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.     

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.     

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.     

Comparative cardiovascular, analgesic, and sedative effects of medetomidine, medetomidine-hydromorphone, and medetomidine-butorphanol in dogs

OBJECTIVE: To compare sedative, analgesic, and cardiopulmonary effects after IV administration of medetomidine (20 microg/kg), medetomidine-hydromorphone (20 microg of medetomidine/kg and 0.1 mg of hydromorphone/kg), and medetomidine-butorphanol (20 microg of medetomidine/kg and 0.2 mg of butorphanol tartrate/kg) in dogs. ANIMALS: 6 dogs healthy mixed-breed dogs. PROCEDURE: Instruments were surgically inserted, and heart rate (HR), respiratory rate (RR), systolic arterial pressure (SAP), mean arterial pressure (MAP), diastolic arterial pressure (DAP), mean pulmonary arterial pressure (MPAP), pulmonary capillary wedge pressure (PCWP), central venous pressure (CVP), core body temperature, and cardiac output (CO) were measured 0, 5, 10, 15, 30, 45, and 60 minutes after injection. Cardiac index (CI), stroke volume (SV), stroke index (SI), systemic vascular resistance (SVR), and pulmonary vascular resistance (PVR) were calculated. Arterial samples for blood gas analysis were collected 0, 15, and 45 minutes after injection. Intensity of analgesia, degree of sedation, and degree of muscle relaxation were evaluated at aforementioned time points and 75, 90, 120, 150, 180, and 210 minutes after injection. RESULTS: Administration of medetomidine, medetomidine-hydromorphone, and medetomidine-butorphanol was associated with increases in SAP, MAP, DAP, MPAP, PCWP, CVP, SVR, PVR, core body temperature, and PaCO2 and decreases in HR, CO, CI, SV, SI, RR, pH, and PaO2. Clinically important differences were not detected among treatments. Medetomidine-hydromorphone and medetomidine-butorphanol provided a longer duration of sedation and better quality of analgesia, compared with medetomidine alone. CONCLUSIONS AND CLINICAL RELEVANCE: Medetomidine-hydromorphone or medetomidine-butorphanol is associated with improved analgesia and sedation but has cardiopulmonary effects comparable to those for medetomidine alone.     

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.     

Comparison of two pre-anaesthetic medetomidine doses in isoflurane anaesthetized sheep

OBJECTIVE: To compare the sedative, anaesthetic-sparing and arterial blood-gas effects of two medetomidine (MED) doses used as pre-anaesthetic medication in sheep undergoing experimental orthopaedic surgery. STUDY DESIGN: Randomized, prospective, controlled experimental trial. ANIMALS: Twenty-four adult, non-pregnant, female sheep of various breeds, weighing 53.9 +/- 7.3 kg (mean +/- SD). METHODS: All animals underwent experimental tibial osteotomy. Group 0 (n = 8) received 0.9% NaCl, group L (low dose) (n = 8) received 5 microg kg(-1) MED and group H (high dose) (n = 8) received 10 microg kg(-1) MED by intramuscular (IM) injection 30 minutes before induction of anaesthesia with intravenous (IV) propofol 1% and maintenance with isoflurane delivered in oxygen. The propofol doses required for induction and endtidal isoflurane concentrations (F(E')ISO) required to maintain anaesthesia were recorded. Heart and respiratory rates and rectal temperature were determined before and 30 minutes after administration of the test substance. The degree of sedation before induction of anaesthesia was assessed using a numerical rating scale. Arterial blood pressure, heart rate, respiratory rate, FE'ISO, end-tidal CO2 (FE'CO2) and inspired O2 (FIO2) concentration were recorded every 10 minutes during anaesthesia. Arterial blood gas values were determined 10 minutes after induction of anaesthesia and every 30 minutes thereafter. Changes over time and differences between groups were examined by analysis of variance (anova) for repeated measures followed by Bonferroni-adjusted t-tests for effects over time. RESULTS: Both MED doses produced mild sedation. The dose of propofol for induction of anaesthesia decreased in a dose-dependent manner: mean (+/-SE) values for group 0 were 4.7 (+/-0.4) mg kg(-1), for group L, 3.2 (+/-0.4) mg kg(-1) and for group H, 2.3 (+/-0.3) mg kg(-1)). The mean (+/-SE) FE'ISO required to maintain anaesthesia was 30% lower in both MED groups [group L: 0.96 (+/-0.07) %; group H: 1.06 (+/-0.09) %] compared with control group values [(1.54 +/- 0.17) %]. Heart rates were constantly higher in the control group with a tendency towards lower arterial blood pressures when compared with the MED groups. Respiratory rates and PaCO2 were similar in all groups while PaO2 increased during anaesthesia with no significant difference between groups. In group H, one animal developed a transient hypoxaemia: PaO2 was 7.4 kPa (55.7 mmHg) 40 minutes after induction of anaesthesia. Arterial pH values and bicarbonate concentrations were higher in the MED groups at all time points. CONCLUSION AND CLINICAL RELEVANCE: Intramuscular MED doses of 5 and 10 microg kg(-1) reduced the propofol and isoflurane requirements for induction and maintenance of anaesthesia respectively. Cardiovascular variables and blood gas measurements remained stable over the course of anaesthesia but hypoxaemia developed in one of 16 sheep receiving MED.     

