Comparison of detomidine and romifidine as premedicants before ketamine and halothane anesthesia in horses undergoing elective surgery

OBJECTIVE: To compare detomidine hydrochloride and romifidine as premedicants in horses undergoing elective surgery. ANIMALS: 100 client-owned horses. PROCEDURE: After administration of acepromazine (0.03 mg/kg, IV), 50 horses received detomidine hydrochloride (0.02 mg/kg of body weight, IV) and 50 received romifidine (0.1 mg/kg, IV) before induction and maintenance of anesthesia with ketamine hydrochloride (2 mg/kg) and halothane, respectively. Arterial blood pressure and blood gases, ECG, and heart and respiratory rates were recorded. Induction and recovery were timed and graded. RESULTS: Mean (+/- SD) duration of anesthesia for all horses was 104 +/- 28 minutes. Significant differences in induction and recovery times or grades were not detected between groups. Mean arterial blood pressure (MABP) decreased in both groups 30 minutes after induction, compared with values at 10 minutes. From 40 to 70 minutes after induction, MABP was significantly higher in detomidine-treated horses, compared with romifidine-treated horses, although more romifidine-treated horses received dobutamine infusions. In all horses, mean respiratory rate ranged from 9 to 11 breaths/min, PaO2 from 200 to 300 mm Hg, PaCO2 from 59 to 67 mm Hg, arterial pH from 7.33 to 7.29, and heart rate from 30 to 33 beats/min, with no significant differences between groups. CONCLUSIONS AND CLINICAL RELEVANCE: Detomidine and romifidine were both satisfactory premedicants. Romifidine led to more severe hypotension than detomidine, despite administration of dobutamine to more romifidine-treated horses. Both detomidine and romifidine are acceptable alpha2-adrenoceptor agonists for use as premedicants before general anesthesia in horses; however, detomidine may be preferable when maintenance of blood pressure is particularly important.     

Detomidine-Propofol Anesthesia for Abdominal Surgery in Horses

OBJECTIVE: To evaluate propofol for induction and maintenance of anesthesia, after detomidine premedication, in horses undergoing abdominal surgery for creation of an experimental intestinal adhesion model. STUDY DESIGN: Prospective study. ANIMALS: Twelve horses (424 +/- 81 kg) from 1 to 20 years of age (5 females, 7 males). METHODS: Horses were premedicated with detomidine (0.015 mg/kg i.v.) 20 to 25 minutes before induction, and a propofol bolus (2 mg/kg i.v.) was administered for induction. Propofol infusion (0.2 mg/kg/min i.v.) was used to maintain anesthesia. The infusion rate was adjusted to maintain an acceptable anesthetic plane as determined by muscle relaxation, occular signs, response to surgery, and cardiopulmonary responses. Oxygen (15 L/min) was insufflated through an endotracheal tube as necessary to maintain the SpO2 greater than 90%. Systolic (SAP), mean (MAP), and diastolic (DAP) arterial pressures, heart rate (HR), electrocardiogram (ECG), respiratory rate (RR), SpO2 (via pulse oximetry), and nasal temperature were recorded at 15 minute intervals, before premedication and after induction of anesthesia. Arterial blood gas samples were collected at the same times. Objective data are reported as mean (+/-SD); subjective data are reported as medians (range). RESULTS: Propofol (2.0 mg/kg i.v.) induced anesthesia (mean bolus time, 85 sec) within 24 sec (+/-22 sec) after the bolus was completed. Induction was good in 10 horses; 2 horses showed signs of excitement and these two inductions were not smooth. Propofol infusion (0.18 mg/kg/min +/- 0.04) was used to maintain anesthesia for 61 +/- 19 minutes with the horses in dorsal recumbency. Mean SAP, DAP, and MAP increased significantly over time from 131 to 148, 89 to 101, and 105 to 121 mm Hg, respectively. Mean HR varied over time from 43 to 45 beats/min, whereas mean RR increased significantly over anesthesia time from 4 to 6 breaths/min. Mean arterial pH decreased from a baseline of 7.41 +/- 0.07 to 7.30 +/- 0.05 at 15 minutes of anesthesia, then increased towards baseline values. Mean PaCO2 values increased during anesthesia, ranging from 47 to 61 mm Hg whereas PaO2 values decreased from baseline (97 +/- 20 mm Hg), ranging from 42 to 57 mm Hg. Muscle relaxation was good and no horses moved during surgery: Recovery was good in 9 horses and acceptable in 3; mean recovery time was 67 +/- 29 minutes with 2.4 +/- 2.4 attempts necessary for the horses to stand. CONCLUSIONS: Detomidine-propofol anesthesia in horses in dorsal recumbency was associated with little cardiovascular depression, but hypoxemia and respiratory depression occurred and some excitement was seen on induction. CLINICAL RELEVANCE: Detomidine-propofol anesthesia is not recommended for surgical procedures in horses if dorsal recumbency is necessary and supplemental oxygen is not available (eg, field anesthesia).     

