Electroencephalographic Power Spectrum Analysis as a Monitor of Anesthetic Depth in Horses

Electroencephalographic (EEG) power spectrum analysis was performed in 18 conscious, adult horses for evaluation as control values for EEG data obtained during anesthesia. Computer-processed total amplitudes for the frequency range 0 to 32 Hz were mainly between 400 and 600 microV, with 80% spectral edge frequency between 16.6 and 32.5 Hz. The highest electrical activity was in the delta band (41.3 +/- 4.4% of total amplitude); there was a less pronounced activity in the beta (34.2 +/- 5.2%), theta (13.6 +/- 1.5%), and alpha (10.0 +/- 1.0%) bands. The applicability of EEG power spectrum analysis as a guide to depth of anesthesia was evaluated in four horses by comparing simultaneously recorded EEG data and clinical signs of anesthesia. Global changes in cerebrocortical electrical activity were detected with a single, monopolar (left frontoatlanto-occipital) EEG lead. Increasing depth of halothane anesthesia was accompanied by a pronounced shift in EEG activity from beta to theta and delta frequency bands, a decrease in 80% spectral edge frequency from 21.5 +/- 2.4 Hz to 12.6 +/- 2.2 Hz, a reduction in the beta/delta ratio of fractional amplitudes from 2.37 +/- 0.84 to 0.49 +/- 0.04, and a slight inconsistent increase in total amplitude from 96.1 +/- 37.3 microV to 185.5 +/- 53 microV. These results show that changes in the clinical signs of anesthetic depth in horses can be described numerically by use of EEG power spectrum analysis.     

Cardiopulmonary and sedative effects of intravenous administration of low doses of medetomidine and xylazine to adult horses

OBJECTIVE: To determine the cardiopulmonary and sedative effects of medetomidine hydrochloride in adult horses and to compare those effects with effects of an equipotent dose of xylazine hydrochloride. ANIMALS: 10 healthy adult female horses. PROCEDURE: 5 horses were given medetomidine (4 microg/kg of body weight, i.v.), and the other 5 were given xylazine (0.4 mg/kg, i.v.). Heart rate, respiratory rate, arterial blood pressures, pulmonary arterial blood pressures, and cardiac output were recorded, and sedation and ataxia scores were assigned before and every 5 minutes after drug administration for 60 minutes. Rectal temperature and blood gas partial pressures were measured every 15 minutes after drug administration. RESULTS: Arterial blood pressure was significantly decreased throughout the study among horses given medetomidine and was significantly decreased for 40 minutes among horses given xylazine. Compared with baseline values, cardiac output was significantly decreased 10, 20, and 40 minutes after administration of medetomidine and significantly increased 40 and 60 minutes after administration of xylazine. Despite the significant decrease in respiratory rate in both groups, results of blood gas analyses were not significantly changed over time. Ataxia and sedation scores were of similar magnitude for the 2 groups, but ataxia persisted slightly longer among horses given medetomidine. Horses resumed eating hay 10 to 55 minutes after drug administration. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that equipotent low doses of medetomidine and xylazine induce comparable levels of ataxia and sedation and similar cardiopulmonary changes in adult horses.     

Cardiovascular and respiratory effects of acetylpromazine and xylazine on halothaneanesthetized horses

Circulatory and respiratory effects of intravenously administered acetylpromazine (0.033 and 0.067 mg/kg) and xylazine (0.5 and 1.0 mg/kg) were studied in drug cross-over fashion in eight laterally recumbent horses anesthetized only with halothane (1.06%, end-tidal) in O2. Both doses of acetylpromazine caused a significant and sustained elevation in cardiac output via a rise in stroke volume. Xylazine produced an initial significant fall in cardiac output followed by a return to control levels. Halothane anesthesia did not prevent xylazine-related atrioventricular conduction block. All treatments caused a similar significant fall in arterial blood pressure (acetylpromazine, total peripheral resistance-related; xylazine, cardiac output-related). PaCO2 significantly increased after all treatments. PaCO2 decreased significantly only following xylazine treatment. One horse (not included in the tabulation) developed ventricular fibrillation and died 15 min after receiving its first injection (0.5 mg/kg) of xylazine.     