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 sevoflurane, isoflurane and halotane anaesthesia on fluorescein angiographic phases of dogs: a comparative study

A fluorescein angiography method was developed to compare the onset and the total duration of the fluorangiographic phases between three anaesthetic protocols in six healthy mixed-breed dogs. The animals were anaesthetized three times. Each dog received, as pre-anaesthetic protocol, atropine (10 micrograms/kg intramuscularly), and as a sedative, romifidine (80 micrograms/kg intravenously). Fifteen minutes later, induction of anaesthesia was delivered with propofol (1 mg/kg intravenously) and maintained either with sevoflurane (SEVO group), isoflurane (ISO group) or halothane (HAL group) for 30 min in all cases. Some angiographic, cardiovascular and respiratory variables were registered during the procedure. Recovery times were also registered. Angiographic variables recorded were: onset of the arterial phase (TA), onset of the arteriovenous phase (TAV), onset of the venous phase (TV), complete arterial phase duration (I1), complete arteriovenous phase duration (I2) and I1 plus I2 (I3). Mean heart rate, mean arterial pressure, systolic arterial pressure, diastolic arterial pressure, respiratory rate, tidal volume, arterial oxygen saturation and end-tidal CO2 during SEVO and ISO anaesthesia, were similar in dogs. Minute ventilation and rectal temperature were higher in dogs with SEVO than ISO. HAL produced higher arterial pressures and a lower arterial oxygen saturation than ISO and SEVO. Mean respiratory rate, rectal temperature and minute ventilation were higher in HAL. Pulse rate, end-tidal CO2 and tidal volume were similar in the dogs of the three groups. No differences in recovery times were found. The fluorescein angiographic times were within the normal range. There were no significant differences between protocols in I1, I2 or I3. HAL produced a significant increase of all temporal variables (TA, TAV and TV) when compared with ISO; TA was higher in HAL than SEVO-treated dogs. All protocols appear to be safe and effective for inducing and maintaining general anaesthesia in healthy dogs for performing fluorescein angiography.     

Normal values and incidence of cardiorespiratory complications in dogs during general anaesthesia. A review of 1281 cases