The Influence of Detomidine and Epinephrine on Heart Rate, Arterial Blood Pressure, and Cardiac Arrhythmia in Horses

Detomidine (10 micrograms/kg and 20 micrograms/kg) was administered to seven horses with and without epinephrine infusion (0.1 microgram/kg/min) from 5 minutes before to 5 minutes after detomidine injection. One or more single supraventricular premature heartbeats were observed in three horses after detomidine administration. Epinephrine infusion did not modify the incidence of cardiac arrhythmias in detomidine-treated horses at the doses tested. Relatively high momentary peak systolic pressures were registered in some horses after detomidine administration during epinephrine infusion. The highest systolic arterial blood pressure was 290 mm Hg, but this value was not higher than that reported in horses during maximum physical exercise. Epinephrine infusion did not alter blood gases, arterial pH, or base excess.     

Effects of an infusion of dopamine on the cardiopulmonary effects of Escherichia coli endotoxin in anaesthetised horses

Horses with colic may be endotoxaemic and subsequently develop hypotension during anaesthesia for surgical operation. The aim of this study was to evaluate the efficacy of dopamine as a means to improve cardiovascular function in anaesthetised endotoxaemic horses. Nine horses (five in group 1 and four in group 2) were anaesthetised with thiopentone and guaifenesin and anaesthesia was maintained with halothane. After approximately one hour, facial artery pressure, heart rate, pulmonary artery pressure, cardiac output, temperature, pHa, PaCO2, PaO2, base excess, packed cell volume, plasma protein concentration and white cell count were measured (time 0). Escherichia coli endotoxin was infused intravenously over 15 minutes in both groups. Group 2 horses were given an intravenous infusion of dopamine (5 micrograms kg-1 min-1) starting five minutes after the start of the endotoxin infusion and continuing for 60 minutes. Measurements were made at 15 minute intervals for 120 minutes. In group 1, one horse died during the endotoxin infusion and in two other horses mean facial artery pressures decreased to 50 mm Hg. Total pulmonary vascular resistance and packed cell volume were significantly increased. Cardiac output, cardiac index and change in mean arterial pressure were significantly greater in group 2 horses than in group 1 horses. Conversely, diastolic pulmonary artery pressure, total vascular resistance and total pulmonary resistance were significantly less in group 2 than in group 1. PaO2, base excess and white blood cell count were significantly decreased in both groups. It was concluded that dopamine improved cardiovascular function in the presence of endotoxaemia and attenuated the rate of haemoconcentration, but had no effect on the development of decreased PaO2 or metabolic acidosis.     

Changes in pH of peritoneal fluid associated with carbon dioxide insufflation during laparoscopic surgery in dogs

OBJECTIVE: To evaluate changes in pH of peritoneal fluid associated with CO2 insufflation during laparoscopy in dogs. ANIMALS: 13 client-owned dogs and 10 purpose-bred teaching dogs. PROCEDURES: Laparotomy was performed on control dogs; peritoneal fluid pH was measured at time of incision of the abdominal cavity (time 0) and 30 minutes later. Laparoscopic insufflation with CO2 was performed and routine laparoscopic procedures conducted on the teaching dogs. Insufflation pressure was limited to 12 mm Hg. Intraperitoneal fluid pH was measured by use of pH indicator paper at 4 time points. Arterial blood gas analysis was performed at the same time points. RESULTS: Peritoneal fluid pH did not change significantly between 0 and 30 minutes in the control dogs. For dogs with CO2 insufflation, measurements obtained were a mean of 8.5, 24.5, 44.5, and 72.0 minutes after insufflation. The pH of peritoneal fluid decreased significantly between the first (7.825 +/- 0.350) and second (7.672 +/- 0.366) time point. Blood pH decreased significantly between the first (7.343 +/- 0.078), third (7.235 +/- 0.042), and fourth (7.225 +/- 0.038) time points. The PaCO2 increased significantly between the first (39.9 +/- 9.8 mm Hg) and fourth (54.6 +/- 4.4 mm Hg) time points. Base excess decreased significantly between the first and all subsequent time points. CONCLUSIONS AND CLINICAL RELEVANCE: Pneumoperitoneum attributable to CO2 insufflation caused a mild and transient decrease in peritoneal fluid pH in dogs. Changes in peritoneal fluid associated with CO2 insufflation in dogs were similar to those in other animals.     

