine. Medetomidine significantly reduced cerebral activity as demonstrated by recordings of total amplitude and frequency evaluation of the EEG with compressed spectral analysis. This analytical method was effective in confirming clinical signs of sedation, analgesia, and anesthesia in canine subjects.     

Effect of medetomidine on breathing and inspiratory neuromuscular drive in conscious dogs

OBJECTIVE: To evaluate the effects of the alpha2-adrenoceptor agonist medetomidine on respiratory rate (RR), tidal volume (V(T)), minute volume (V(M)), and central respiratory neuromuscular drive as determined by inspiratory occlusion pressure (IOP) during increasing fractional inspired concentrations of carbon dioxide (FiCO2) in conscious dogs. ANIMALS: 6 healthy dogs (3 males and 3 females). PROCEDURE: Dogs were administered 0, 5, or 10 microg of medetomidine/kg i.v. We measured RR, V(T), V(M), and IOP for the first 0.1 second of airway occlusion (IOP0.1) during FiCO2 values of 0%, 2.5%, 5.0%, and 75% at 15 minutes before and 5, 30, and 60 minutes after administration of medetomidine. RESULTS: Increases in FiCO2 significantly increased RR, V(T), and V(M). The i.v. administration of 5 and 10 microg of medetomidine/kg significantly decreased RR and V(M) at 5, 30, and 60 minutes for FiCO2 values of 2.5% and 5.0% and at 30 and 60 minutes for an FiCO2 value of 75%. The IOP0.1 was decreased after 30 minutes only for an FiCO2 value of 7.5% in dogs administered 5 and 10 microg of medetomidine/kg. The IOP0.1 was decreased at 60 minutes after administration of 10 microg of medetomidine/kg for an FiCO2 value of 7.5%. CONCLUSIONS AND CLINICAL RELEVANCE: The i.v. administration of medetomidine decreases RR, V(M), and central respiratory drive in conscious dogs. Medetomidine should be used cautiously and with careful monitoring in dogs with CNS depression or respiratory compromise.