This paper describes the cardiorespiratory variables and the incidence of anaesthetic complications in dogs. For this, a retrospective study of 1281 anaesthesias was performed. Heart rate (HR), non-invasive mean arterial (MAP), systolic (SP) and diastolic pressures (DP), invasive mean arterial (IMAP), systolic (ISP) and diastolic pressures (IDP), central venous pressure (CVP), respiratory rate (RR), tidal volume (V(T)), minute volume (V(M)), end-tidal CO(2) (EtCO(2)), arterial oxygen saturation (SpO(2)), temperature (T) and death are reported. Data were described both globally and separately for each ASA (American Society of Anaesthesiologists classification) status. An ANOVA and a Tukey's test were used for comparing the different ASA status' values (alpha=0.05). During anaesthetic maintenance, the mean +/- SD of the studied variables were: HR: 91+/-27 bpm. MAP: 86+/-24 mmHg. IMAP: 80+/-22 mmHg. SP: 114+/-25 mmHg. ISP: 109+/-26 mmHg. DP: 67+/-23 mmHg. IDP: 66+/-22 mmHg. CVP: 5+/-3 mmHg. RR: 19+/-11 rpm. V(T): 14+/-7 ml/kg. V(M): 191+/-93 ml/kg/min. EtCO(2): 40+/-8 mmHg. T: 37.1+/-1.7 degrees C. ASA III and ASA IV patients, compared with those with ASA I, showed higher values of HR, RR, V(T) and V(M) and lower in IMAP, CVP, EtCO(2), SpO(2) and T. The most frequent complications were bradycardia (36.3% of the patients), hypotension (37.9%), hypoventilation (63.4%), hypoxia (16.4%), hypothermia (4.8%) and death (0.9%). Cardiorespiratory complications frequently occur in dogs during general anaesthesia.     

Cardiovascular Effects of 1.0, 1.5, and 2.0 Minimum Alveolar Concentrations of Isoflurane in Experimentally Induced Hypothyroidism in Dogs

This study was performed to determine the cardiovascular responses to isoflurane in euthyroid and hypothyroid dogs. Four healthy mixed-breed dogs were studied prior to thyroidectomy (PRE), 6 months after thyroidectomy (HYP), and after 2 months of oral supplementation with 1-thyroxine (SUP). Heart rate (HR), cardiac output (), stroke volume (SV), systolic, diastolic, mean arterial blood pressure (SAP, DAP, MAP), and total peripheral resistance (TPR) were determined in awake dogs and in the same dogs when end-tidal isoflurane concentrations were 1.28%, 1.92%, and 2.56%. Ventilation was controlled in anesthetized dogs and Paco₂ maintained between 38 to 42 mm Hg. Isoflurane caused significant ( P <.05) dose-dependent reduction in , SV, SAP, DAP, and MAP in the PRE, HYP, and SUP dogs. Cardiac output was lower in the HYP dogs than in the PRE or SUP dogs during awake measurement. TPR was increased in the awake HYP dogs compared with the PRE or SUP dogs. During anesthesia, HYP dogs tended to have lower , SV, SAP, and MAP than the PRE or SUP groups, but the only significant reduction was SAP during 1.5 MAC. The cardiovascular responses to isoflurane in hypothyroid dogs are similar to euthyroid animals with a dose-dependent depression in , SV, and arterial pressure.     

A comparison in dogs of medetomidine,with or without MK‐467, and the combination acepromazine‐butorphanol as premedication prior to anaesthesia induced by propofol and maintained with isoflurane