Cardiopulmonary,blood and peritoneal fluid alterations associated with abdominal insufflation of carbon dioxide in standing horses

REASONS FOR PERFORMING STUDY: Abdominal insufflation is performed routinely during laparoscopy in horses to improve visualisation and facilitate instrument and visceral manipulations during surgery. It has been shown that high-pressure pneumoperitoneum with carbon dioxide (CO2) has deleterious cardiopulmonary effects in dorsally recumbent, mechanically ventilated, halothane-anaesthetised horses. There is no information on the effects of CO2 pneumoperitoneum on cardiopulmonary function and haematology, plasma chemistry and peritoneal fluid (PF) variables in standing sedated horses during laparoscopic surgery. OBJECTIVES: To determine the effects of high pressure CO2 pneumoperitoneum in standing sedated horses on cardiopulmonary function, blood gas, haematology, plasma chemistry and PF variables. METHODS: Six healthy, mature horses were sedated with an i.v. bolus of detomidine (0.02 mg/kg bwt) and butorphanol (0.02 mg/kg bwt) and instrumented to determine the changes in cardiopulmonary function, haematology, serum chemistry and PF values during and after pneumoperitoneum with CO2 to 15 mmHg pressure for standing laparoscopy. Each horse was assigned at random to either a standing left flank exploratory laparoscopy (LFL) with CO2 pneumoperitoneum or sham procedure (SLFL) without insufflation, and instrumented for measurement of cardiopulmonary variables. Each horse underwent a second procedure in crossover fashion one month later so that all 6 horses had both an LFL and SLFL performed. Cardiopulmonary variables and blood gas analyses were obtained 5 mins after sedation and every 15 mins during 60 mins baseline (BL), insufflation (15 mmHg) and desufflation. Haematology, serum chemistry analysis and PF analysis were performed at BL, insufflation and desufflation, and 24 h after the conclusion of each procedure. RESULTS: Significant decreases in heart rate, cardiac output and cardiac index and significant increases in mean right atrial pressure, systemic vascular resistance and pulmonary vascular resistance were recorded immediately after and during sedation in both groups of horses. Pneumoperitoneum with CO2 at 15 mmHg had no significant effect on cardiopulmonary function during surgery. There were no significant differences in blood gas, haematology or plasma chemistry values within or between groups at any time interval during the study. There was a significant increase in the PF total nucleated cell count 24 h following LFL compared to baseline values for LFL or SLFL at 24 h. There were no differences in PF protein concentrations within or between groups at any time interval. CONCLUSIONS: Pneumoperitoneum with CO2 during standing laparoscopy in healthy horses does not cause adverse alterations in cardiopulmonary, haematology or plasma chemistry variables, but does induce a mild inflammatory response within the peritoneal cavity. POTENTIAL RELEVANCE: High pressure (15 mmHg) pneumoperitoneum in standing sedated mature horses for laparoscopic surgery can be performed safely without any short-term or cumulative adverse effects on haemodynamic or cardiopulmonary function.     