Electroencephalographic studies of adult cattle associated with electrical stunning, throat cutting and carcass electro-immobilization

Twelve adult cattle were electrically stunned head-only (400 V, 2.5 A, 50 Hz) behind the ears for four seconds. Within ten seconds of stun initiation, the carotid arteries, jugular veins, trachea and oesophagus were severed. Twenty seconds after the stun initiation, ten animals received an electro-immobilization current (80 V peak, 14.3 Hz, 5 ms square wave, 300 mA) nose to anus for periods ranging from 30-37 seconds. Electroencephalographic (EEG) traces were recorded before and after the stun up until electroimmobilization and at cessation of electro-immobilization by means of implanted electrodes, and animal movement was recorded on videotape. Before the stun, the EEG trace was within a window of sensibility (10-40 microV amplitude). During the stun, the amplitude increased and sometimes exceeded 500 microV. At the end of electro-immobilization, EEG amplitude was less than 10 microV, indicating insensibility. This amplitude was reached in the two non-immobilized animals 57 seconds and 63 seconds after stun initiation. During stunning, the forelegs and hindlegs usually tucked under the animals. Various degrees of foreleg extension then occurred. From about ten seconds post-stun, paddling movements occurred, at which time the EEG trace showed large-amplitude waves characteristic of a stunned animal. During immobilization, the animals stiffened and breathing stopped. After immobilization weak muscle spasms occurred that did not interfere with dressing operations. Non-immobilized animals moved excessively, inhibiting dressing. It is concluded that adult cattle rendered insensible by stunning do not recover sensibility during the stun/throat-cut/immobilization operation and therefore this procedure is humane.     

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.     

A method of assessing auditory and brainstem function in horses

Brainstem auditory evoked potential (BAEP) waveforms were recorded as a means of objectively evaluating auditory and brainstem function in horses. BAEP recordings were readily and repeatably recorded from horses, under minimal restraint, using signal averaging equipment. Clearly identified BAEP waveforms were obtained with compression clicks of 30-100 dB (HHL) at 10 Hz applied in the external auditory meatus of one ear and masking white noise (10 dB lower) in the other ear. Vertex positive (upwards) waveforms I through V were obtained with an active, subdermal electrode over the ipsilateral and contralateral zygomatic processes of the temporal bones and the reference electrode over the vertex. Recording sweep duration was 10 ms, amplifier sensitivity 10 microV/division, display gain x 10 and low and high amplifier filters set at 200 Hz to 2 kHz. Such recordings can be useful in evaluation of all clinical cases suspected of showing degrees of deafness, vestibular disease or brainstem disease, and in monitoring the progress of such cases.     

Effects of treatment with oxytocin,xylazine butorphanol,guaifenesin, acepromazine,and detomidine on esophageal manometric pressure in conscious horses