ObjectiveTo compare the haemodynamic effects of three premedicant regimens during propofol-induced isoflurane anaesthesia.Study designProspective, randomized cross-over study.AnimalsEight healthy purpose-bred beagles aged 4 years and weighing mean 13.6 ± SD 1.9 kg.MethodsThe dogs were instrumented whilst under isoflurane anaesthesia prior to each experiment, then allowed to recover for 60 minutes. Each dog was treated with three different premedications given intravenously (IV): medetomidine 10 μg kg^?1 (MED), medetomidine 10 μg kg^?1 with MK-467 250 μg kg^?1 (MMK), or acepromazine 0.01 mg kg^?1 with butorphanol 0.3 mg kg^?1 (AB). Anaesthesia was induced 20 minutes later with propofol and maintained with isoflurane in oxygen for 60 minutes. Heart rate (HR), cardiac output, arterial blood pressures (ABP), central venous pressure (CVP), respiratory rate, inspired oxygen fraction, rectal temperature (RT) and bispectral index (BIS) were measured and arterial and venous blood gases analyzed. Cardiac index (CI), systemic vascular resistance index (SVRI), oxygen delivery index (DO₂I), systemic oxygen consumption index (VO₂I) and oxygen extraction (EO₂) were calculated. Times to extubation, righting, sternal recumbency and walking were recorded. The differences between treatment groups were evaluated with repeated measures analysis of covariance.ResultsHR, CI, DO₂I and BIS were significantly lower with MED than with MMK. ABP, CVP, SVRI, EO₂, RT and arterial lactate were significantly higher with MED than with MMK and AB. HR and ABP were significantly higher with MMK than with AB. However, CVP, CI, SVRI, DO₂I, VO₂I, EO₂, T, BIS and blood lactate did not differ significantly between MMK and AB. The times to extubation, righting, sternal recumbency and walking were significantly shorter with MMK than with MED and AB.Conclusions and clinical relevanceMK-467 attenuates certain cardiovascular effects of medetomidine in dogs anaesthetized with isoflurane. The cardiovascular effects of MMK are very similar to those of AB.     

Cardiopulmonary effects of three different anaesthesia protocols in cats.

To develop an alternative anaesthetic regimen for cats with cardiomyopathy, the cardiopulmonary effects of three different premedication-induction protocols, followed by one hour maintenance with isoflurane in oxygen: air were evaluated in six cats. Group I: acepromazine (10 microg/kg) + buprenorphine (10 microg/kg) IM, etomidate (1-2 mg/kg) IV induction. Group II: midazolam (1 mg/kg) + ketamine (10 mg/kg) IM induction. Group III: medetomidine (1.5 mg/m2 body surface) IM, propofol (1-2 mg/kg) IV induction. Heart rate, arterial blood pressure, arterial blood gases, respiration rate, and temperature were recorded for the duration of the experiment. In group I the sedative effect after premedication was limited. In the other groups the level of sedation was sufficient. In all groups premedication resulted in a reduced blood pressure which decreased further immediately following induction. The reduction in mean arterial pressure (MAP) reached statistical significance in group I (142+/-22 to 81+/-14 mmHg) and group II (153+/-28 to 98+/-20 mmHg) but not in group III (165+/-24 to 134+/-29 mmHg). Despite the decrease in blood pressure, MAP was judged to have remained within an acceptable range in all groups. During maintenance of anaesthesia, heart rate decreased significantly in group III (from 165+/-24 to 125+/-10 b.p.m. at t=80 min). During anaesthesia the PCO2 and PO2 values increased significantly in all groups. On the basis of the results, the combination acepromazine-buprenorphine is preferred because heart rate, MAP, and respiration are acceptable, it has a limited sedative effect but recovery is smooth.     

Comparison of medetomidine and dexmedetomidine as premedicants in dogs undergoing propofol-isoflurane anesthesia.

OBJECTIVE: To compare 3 dose levels of medetomidine and dexmedetomidine for use as premedicants in dogs undergoing propofol-isoflurane anesthesia. ANIMALS: 6 healthy Beagles. PROCEDURE: Dogs received medetomidine or dexmedetomidine intravenously at the following dose levels: 0.4 microg of medetomidine or 0.2 microg of dexmedetomidine/kg of body weight (M0.4/D0.2), 4.0 microg of medetomidine or 2.0 microg of dexmedetomidine/kg (M4/D2), and 40 microg of medetomidine or 20 microg of dexmedetomidine/kg (M40/D20). Sedation and analgesia were scored before induction. Anesthesia was induced with propofol and maintained with isoflurane. End-tidal isoflurane concentration, heart rate, and arterial blood pressures and gases were measured. RESULTS: Degrees of sedation and analgesia were significantly affected by dose level but not drug. Combined mean end-tidal isoflurane concentration for all dose levels was higher in dogs that received medetomidine, compared with dexmedetomidine. Recovery time was significantly prolonged in dogs treated at the M40/D20 dose level, compared with the other dose levels. After induction, blood pressure decreased below reference range and heart rate increased in dogs treated at the M0.4/D0.2 dose level, whereas blood pressure was preserved in dogs treated at the M40/D20 dose level. However, dogs in these latter groups developed profound bradycardia and mild metabolic acidosis during anesthesia. Treatment at the M4/D2 dose level resulted in more stable cardiovascular effects, compared with the other dose levels. In addition, PaCO2 was similar among dose levels. CONCLUSIONS AND CLINICAL RELEVANCE: Dexmedetomidine is at least as safe and effective as medetomidine for use as a premedicant in dogs undergoing propofol-isoflurane anesthesia.     