Surface oximetry of healthy and ischemic equine intestine

Measurements of jejunal, ileal, and large colon (pelvic flexure) surface O2 tension (PSO2) were made in halothane-anesthetized horses with a nonheated miniature oxygen polarographic electrode. Assisted ventilation with 100% O2 was used to maintain PaCO2 tension at 50 +/- 8 mm of Hg while mean arterial blood pressure was maintained greater than or equal to 70 mm of Hg. Mean +/- SD PSO2 for the intestinal segments were: jejunum (horses 1 to 4), 71 +/- 20 mm of Hg; ileum (horses 1 to 4), 61 +/- 8 mm of Hg; and pelvic flexure of the large colon (horses 1 to 10), 55 +/- 13 mm of Hg. The response of the sensor to intestinal ischemia was studied in the large colon of an additional 12 halothane-anesthetized horses, using 4 types of vascular occlusion: venous (4 horses); arterial and venous (4 horses); venous and intramural vascular obstruction (2 horses); and arterial, venous, and intramural obstruction (2 horses). Venous and arterial occlusions were maintained for 30, 60, 90, and 120 minutes, whereas intramural obstruction combined with either type of vascular obstruction was studied for 60 to 120 minutes. After vascular occlusion, PSO2 decreased to 8 +/- 7 mm of Hg for venous obstruction, 4 +/- 3 mm of Hg for arterial and venous obstruction, 6 +/- 0 mm of Hg for intramural and venous obstruction, and 3 +/- 0 mm of Hg after intramural and arterial and venous obstruction. Thirty minutes after release of the clamps, the PSO2 increased to greater than or equal to 50% of the preoccluded large colon value.(ABSTRACT TRUNCATED AT 250 WORDS)     

Use of right ventricular pressure increase rate to evaluate cardiac contractility in horses

OBJECTIVE: To establish reference values for right ventricular maximal rate of increase in pressure (dP/dt(max)) in horses and determine the usefulness of this variable to evaluate cardiac contractility. ANIMALS: 15 crossbred horses, 3 to 20 years old. PROCEDURE: Cardiac catheterization was performed, using a high-fidelity catheter tip micromanometer, to determine right ventricular dP/dt(max). The following mathematic corrections were made: for preload, (dP/dt(max))/instantaneous total pressure, (dP/dt(max))/instantaneous developed pressure, and (dP/dt(max))/end diastolic pressure; for afterload, (dP/dtCPIP)/common peak isovolumic pressure. Wedge pressure was measured simultaneously, using a Swan-Ganz catheter. A negative inotropic drug, detomidine hydrochloride, was administered to 6 horses to examine the effect of the negative inotropic drug on right ventricular dP/dt(max) and derived variables. RESULTS: The mean right ventricular dP/dt(max) was 477 (+/- 84.1) mm Hg/s in 15 horses. A 40% decrease in dP/dt(max) was found for 30 minutes after detomidine administration. Variables that correct for preload and afterload were influenced similarly. Detomidine administration also caused a 24% increase in mean wedge pressure, probably indicating reduced left-sided cardiac contractility. CONCLUSIONS AND CLINICAL RELEVANCE: Right ventricular dP/dt(max) may be a useful clinical variable for determining acute changes in cardiac contractility in horses.     

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.     

Cardiovascular effects of hydralazine HCl administration in horses

Six standing awake adult horses were instrumented for measurement of mean arterial, central venous, and pulmonary arterial blood pressures (mm of Hg), thermodilution cardiac output (ml/kg/min), and pulmonary arterial blood temperature (C). Total peripheral resistance was calculated from these values. Base-line data were accumulated, and a single dose of hydralazine HCl (0.5 mg/kg) was administered IV. Horses were monitored for 420 minutes after hydralazine administration. Mean arterial and central venous blood pressures did not change from the base-line values. Cardiac output and heart rate were increased above base-line values for 260 minutes. Total peripheral resistance was decreased for 240 minutes. Pulmonary arterial blood temperature was decreased for 60 minutes after drug administration. Mean pulmonary arterial pressure relative to the base-line mean was intermittently decreased during the study. Intravenously administered hydralazine HCl appears to be an effective vasodilator, with moderate duration of action in horses.     

Cardiopulmonary effects of intrathoracic insufflation in dogs

This study was designed to quantify the effects of incremental positive insufflation of the intrathoracic space on cardiac output (CO), heart rate (HR), arterial pressure (AP), central venous pressure (CVP), and percent saturation of hemoglobin with oxygen (SPO2) in anesthetized dogs. Seven healthy, adult dogs from terminal teaching laboratories were maintained under anesthesia with isoflurane delivered with a mechanical ventilator. The experimental variables were recorded before introduction of an intrathoracic catheter, at intrathoracic pressures (IP) of 0 mm Hg, 3 mm Hg insufflation, and additional increments of 1 mm Hg insufflation thereafter until the SPO2 remained <85% despite increases in minute volume. Finally the variables were measured again at 0 mm Hg IP. The cardiac output and systolic and diastolic AP significantly (P < 0.05) decreased at 3 mm Hg IP. Significant decreases in SPO2 were seen at 10 mm Hg IP. Significant increase in CVP was noted at 6 mm Hg IP. Heart rate decreased significantly at 5 to 6 mm Hg IP but was not decreased above 6 mm Hg IP. Given the degree of CO decrease at low intrathoracic pressures, insufflation-aided thoracoscopy should be used with caution and at the lowest possible insufflation pressure. Standard anesthetic monitoring variables such as HR and AP measurements may not accurately reflect the animal's cardiovascular status.     