OBJECTIVE: To compare effects of oxytocin, acepromazine maleate, xylazine hydrochloride-butorphanol tartrate, guaifenesin, and detomidine hydrochloride on esophageal manometric pressure in horses. ANIMALS: 8 healthy adult horses. PROCEDURE: A nasogastric tube, modified with 3 polyethylene tubes that exited at the postpharyngeal area, thoracic inlet, and distal portion of the esophagus, was fitted for each horse. Amplitude, duration, and rate of propagation of pressure waveforms induced by swallows were measured at 5, 10, 20, 30, and 40 minutes after administration of oxytocin, detomidine, acepromazine, xylazine-butorphanol, guaifenesin, or saline (0.9% NaCI) solution. Number of spontaneous swallows, spontaneous events (contractions that occurred in the absence of a swallow stimulus), and high-pressure events (sustained increases in baseline pressure of > 10 mm Hg) were compared before and after drug adminision. RESULTS: At 5 minutes after administration, detomidine increased waveform amplitude and decreased waveform duration at the thoracic inlet. At 10 minutes after administration, detomidine increased waveform duration at the thoracic inlet. Acepromazine administration increased the number of spontaneous events at the thoracic inlet and distal portion of the esophagus. Acepromazine and detomidine administration increased the number of high-pressure events at the thoracic inlet. Guaifenesin administration increased the number of spontaneous events at the thoracic inlet. Xylazine-butorphanol, detomidine, acepromazine, and guaifenesin administration decreased the number of spontaneous swallows. CONCLUSIONS AND CLINICAL RELEVANCE: Detomidine, acepromazine, and a combination of xylazine butorphanol had the greatest effect on esophageal motility when evaluated manometrically. Reduction in spontaneous swallowing and changes in normal, coordinated peristaltic activity are the most clinically relevant effects.     

Prolongation of anesthesia with xylazine, ketamine, and guaifenesin in horses: 64 cases (1986-1989)

On 74 occasions, 54 horses and 6 foals were anesthetized with xylazine and ketamine or xylazine, guaifenesin, and ketamine, with or without butorphanol. On 64 occasions, anesthesia was prolonged for up to 70 minutes (34 +/- 15 min) by administration of 1 to 9 supplemental IV injections of xylazine and ketamine at approximately a third the initial dosage. All horses except 5 were positioned in lateral recumbency, and oxygen was insufflated. In adult horses, the time from induction of anesthesia to the first supplemental xylazine and ketamine injection was 13 +/- 4 minutes and the time between supplemental injections was 12.1 +/- 3.7 minutes. These results were consistent with predicted plasma ketamine concentration calculated from previously published pharmacokinetic data for ketamine in horses. Respiratory and heart rates and coccygeal artery pressure remained consistent for the duration of anesthesia. The average interval between the last injection of ketamine and assumption of sternal position was approximately 30 minutes, and was the same regardless of the number of supplemental injections. The time to standing was significantly longer (P less than 0.05) in horses given 2 supplemental injections, compared with those not given any or only given 1, but was not longer in horses given 3 supplemental injections. Recovery was considered unsatisfactory in 5 horses, but did not appear to be related to prolongation of anesthesia.     

Sedative and cardiopulmonary effects of buprenorphine and xylazine in horses

This study investigated the sedative, cardiopulmonary, and gastrointestinal effects produced by buprenorphine and xylazine given in combination to horses. Six healthy adult horses underwent 4 randomized treatments, with an interval of 1 wk between treatments. A control group was given a saline solution intravenously (IV) and the experimental groups received buprenorphine [10 μg/kg bodyweight (BW)] in combination with 1 of 3 different doses of xylazine: 0.25 mg/kg BW (BX25), 0.50 mg/kg BW (BX50), or 0.75 mg/kg BW (BX75), all of them by IV. Cardiopulmonary parameters were evaluated for 120 min after the drugs were administered and intestinal motility was observed for 12 h after treatment. Sedation was found to be dose-dependent in all groups receiving buprenorphine and xylazine and it was observed that the heart rate decreased in the first 5 min and increased at the end of the sedation period. Arterial blood gas tension analyses showed minimal alterations during the experiment. Gastrointestinal hypomotility was observed for up to 8 h. The combination of buprenorphine and 0.50 mg/kg BW of xylazine (BX50) provided a 30-minute period of sedation without intense ataxia and maintained cardiopulmonary parameters within acceptable limits for the species.     

