Search

OBJECTIVE To determine whether isoflurane-anesthetized cats with demonstrated resistance to the immobilizing effects of fentanyl would exhibit naltrexone-reversible sparing of the minimum alveolar concentration (MAC) of isoflurane when fentanyl was coadministered with the centrally acting catecholamine receptor antagonist acepromazine. ANIMALS 5 healthy male purpose-bred cats. PROCEDURES Anesthesia was induced and maintained with isoflurane in oxygen. Baseline isoflurane MAC was measured by use of a standard tail clamp stimulus and bracketing study design. Afterward, fentanyl was administered IV to achieve a plasma concentration of 100 ng/mL by means of target-controlled infusion, and isoflurane MAC was remeasured. Next, acepromazine maleate (0.1 mg/kg) was administered IV, and isoflurane MAC was remeasured. Finally, isoflurane concentration was equilibrated at 70% of the baseline MAC. Movement of cats in response to tail clamping was tested before and after IV bolus administration of naltrexone. Physiologic responses were compared among treatment conditions. RESULTS Isoflurane MAC did not differ significantly between baseline and fentanyl infusion (mean ± SD, 1.944 ± 0.111% and 1.982 ± 0.126%, respectively). Acepromazine with fentanyl significantly decreased isoflurane MAC to 1.002 ± 0.056% of 1 atm pressure. When isoflurane was increased to 70% of the baseline MAC, no cats moved in response to tail clamping before naltrexone administration, but all cats moved after naltrexone administration. CONCLUSIONS AND CLINICAL RELEVANCE Acepromazine caused fentanyl to decrease the isoflurane MAC in cats that otherwise did not exhibit altered isoflurane requirements with fentanyl alone. Results suggested that opioid-mediated increases in brain catecholamine concentrations in cats counteract the opioid MAC-sparing effect.

Made available in DSpace on 2021-06-25T10:54:23Z (GMT). No. of bitstreams: 0 Previous issue date: 2021-02-16 The lack of standardization of sedation scales in horses limits the reproducibility between different studies. This prospective, randomized, blinded, horizontal and controlled trial aimed to validate a scale for sedation in horses (EquiSed). Seven horses were treated with intravenous detomidine in low/high doses alone (DL 2.5 μg/kg + 6.25 μg/kg/h; DH 5 μg/kg +12.5 μg/kg/h) or associated with methadone (DLM and DHM, 0.2 mg/kg + 0.05 mg/kg/h) and with low (ACPL 0.02 mg/kg) or high (ACPH 0.09 mg/kg) doses of acepromazine alone. Horses were filmed at (i) baseline (ii) peak, (iii) intermediate, and (iv) end of sedation immediately before auditory, visual and pressure stimuli were applied and postural instability evaluated for another study. Videos were randomized and blindly evaluated by four evaluators in two phases with 1-month interval. Intra- and interobserver reliability of the sum of EquiSed (Intraclass correlation coefficient) ranged between 0.84–0.94 and 0.45–0.88, respectively. The criterion validity was endorsed by the high Spearman correlation between the EquiSed and visual analog (0.77), numerical rating (0.76), and simple descriptive scales (0.70), and average correlation with head height above the ground (HHAG) (−0.52). The Friedman test confirmed the EquiSed responsiveness over time. The principal component analysis showed that all items of the scale had a load factor ≥ 0.50. The item-total Spearman correlation for all items ranged from 0.3 to 0.5, and the internal consistency was good (Cronbach's α = 0.73). The area under the curve of EquiSed HHAG as a predictive diagnostic measure was 0.88. The sensitivity of the EquiSed calculated according to the cut-off point (score 7 of the sum of the EquiSed) determined by the receiver operating characteristic curve, was 96% and specificity was 83%. EquiSed has good intra- and interobserver reliabilities and is valid to evaluate tranquilization and sedation in horses. Department of Veterinary Surgery and Animal Reproduction School of Veterinary Medicine and Animal Science São Paulo State University Universidade Estadual Paulista (UNESP) The Royal (Dick) School of Veterinary Studies and The Roslin Institute The University of Edinburgh Section Anaesthesiology Department of Clinical Diagnostics and Services Vetsuisse Faculty University of Zürich Department of Surgery and Anaesthesia of Domestic Animals Faculty of Veterinary Medicine Ghent University Department of Veterinary Surgery and Animal Reproduction School of Veterinary Medicine and Animal Science São Paulo State University Universidade Estadual Paulista (UNESP)