Cardiovascular Effects of Intravenous Sodium Penicillin, Sodium Cefazolin, and Sodium Citrate in Awake and Anesthetized Horses

Sodium penicillin, sodium cefazolin, and sodium citrate were administered to six adult horses on separate occasions, when awake and during anesthesia. The order of administration was randomized and studies were separated by a minimum of 7 days. Arterial blood pressure decreased significantly (less than 0.05) from control 5 minutes after intravenous (IV) sodium penicillin in awake and anesthetized horses. Systolic arterial blood pressure remained significantly (less than 0.05) decreased 10 minutes after IV sodium penicillin in anesthetized horses. Sodium cefazolin and sodium citrate did not significantly affect any of the measured cardiovascular variables. Although the changes in arterial blood pressure were small (8-15 mm Hg), monitoring of arterial blood pressure is advised when sodium penicillin is administered IV to anesthetized horses.     

The Cardiovascular Response of Sheep to Tiletamine–Zolazepam and Butorphanol Tartrate Anesthesia

Butorphanol tartrate (0.5 mg/kg intravenously [IV]) was administered to six ewes (group 1), 10 minutes before administration of tiletamine-zolazepam (12 mg/kg IV). In six ewes (group 2), butorphanol tartrate and tiletamine-zolazepam were administered simultaneously. Time of administration of butorphanol did not alter hemodynamics or duration of anesthesia significantly. Anesthesia was adequate for 25 to 45 minutes (mean, 31 min) in group 1. The sheep in group 2 were anesthetized effectively for 25 to 50 minutes (mean, 39 min). Neither dosing regimen caused significant changes in right atrial pressure, heart rate, pulmonary vascular resistance, or pulmonary capillary wedge pressure. Mean arterial blood pressure (MABP) decreased an average of 18% from baseline values of 113 mm Hg to a minimum of 84 mm Hg at minute 60 in group 1, and from 111 mm Hg to 92 mm Hg at minute 75 in group 2. The decrease was significant only for group 1. Cardiac output (CO) was significantly decreased 24% from 6.6 L/min at minute 45 in group 1, and 32% from 6.3 L/min at minute 15 in group 2. Systemic vascular resistance (SVR) was increased significantly at minute 15, 11% in group 1 and 37% in group 2. Mild respiratory acidosis was measured by significant decreases in arterial pO2 and pH and a significant increase in pCO2 without significant changes in HCO3-. Results of this study show that (1) tiletamine-zolazepam and butorphanol tartrate produce adequate anesthesia for 25 to 50 minutes; (2) the cardiovascular and anesthetic effects of the dosing schedules were similar; and (3) tiletamine-zolazepam and butorphanol result in decreased CO and MABP with a concomitant increase in SVR, and mild respiratory acidosis.     

The influence of atipamezole on the cardiovascular effects of detomidine in horses

The reversal of the cardiovascular effects of the α₂-adrenoceptor agonist detomidine by the α₂-antagonist atipamezole was studied. Nine horses were given detomidine 20 μg/kg iv. On a separate occasion they were given atipamezole 100 μg/kg iv 15 mins after the detomidine injection. Blood gas tensions were measured and clinical signs of sedation were also observed. Bradycardia and the frequency of heart blocks induced by detomidine were reduced after atipamezole and blood pressure decreased. These reversal effects of atipamezole were of short duration (a few minutes) at the dose level tested. Two of the nine horses exhibited premature depolarisations after administration of detomidine, but not after atipamezole injection. PaO₂ decreased and PaCO₂ increased slightly after detomidine injection, but the arterial pH was within reference values or slightly elevated. Administration of atipamezole did not alter these values. Base excess rose after detomidine, and it decreased more quickly towards the baseline level, when the horses were given detomidine alone. No clinical adverse effects were seen from the administration of atipamezole. Atipamezole may be beneficial, if detomidine-induced bradycardia needs to be reversed in horses.     

Does the induction agent affect the course of halothane anaesthesia in horses?