Electroencephalogram of Japanese Black calves affected with cerebrocortical necrosis

Electroencephalogram (EEG) examinations were carried out on three Japanese Black calves (1, 2 and 14 week old) affected with cerebrocortical necrosis (CCN) in order to investigate the relationship between EEG abnormalities and encephalic lesions. Some neurologic signs such as circling, astasia, convulsion and opisthotonus appeared in two of the calves (case 1 and 3). The other calf (case 2), however, showed no neurologic signs. The EEGs obtained from the two calves (case 1 and 2), in the awake state, showed constant high amplitude (50-160 microV) and slow (1-4 Hz) activity (HASA). One of these (case 1) had necrosis mainly in the right hemisphere and showed a markedly asymmetric sharp wave. On the other hand, in case 3, the EEG showed diffuse lowered activity, and almost flat in some leads. A decrease in fast activity observed in common with all three animals. These findings suggest that one of the characteristic EEG patterns of CCN patient may be HASA and decreased fast activity. Histopathologic diagnoses of the calves were CCN in various degrees. The degrees of abnormality of the EEGs seemed to accord with the seriousness of the lesions. Because the EEG obtained from the calf having no obvious neurologic signs showed an abnormal pattern, it was considered that EEG examinations in the early stages of disorders are valuable to diagnose CCN.     

Comparison of detomidine hydrochloride, xylazine, and xylazine plus morphine in horses: a double blind study

Detomidine (30 mcg/kg), xylazine (1.1 mg/kg) and xylazine/morphine (1.1 mg/kg and 0.75 mg/kg with 300 mg maximum dose) were compared in horses admitted for broncho-alveolar lavage. Horses (n=99) were randomized and clinicians performing the procedure were unaware of the sedation used. Horses were assessed during the procedure and for the next 2 hours. A significant number of xylazine/morphine-sedated horses showed excitement (p<0.05). The frequency of sinus block or arrest and second-degree atrioventricular block was significantly greater with detomidine. Detomidine-sedated horses were significantly more depressed than either xylazine or xylazine/morphine treated animals. Heart rate was significantly greater in horses given xylazine/morphine by 60 min. There was no significant difference between drug treatments related to reactions to the procedure or respiratory rate depression. The study indicated that all three methods are suitable for standing restraint. The more frequent adverse side effects (circling, muscle fasciculations, head pressing) accompanying xylazine/morphine should be considered.     

Evaluation of gastrointestinal activity patterns in healthy horses using B mode and Doppler ultrasonography

Healthy adult horses were examined by using transabdominal ultrasonography to quantitatively and qualitatively evaluate activity of the jejunum, cecum, and colon with B mode and Doppler techniques. Doppler ultrasound was used to assess jejunal peristaltic activity. Examinations were performed on multiple occasions under imposed colic evaluation conditions, including fasting, nasogastric intubation, and xylazine sedation. In fasted horses, jejunal visibility was increased and jejunal, cecal, and colonic activity was decreased. The stomach was displaced ventrally and was visualized ventral to the costochondral junction. Xylazine sedation in fed horses had minimal effects; however, in fasted horses, xylazine significantly decreased jejunal and cecal activity. Nasogastric intubation in fasted horses had no observable effects on activity, but moved the stomach dorsally. B mode and Doppler jejunal activity were strongly correlated. Prior feeding and sedation status need to be considered when interpreting the results of equine abdominal ultrasound examinations. Doppler techniques may be useful for assessing jejunal activity.     

Clinical comparison of xylazine and medetomidine for premedication of horses

OBJECTIVE: To compare the analgesic and cardiopulmonary effects of medetomidine and xylazine when used for premedication of horses undergoing general anesthesia. DESIGN: Randomized clinical trial. ANIMALS: 40 horses. PROCEDURE: Twenty horses were premedicated with medetomidine (10 microg/kg [4.5 microg/lb], i.m.) and the other 20 were premedicated with xylazine (2 mg/kg [0.9 mg/kg], i.m.). Horses were then anesthetized with a combination of guaifenesin and ketamine; anesthesia was maintained with halothane. Additional doses of medetomidine or xylazine were given if horses were not sufficiently sedated at the time of anesthetic induction. After induction of anesthesia, sodium pentothal was administered as necessary to prevent limb movements. Hypotension was treated with dobutamine; hypoventilation and hypoxemia were treated with intermittent positive-pressure ventilation. The quality of anesthetic induction, maintenance, and recovery and the quality of the transition to inhalation anesthesia were scored. RESULTS: Scores for the quality of the transition to inhalation anesthesia were significantly higher for horses premedicated with medetomidine than for horses premedicated with xylazine. However, other scores, recovery times, and numbers of attempts needed to achieve sternal recumbency and to stand were not significantly different between groups. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that medetomidine is suitable for premedication of horses undergoing general anesthesia. Analgesic and cardiopulmonary effects of medetomidine were similar to those of xylazine, except that the transition to inhalation anesthesia was smoother when horses were premedicated with medetomidine, rather than xylazine.     