The isoflurane-sparing and clinical effects of a constant rate infusion of remifentanil in dogs

OBJECTIVE: To evaluate the isoflurane-sparing and clinical effects of two constant rate infusions of remifentanil in healthy dogs undergoing orthopaedic surgery. STUDY DESIGN: Prospective, randomized clinical study. ANIMALS: Forty-one American Society of Anesthesiologists I-II client-owned dogs (age, 7 months-9 years; body mass 11-59 kg). METHODS: Dogs were randomly assigned to one of three groups and received either: intramuscular (IM) meperidine 2 mg kg(-1) every 2 hours throughout surgery (control group (C); n = 13); remifentanil infused intravenously (IV) at 0.1 microg kg(-1) minute(-1) (low remifentanil group (L); n = 14) or remifentanil infused at 0.25 microg kg(-1) minute(-1) IV (high remifentanil group (H); n = 14). Anaesthesia was induced with thiopental administered to effect and maintained using isoflurane in 100% oxygen. During controlled ventilation when the end-tidal CO(2) was maintained between 4.65 and 5.98 kPa [35-45 mmHg], the end-tidal isoflurane concentration (e'iso%), mean arterial blood pressure (MAP) and heart rate (HR) were measured every 5 minutes. Bradycardia (HR < 40 minute(-1) lasting >5 minutes) was corrected with 0.01 mg kg(-1) IV glycopyrrolate. Data were analysed using the Kruskal-Wallis test with a post-hoc Mann-Whitney U-test and Bonferroni correction. Statistical significance was accepted at < or = 0.05. Data are expressed as mean +/- standard deviation. RESULTS: The e'iso% was reduced in a dose-dependent manner by remifentanil. In C, e'iso% was 1.28 +/-0.13 and was significantly different from L (0.78 +/- 0.17, p < 0.001) and H (0.65 +/- 0.16, p < 0.001). HR was significantly different between groups (p < 0.001). There were no significant differences in MAP between groups. Glycopyrrolate was required in two, three and six dogs in the C, L and H groups respectively. CONCLUSIONS: Remifentanil infusion reduced the isoflurane concentration required for surgical anaesthesia during orthopaedic surgery. CLINICAL RELEVANCE: Remifentanil infusions may be a useful additive to isoflurane anaesthesia in healthy dogs.     

Effect of butorphanol administration on cardiovascular parameters in isoflurane-anesthetized horses - a retrospective clinical evaluation.

OBJECTIVE: To determine cardiovascular responses to administration of butorphanol in isoflurane-anesthetized horses. STUDY DESIGN: Retrospective evaluation of anesthetic records. ANIMALS: Seventy-six horses anesthetized for a variety of clinical surgical procedures. METHODS: Anesthetic records of clinical equine patients anesthetized between January 1999 and December 2003 were searched. The records were reviewed for horses in which anesthesia was induced with ketamine and a benzodiazepine and maintained with isoflurane, and horses that received butorphanol intraoperatively. Exclusion criteria included horses in which the rate of infusion of an inotrope or end-tidal isoflurane concentration was changed 10 minutes before or after the butorphanol bolus. The horses were separated into two groups: group 1 horses received butorphanol at intervals as part of a balanced protocol, group 2 horses had > or = 10% increase in heart rate (HR) or blood pressure within 10 minutes prior to butorphanol administration. RESULTS: Eighty-nine butorphanol administration events matched the criteria for inclusion, 49 in group 1 and 40 in group 2. There were no significant changes after butorphanol administration in systolic arterial pressure (SAP), mean arterial pressure (MAP), diastolic arterial pressure (DAP), and heart rate (HR) in group 1, or in end-tidal carbon dioxide concentration or hemoglobin oxygen saturation in either group. There were significant decreases in SAP (p < 0.0001), MAP (p < 0.0005), and DAP (p < 0.0008) after butorphanol administration in group 2. CONCLUSIONS AND CLINICAL RELEVANCE: The results presented here confirm that butorphanol can be administered to horses during isoflurane anesthesia without adverse effects on HR and arterial blood pressure. The results imply that butorphanol can deepen the plane of anesthesia and obtund sympathetic stimulation from a surgical procedure.     