Four hundred and ninety horses were anaesthetised with halothane for clinical surgical or diagnostic procedures following induction with either detomidine/keta-mine, detomidine/thiopentone, xylazine/ketamine or guaiphenesin/thiopentone. Routine clinical monitoring was performed during anaesthesia. All horses developed hypotension (mean arterial pressures below 80 mm Hg) and respiratory depression (significant fall in respiratory rate and arterial carbon dioxide tension above 7 kPa (53 mm Hg)) consistent with the recognised effects of halothane. All anaesthetic procedures incorporating xylazine or detomidine resulted in lower pulse rates (28–35 per min) than after guaiphenesin/thiopentone (36–44 per min) and there was greater respiratory depression after techniques employing thiopentone rather than keta-mine. Development of hypotension was delayed after techniques using the α₂ adrenoceptor agonist agents (xylazine and detomidine), particularly detomidine. Prernedication with acepromazine did not affect any of the physiological variables measured after techniques employing detomidine. Recovery to standing was fastest after xylazine/ketamine (31±1 min) and slowest after detomidine/thiopentone (53±2 min). Recovery quality was best after detomidine/thiopentone and all techniques employing an α₂ adrenoceptor agonist agent resulted in smoother recovery than after guaiphenesin/thiopentone. This study demonstrates that most of the physiological effects of individual induction agents are overridden by the cardiovascular and respiratory depressant effects of halothane. The study also shows that detomidine is an acceptable sedative for use before general anaesthesia with halothane in horses.     

The effect of hyoscine on dobutamine requirement in spontaneously breathing horses anaesthetized with halothane

OBJECTIVE: To determine whether hyoscine has a sparing effect on the volume of dobutamine required to maintain mean arterial pressure (MAP) at 70 mmHg in horses anaesthetized with halothane. STUDY DESIGN: Prospective, randomized, controlled clinical trial. ANIMALS: Twenty adult horses weighing 507 +/- 97 kg (mean +/- SD), aged 10 +/- 5 years. MATERIALS AND METHODS: Pre-anaesthetic medication in all horses was intramuscular (IM) acepromazine (40 mug kg(-1)) and intravenous (IV) detomidine (0.02 mg kg(-1)). Anaesthesia was induced with ketamine (2.2 mg kg(-1) IV) and diazepam (0.02 mg kg(-1) IV), and maintained with halothane in oxygen. Horses breathed spontaneously. Flunixin (1.1 mg kg(-1) IV) was given to provide analgesia. Heart rate, ECG, invasive arterial pressure, respiratory rate, percentage end-tidal carbon dioxide, percentage end-tidal halothane and partial pressure of oxygen and carbon dioxide in arterial blood and blood pH were monitored. Dobutamine was infused by an infusion pump to maintain MAP at 70 mmHg. Horses were randomly assigned to receive saline or hyoscine (0.1 mg kg(-1)) IV 30 minutes after induction. The heart rate, MAP and volume of dobutamine infused over 30-minute periods were measured and analysed statistically using a one-way anova. RESULTS: After administration of hyoscine, heart rate increased for 10 minutes (p < 0.01) and MAP for 5 minutes (p < 0.01). There was no difference in the volume of dobutamine infused over 30 minutes between horses given hyoscine or saline, although there was a wide individual variation in dobutamine requirements. No side effects of hyoscine were seen. CONCLUSIONS: The increase in heart rate and blood pressure that occurs after 0.1 mg kg(-1) hyoscine is given IV in anaesthetized horses, is of short duration and does not significantly alter the amount of dobutamine required to maintain arterial pressure over the next 30 minutes. Clinical relevance The short duration of action of 0.1 mg kg(-1) hyoscine IV may limit its usefulness for correction of hypotension in horses anaesthetized with halothane. Further work is necessary to investigate the effects of higher or repeated doses or constant rate infusions of hyoscine.     

Effects of alpha2-adrenergic receptor agonists on urine production in horses deprived of food and water