Evaluation of Nociception,Sedation, and Cardiorespiratory Effects of a Constant Rate Infusion of Xylazine Alone or in Combination with Lidocaine in Horses

This study aimed to evaluate the effects of a constant rate infusion (CRI) of xylazine or xylazine in combination with lidocaine on nociception, sedation, and physiologic values in horses. Six horses were given intravenous (IV) administration of a loading dose (LD) of 0.55 mg/kg of xylazine followed by a CRI of 1.1 mg/kg/hr. The horses were randomly assigned to receive three treatments, on different occasions, administered 10 minutes after initiation of the xylazine CRI, as follows: control, physiologic saline; lidocaine low CRI (LLCRI), lidocaine (LD: 1.3 mg/kg, CRI: 0.025 mg/kg/min); and lidocaine high CRI (LHCRI), lidocaine (LD: 1.3 mg/kg, CRI: 0.05 mg/kg/min). A blinded observer assessed objective and subjective data for 50 minutes during the CRIs. In all treatments, heart and respiratory rates decreased, end-tidal carbon dioxide concentration increased, and moderate to intense sedation was observed, but no significant treatment effect was detected in these variables. Ataxia was significantly higher in LHCRI than in the control treatment at 20 minutes of infusion. Compared with baseline values, nociceptive threshold increased to as much as 79% in the control, 190% in LLCRI, and 158% in LHCRI. Nociceptive threshold was significantly higher in LLCRI (at 10 and 50 minutes) and in LHCRI (at 30 minutes) than in the control treatment. The combination of CRIs of lidocaine with xylazine produced greater increases in nociceptive threshold compared with xylazine alone. The effects of xylazine on sedation and cardiorespiratory variables were not enhanced by the coadministration of lidocaine. The potential to increase ataxia may contraindicate the clinical use of LHCRI, in combination with xylazine, in standing horses.     

Effects of xylazine and acetylpromazine upon induced ventricular fibrillation in dogs anesthetized with thiamylal and halothane.

Ventricular arryhythmias including ventricular fibrillation were produced with epinephrine in dogs induced to an anesthetic state with thiamylal and maintained with halothane. In dogs given (premedicated) xylazine 20 minutes prior to anesthesia, ventricular arrhythmias, including ventricular fibrillation, were induced with much smaller doses of epinephrine than in nonpremedicated dogs. Dogs premedicated with acetylpromazine 20 minutes prior to anesthesia with thiamylal and halothane displayed protection from epinephrine-induced arrhythmias. Caution is advised from using xylazine in the presence of halothane if epinephrine is to be administered.     

Electroencephalographic studies of calves associated with electrical stunning, throat cutting and carcass electro-immobilisation