Influence of a preload of hydroxyethylstarch 6% on the cardiovascular effects of epidural administration of ropivacaine 0.75% in anaesthetized dogs

ObjectiveTo evaluate the cardiovascular effects of a preload of hydroxyethylstarch 6% (HES), preceding an epidural administration of ropivacaine 0.75% in isoflurane anaesthetized dogs.AnimalsSix female, neutered Beagle dogs (mean 13.3 ± SD 1.0 kg; 3.6 ± 0.1 years).Study designRandomized experimental cross-over study (washout of 1 month).MethodsAnaesthesia was induced with propofol and maintained with isoflurane in oxygen/air. All dogs were anaesthetized twice to receive either treatment HESR (continuous rate infusion [CRI] of 7 mL kg^?1 HES started 30 minutes [T-30] prior to epidural administration of ropivacaine 0.75% 1.65 mg kg^?1 at T0) or treatment R (no HES preload and similar dose and timing of epidural ropivacaine administration). Baseline measurements were obtained at T-5. Heart rate (HR), mean (MAP), diastolic (DAP) and systolic (SAP) invasive arterial pressures, cardiac output (Lithium dilution and pulse contour analysis) and derived parameters were recorded every 5 minutes for 60 minutes. Statistical analysis was performed on five dogs, due to the death of one dog.ResultsClinically relevant decreases in MAP (<60 mmHg) were observed for 20 and 40 minutes following epidural administration in treatments HESR and R respectively. Significant decreases in MAP and DAP were present after treatment HESR for up to 20 minutes following epidural administration. No significant within-treatment and overall differences were observed for other cardiovascular parameters. A transient unilateral Horner's syndrome occurred in two dogs (one in each treatment). One dog died after severe hypotension, associated with epidural anaesthesia.Conclusions and clinical relevanceA CRI of 7 mL kg^?1 HES administered over 30 minutes before epidural treatment did not prevent hypotension induced by epidural ropivacaine 0.75%. Epidural administration of ropivacaine 0.75% in isoflurane anaesthetized dogs was associated with a high incidence of adverse effects in this study.     

Comparison of isoflurane and propofol for maintenance of anesthesia in dogs with intracranial disease undergoing magnetic resonance imaging