OBJECTIVE: To quantitate the dose- and time-related effects of IV administration of xylazine and detomidine on urine characteristics in horses deprived of feed and water. ANIMALS: 6 horses. PROCEDURE: Feed and water were withheld for 24 hours followed by i.v. administration of saline (0.9% NaCI) solution, xylazine (0.5 or 1.0 mg/kg), or detomidine (0.03 mg/kg). Horses were treated 4 times, each time with a different protocol. Following treatment, urine and blood samples were obtained at 15, 30, 60, 120, and 180 minutes. Blood samples were analyzed for PCV and serum concentrations of total plasma solids, sodium, and potassium. Urine samples were analyzed for pH and concentrations of glucose, proteins, sodium, and potassium. RESULTS: Baseline (before treatment) urine flow was 0.30 +/- 0.03 mL/kg/h and did not significantly change after treatment with saline solution and low-dose xylazine but transiently increased by 1 hour after treatment with high-dose xylazine or detomidine. Total urine output at 2 hours following treatment was 312 +/- 101 mL versus 4,845 +/- 272 mL for saline solution and detomidine, respectively. Absolute values of urine concentrations of sodium and potassium also variably increased following xylazine and detomidine administration. CONCLUSIONS AND CLINICAL RELEVANCE: Xylazine and detomidine administration in horses deprived of feed and water causes transient increases in urine volume and loss of sodium and potassium. Increase in urine flow is directly related to dose and type of alpha2-adrenergic receptor agonist. Dehydration in horses may be exacerbated by concurrent administration of alpha2-adrenergic receptor agonists.     

Effects of Intravenous Detomidine on Schirmer Tear Test Results in Clinically Normal Horses

This study was conducted to determine the effects of intravenous detomidine on Schirmer tear test (STT) results in clinically normal horses. Eighteen adult horses were randomly divided into two groups of nine horses each. The treatment group was sedated with intravenous detomidine alone (20 μg/kg), and the control group received only intravenous saline (0.2 mL/100 kg). Schirmer tear test was performed just before intravenous administration of detomidine or saline in treatment and control groups, respectively. Schirmer tear tests were repeated 5, 20, 60, and 120 minutes later. Horses enrolled in this study consisted of nine males and nine females. Breeds were Arabian and Hanoverian, ranging from 3 to 6 years in age. In the treatment group, the pretreatment and subsequent posttreatment mean ± standard deviation values were 17.0 ± 6.9 (0 minutes), 11.8 ± 2.9 (5 minutes), 12.1 ± 2.0 (20 minutes), 12.1 ± 3.1 (60 minutes), and 15.0 ± 2.8 (120 minutes) mm wetting/min. In this group of horses, a significant reduction was observed in STT values at 5, 20, and 60 minutes after treatment with detomidine hydrochloride in comparison to the pretreatment values (analysis of variance with post hoc testing; P₅ = 0.004, P₂₀ = 0.007, P₆₀ = 0.006). There was no significant difference between baseline values and posttreatment values in the control saline group (P ≥ .08). We conclude that intravenous detomidine causes a significant reduction in STT values in clinically normal horses. In horses, practitioners should measure STT values before intravenous administration of detomidine to accurately assess the results.     

Anesthesia of horses with a combination of detomidine, zolazepam, tiletamine, and isoflurane immediately after strenuous treadmill exercise.

OBJECTIVES: To evaluate effects of strenuous exercise in adult horses immediately before anesthesia and to determine whether prior exercise affects anesthesia induction, recovery, or both. ANIMALS: 6 healthy Thoroughbreds in good condition and trained to run on a treadmill, each horse serving as its own control. PROCEDURE: Horses ran on a treadmill until fatigued, then were sedated immediately with detomidine hydrochloride and anesthetized with a zolazepam hydrochloride-tiletamine combination. Anesthesia was maintained with isoflurane in oxygen for another 90 minutes. Blood samples were taken before, during, and after exercise and during anesthesia. RESULTS: During exercise, changes in heart rate, core body temperature, plasma lactate concentration, arterial pH, and PaCO2 were significant. Plasma ionized calcium concentration was lower after exercise, compared with baseline values, and remained lower at 30 minutes of isoflurane anesthesia. Compared with baseline values, plasma chloride concentration decreased significantly during anesthesia after exercise. Cardiac output during anesthesia was significantly lower than that during preexercise, but significant differences between experimental and control periods were not observed. Arterial blood pressure during anesthesia was significantly lower than that during preexercise and initially was maintained better during isoflurane anesthesia after exercise. Cardiac output and blood pressure values were clinically acceptable throughout anesthesia. CONCLUSION: Administration of detomidine hydrochloride followed by zolazepam hydrochloride-tiletamine appeared to be safe and effective for sedation and anesthesia of horses that had just completed strenuous exercise. CLINICAL RELEVANCE: Anesthetic given in accordance with this protocol can be used to anesthetize horses that are injured during athletic competition to assess injuries, facilitate first aid, and possibly allow salvage of injured horses.