Electroencephalographic (EEG) recordings were made on 34 calves (two days to six weeks old, 30-50 kg) during the slaughter process. The calves, supported in a V-shaped box or polypropylene net, were either head-only electrically stunned (50 Hz, 1.0 A) across the head and allowed to recover, head-only stunned followed by throat cutting or head-only stunned followed by throat cutting and electro-immobilisation. All time intervals were measured from the commencement of the stun. The electro-immobilisation (80 V peak, 14.3 Hz, 5 ms square wave) at 15-26 seconds post-stun was applied through electrodes attached to nose and anus, for periods ranging from 5-60 seconds. The head only stun produced an elevated EEG amplitude of the electroplectic fit which lasted approximately 34 seconds followed by a quiescent period before the EEG amplitude again became elevated above normal. A normal pre-stun pattern was not reached until many minutes had elapsed. Following the stun, the forelegs were usually flexed and then extended, gradually becoming part of the paddling movements commencing as early as eight seconds post-stun. Such movements were taking place while the animal was still stunned. With a head-only stun followed by throat cutting, the electroplectic fit was reduced to about 23 seconds and the amplitude of the EEG fell to about 10 microV after 50-73 seconds and breathing was inhibited for at least 20 seconds after stun commencement. If inadvertently only one carotid was severed, the EEG did not fall as rapidly as when both carotids were cut. The increase in amplitude of the EEG tracings was caused by stunning but the reduced duration of this increase in calves in which the throat was cut, suggests that there is an impairment of recovery of brain function from the moment of cutting and recovery of sensibility is unlikely. In reviewing the criteria of sensibility, we believe that insensibility can be presumed to continue from stun initiation, through the throat cut until the EEG falls below 10/microV provided that there is no resurgence of activity and the EEG amplitude continually falls rapidly enough. By this criteria, calves which are electrically stunned and rapidly exsanguinated remain permanently and irreversibly insensible. The addition of at least 15 seconds electro-immobilisation causes an even more rapid fall in the amplitude of the EEG (<10 microV at 50 seconds) making insensibility more certain as well as abolishing animal movement.     

A comparison of the sedative effects of three α2-adrenoceptor agonists (romifidine, detomidine and xylazine) in the horse

The sedative effects of a new alpha 2-adrenoceptor agonist, romifidine, were compared with those of xylazine and detomidine. Five horses were treated with two doses of romifidine (40 micrograms/kg body weight and 80 micrograms/kg body weight), two doses of detomidine (10 micrograms/kg body weight and 20 micrograms/kg body weight) and one dose of xylazine (1 mg/kg body weight) given by intravenous injection using a Latin-square design. The dose of 80 micrograms/kg romifidine appeared equipotent to 1 mg/kg xylazine and 20 micrograms/kg detomidine, although at these doses both xylazine and detomidine had a shorter action. Detomidine 20 micrograms/kg and xylazine both produced greater lowering of the head and a greater degree of ataxia than romifidine at either dose. Romifidine produced sedation similar to that of the other drug regimes. The effect upon imposed stimuli was similar.     

Comparison of the effects of the alpha-2 agonists detomidine, romifidine and xylazine on nociceptive withdrawal reflex and temporal summation in horses

ObjectiveTo evaluate and compare the antinociceptive effects of the three alpha-2 agonists, detomidine, romifidine and xylazine at doses considered equipotent for sedation, using the nociceptive withdrawal reflex (NWR) and temporal summation model in standing horses.Study designProspective, blinded, randomized cross-over study.AnimalsTen healthy adult horses weighing 527–645 kg and aged 11–21 years old.MethodsElectrical stimulation was applied to the digital nerves to evoke NWR and temporal summation in the left thoracic limb and pelvic limb of each horse. Electromyographic reflex activity was recorded from the common digital extensor and the cranial tibial muscles. After baseline measurements a single bolus dose of detomidine, 0.02 mg kg^?1, romifidine 0.08 mg kg^?1, or xylazine, 1 mg kg^?1, was administered intravenously (IV). Determinations of NWR and temporal summation thresholds were repeated at 10, 20, 30, 40, 60, 70, 90, 100, 120 and 130 minutes after test-drug administration alternating the thoracic limb and the pelvic limb. Depth of sedation was assessed before measurements at each time point. Behavioural reaction was observed and recorded following each stimulation.ResultsThe administration of detomidine, romifidine and xylazine significantly increased the current intensities necessary to evoke NWR and temporal summation in thoracic limbs and pelvic limbs of all horses compared with baseline. Xylazine increased NWR thresholds over baseline values for 60 minutes, while detomidine and romifidine increased NWR thresholds over baseline for 100 and 120 minutes, respectively. Temporal summation thresholds were significantly increased for 40, 70 and 130 minutes after xylazine, detomidine and romifidine, respectively.Conclusions and clinical relevanceDetomidine, romifidine and xylazine, administered IV at doses considered equipotent for sedation, significantly increased NWR and temporal summation thresholds, used as a measure of antinociceptive activity. The extent of maximal increase of NWR and temporal summation thresholds was comparable, while the duration of action was drug-specific.     