ObjectiveTo compare isoflurane and propofol for maintenance of anesthesia and quality of recovery in client-owned dogs with intracranial disease undergoing magnetic resonance imaging (MRI).Study designProspective, randomized, clinical trial.AnimalsTwenty-five client-owned dogs with intracranial pathology, 13 females and 12 males, ages 11 months to 13 years, weighing between 3.0 and 48.0 kg.MethodsEach dog was randomly assigned to receive propofol or isoflurane for maintenance of anesthesia. All dogs were not premedicated, were administered propofol intravenously to effect for induction, intubated and mechanically ventilated to maintain an end-tidal carbon dioxide tension 30–35 mmHg (4.0–4.7 kPa). Temperature and cardiac output were measured pre- and post-MRI. Scores for mentation, neurological status, ease of maintenance, and recovery were obtained pre- and post-anesthesia. Pulse oximetry, end-tidal gases, arterial blood pressure, heart rate (HR) and requirements for dopamine administration to maintain mean arterial pressure (MAP) >60 mmHg were recorded throughout anesthesia.ResultsEnd-tidal isoflurane concentration was 0.73 ± 0.35% and propofol infusion rate was 292 ± 119 μg kg^?1 minute^?1. Cardiac index was higher, while HR was lower, with propofol than isoflurane in dogs younger than 5 years, but not in older dogs. Dogs maintained with isoflurane were 14.7 times more likely to require dopamine than propofol dogs. Mentation and maintenance scores and temperature were not different. MAP and diastolic arterial pressure were higher in the propofol group. Recovery scores were better with propofol, although times to extubation were similar. Change in neurological score from pre- to post-anesthesia was not different between treatments.ConclusionsDogs maintained with propofol during MRI had higher arterial pressures, decreased requirements for dopamine, and better recovery scores, compared to dogs maintained with isoflurane.Clinical relevancePropofol anesthesia offered cardiovascular and recovery advantages over isoflurane during MRI in dogs with intracranial disease in this study.     

A clinical comparison of two anaesthetic protocols using lidocaine or medetomidine in horses

OBJECTIVE: To compare the effects of two balanced anaesthetic protocols on end-tidal isoflurane (Fe'ISO), cardiopulmonary performance and quality of recovery in horses. DESIGN: Prospective blinded randomized clinical study. ANIMALS: Sixty-nine client-owned horses, American Society of Anesthesiologists category I and II, undergoing elective surgery. METHODS: The horses were premedicated with acepromazine (0.03 mg kg(-1)) IM 30-60 minutes before induction of anaesthesia and were randomly assigned to one of two treatments: in group L (37 horses) xylazine (1 mg kg(-1)) and in group M (31 horses) medetomidine (7 microg kg(-1)) was administered IV for sedation. Anaesthesia was induced 5 minutes later with ketamine (2.2 mg kg(-1)) and diazepam (0.02 mg kg(-1)) IV and maintained with isoflurane in oxygen/air (initial FIO2 0.40-0.50) and a constant rate infusion (CRI) of either lidocaine (2 mg kg(-1)/15 minutes loading dose followed by 50 microg kg(-1) minute(-1)) (group L) or medetomidine (3.5 microg kg(-1) hour(-1)) (group M). If horses showed movement or nystagmus, additional thiopental or ketamine was administered. Heart rate, mean arterial pressure (MAP), Fe'ISO and arterial blood gases were measured. Cardiac output was measured with the lithium dilution method in 10 (group L) and 11 (group M) horses every 45 minutes. Recovery was scored. RESULTS: Heart rate and the cardiac index (CI) were significantly higher in group L with changes over time. In group M, MAP was significantly higher during the first 50 minutes. Group L needed more additional ketamine and thiopental to maintain a surgical plane of anaesthesia and Fe'ISO was significantly higher from 70 minutes. Recovery was longer in group M and of better quality. The significance level was set at p < 0.05. CONCLUSIONS AND CLINICAL RELEVANCE: In group M, maintenance of stable anaesthetic depth was easier and lower Fe'ISO was required to maintain a surgical plane of anaesthesia. Recoveries were longer but of better quality. The CI was higher in group L but cardiovascular function was generally well maintained in both groups.     

The cardiopulmonary effects of a peripheral alpha‐2‐adrenoceptor antagonist,MK‐467, in dogs sedated with a combination of medetomidine and butorphanol