Effect of aerosolized albuterol sulfate on resting energy expenditure determined by use of open-flow indirect calorimetry in horses with recurrent airway obstruction

OBJECTIVE: To evaluate effects of sedation on stability of resistance of the respiratory system (RRS) and measures of resting energy expenditure (REE) by use of open-flow indirect calorimetry (IC) and treatment with aerosolized albuterol on REE in horses with recurrent airway obstruction (RAO). ANIMALS: 9 clinically normal horses and 8 horses with RAO. PROCEDURE: In phase 1, RRS was measured by using forced oscillometry (FOT) in 5 clinically normal horses before and after sedation with xylazine. In phase 2, REE was measured in 4 clinically normal horses between 20 and 25 minutes and again 35 to 40 minutes after sedation with xylazine. In phase 3, IC was performed between 20 and 25 minutes and FOT was performed between 30 and 35 minutes after xylazine administration in 8 horses with RAO; after administration of 450 microg of albuterol, IC and FOT were repeated. RESULTS: In phase 1, RRS values were significantly lower 5 and 10 minutes after sedation. In phase 2, diminishing sedation did not significantly affect REE. In phase 3, there was a significant decrease in mean RRS (1.15 +/- 0.25 vs 0.84 +/- 0.14 cm H20/L/s) and REE (30.68 +/- 17.89 vs 27.46 = 16.54 kcal/kg/d) after albuterol administration. CONCLUSIONS AND CLINICAL RELEVANCE: FOT and IC are useful in obtaining repeatable measurements of RRS and REE, respectively, in sedated horses. Concurrent bronchodilation and decreased REE after albuterol administration suggest that increased work of breathing as a result of airway obstruction may contribute to increased energy demands in horses with RAO.     

Qualitative and quantitative characteristics of the electroencephalogram in normal horses after sedation

Background

The administration of certain sedatives has been shown to promote sleep in humans. Related agents induce sleep‐like behavior when administered to horses. Interpretation of electroencephalograms (EEGs) obtained from sedated horses should take into account background activity, presence of sleep‐related EEG events, and the animal's behavior.

Hypothesis

Sedatives induce states of vigilance that are indistinguishable on EEGs from those that occur naturally.

Animals

Six healthy horses.

Methods

Digital EEG with video was recorded after administration of 1 of 4 sedatives (acepromazine, butorphanol, xylazine, or detomidine). Serum drug concentrations were measured. Recordings were reviewed, states were identified, and representative EEG samples were analysed. These data were compared with data previously obtained during a study of natural sleep.

Results

Butorphanol was associated with brief episodes resembling slow wave sleep in 1 horse. Acepromazine led to SWS in 3 horses, including 1 that also exhibited rapid eye movement sleep. Periods of SWS were observed in all horses afer xylazine or detomidine administration. Normal sleep‐related EEG events and heart block, occurred in association with SWS regardless of which sedative was used. Spectral data varied primarily by state, but some differences were observed between sedative and natural data.

Conclusions and Clinical Importance

Qualitatively, EEG findings appeared identical whether sedation‐induced or naturally occurring. The startle response and heart block associated with some sedatives may be related to sleep. Alpha₂ agonists can be used to obtain high quality EEGs in horses, but acepromazine does not promote a relaxed state in all animals.