ObjectiveTo compare the cardiopulmonary effects of intravenous (IV) and intramuscular (IM) medetomidine and butorphanol with or without MK-467.Study designProspective, randomized experimental cross-over.AnimalsEight purpose–bred beagles (two females, six males), 3–4 years old and weighing 14.5 ±1.6 kg (mean ± SD).MethodsAll dogs received four different treatments as follows: medetomidine 20 μg kg^?1 and butorphanol tartrate 0.1 mg kg^?1 IV and IM (MB), and MB combined with MK-467,500 μg kg^?1 (MBMK) IV and IM. Heart rate (HR), arterial blood pressures (SAP, MAP, DAP), central venous pressure (CVP), cardiac output, respiratory rate (f_R), rectal temperature (RT) were measured and arterial blood samples were obtained for gas analysis at baseline and at 3, 10, 20, 30, 45 and 60 minutes after drug administration. The cardiac index (CI), systemic vascular resistance index (SVRI) and oxygen delivery index (DO₂I) were calculated. After the follow-up period atipamezole 50 μg kg^?1 IM was given to reverse sedation.ResultsHR, CI and DO₂I were significantly higher with MBMK after both IV and IM administration. Similarly, SAP, MAP, DAP, CVP, SVRI and RT were significantly lower after MBMK than with MB. There were no differences in f_R between treatments, but arterial partial pressure of oxygen decreased transiently after all treatments. Recoveries were uneventful following atipamezole administration after all treatments.Conclusions and clinical relevanceMK-467 attenuated the cardiovascular effects of a medetomidine-butorphanol combination after IV and IM administration.     

Comparative cardiovascular, analgesic, and sedative effects of medetomidine, medetomidine–hydromorphone, and medetomidine–butorphanol in dogs

The purpose of this study was to determine the cardiovascular, analgesic, and sedative effects of IV medetomidine (M, 20 µg kg^?1), medetomidine–hydromorphone (MH, 20 µg kg^?1 ? 0.1 mg kg^?1), and medetomidine–butorphanol (MB, 20 µg kg^?1 ? 0.2 mg kg^?1) in dogs. Using a randomized cross‐over design and allowing 1 week between treatments, six healthy, mixed‐breed dogs (five males and one female) weighing 20 ± 3 kg, were induced to anesthesia by face‐mask administration of 2.9% ET sevoflurane to facilitate instrumentation prior to administration of the treatment combinations. Dogs were intubated and instrumented to enable measurement of heart rate (HR), systolic arterial pressure (SAP), mean arterial pressure (MAP), diastolic arterial pressure (DAP), mean pulmonary arterial pressure (PAP), pulmonary arterial occlusion pressure (PAOP), central venous pressure (CVP), pulmonary arterial temperature (TEMP), and cardiac output via thermodilution using 5 mL of 5% dextrose, and recording the average of the three replicate measurements. Cardiac index (CI) and systemic (SVR) and pulmonary vascular resistances were calculated. After instrumentation was completed, administration of sevoflurane was discontinued, and the dogs were allowed to recover for 30 minutes prior to administration of the treatment drugs. After collection of the baseline samples for blood gas analysis and recording the baseline cardiovascular variables, the test agents were administered IV over 10 seconds and the CV variables recorded at 5, 10, 15, 30, 45, and 60 minutes post‐injection. In addition, arterial blood was sampled for blood gas analysis at 15 and 45 minutes following injection. Intensity and duration of analgesia (assessed by toe‐pinch response using a hemostat) and level of sedation were evaluated at the above time points and at 75 and 90 minutes post‐injection. Data were analyzed using anova for repeated measures with posthoc differences between means identified using Bonferroni's method (p < 0.05). Administration of M, MH, or MB was associated with increases in SAP, MAP, DAP, PAP, PAOP, CVP, SVR, and TEMP and with decreases in HR and CI. No differences in CV variables between treatment groups were identified at any time. PaO₂ increased over time in all groups and was significantly higher when MH was compared with M. At 45 minutes, PaO₂ tended to decrease over time and was significantly lower when MH and MB were compared with M at 15 minutes. Analgesia scores for MH and MB were significantly higher compared with M through 45 minutes, while analgesia scores for MH were significantly higher compared with M through 90 minutes. Sedation scores were higher for MH and MB compared with M throughout 90 minutes. Durations of lateral recumbency were 108 ± 10.8, 172 ± 15.5, and 145 ± 9.9 minutes for M, MH, and MB, respectively. We conclude that MH and MB are associated with improved analgesia and sedation and have similar CV effects when compared with M.