Submitted by Alice Rodrigues de Oliveira (alice.oliveira@unesp.br) on 2020-08-14T20:02:59Z No. of bitstreams: 1 Tese.repositório,unesp.ficha catalográfica.pdf: 2349522 bytes, checksum: 1e4ce6249eb0a1409cf95a46d88cc57d (MD5) Approved for entry into archive by ROSANGELA APARECIDA LOBO null (rosangelalobo@btu.unesp.br) on 2020-08-17T14:36:56Z (GMT) No. of bitstreams: 1 oliveira_ar_dr_bot_par.pdf: 359360 bytes, checksum: ead43ce5ea8cf812e7f0566c913c73af (MD5) Made available in DSpace on 2020-08-17T14:36:57Z (GMT). No. of bitstreams: 1 oliveira_ar_dr_bot_par.pdf: 359360 bytes, checksum: ead43ce5ea8cf812e7f0566c913c73af (MD5) Previous issue date: 2020-06-15 Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) A sedação em equinos é alvo de estudos que avaliam os efeitos sedativos de fármacos em situações experimentais e clínicas. Há diferentes descrições para estimar sedação em equinos, porém sem padronização e validação o que dificulta a reprodutibilidade. Objetivou-se desenvolver e validar uma Escala numérica composta de sedação em equinos (EquiSed) e Escala numérica facial de sedação em equinos (FaceSed). Sete animais foram submetidos à seis diferentes protocolos: Detomidina em dose baixa isolada (DL, 2,5 μg/kg + 6,25 μg/kg/h, por 120 min) ou associada à metadona (DLM, 0,2 mg/kg de metadona + metadona 0,05 mg/kg/h, por 120 min), detomidina em dose alta isolada (DH, 5 μg/kg + 12,5 μg/kg/h, por 120 min) ou associada à metadona (DHM, 0,2 mg/kg de metadona + metadona 0,05 mg/kg/h, por 120 min), bolus de acepromazina em dose baixa (ACPL 0,02 mg/kg) e dose alta (ACPH 0,09 mg/kg). Quando submetidos à infusão contínua, os animais foram avaliados por 240 minutos e quando submetidos a bolus, avaliados por 120 minutos. Os cavalos foram fotografados e filmados nos momentos basal, pico de sedação, sedação intermediária e recuperação da sedação. Tirou-se a fotografia da face dos cavalos e na sequencia foram filmados enquanto aplicavam-se os estímulos auditivo, visual, pressórico mediante o toque nas orelhas, nos membros torácico e pélvico e estabilidade postural. Os vídeos e fotos foram aleatorizados e avaliados duas vezes por quatro avaliadores com intervalo de um mês. Comprovou-se a responsividade da somatória de ambas as escalas ao longo do tempo (p0,70) em animais tratados com detomidina em dose alta. Já com a altura da cabeça acima do chão (ACAC) foi média (-0,69). Confiabilidades intraobservadores boas e muito boas da somatória da EquiSed foram identificadas (0,89 – 0,91) e as concordâncias interobservadores em matriz dos avaliadores variaram de 0,53 a 0,86. A sensibilidade foi >78 para estímulo toque nas orelhas, auditivo, visual e instabilidade postural. Detectou-se especificidade para pressão nos membros (>74). A FaceSed apresentou alta consistência interna (α de Cronbach = 0,83) e correlação item-total entre 0,60 – 0,73. A correlação de Spearman da somatória da FaceSed versus a EN foram altas (>0.85) e a ACAC% foram médias (-0,38 a -0,56). A correlação intraobservadores variou de 0,82 a 0,91 e a interobservadores 0,64 a 0,84. A sensibilidade foi >82 e a especificidade variou de 44 a 82. Conclui-se que a EquiSed e a FaceSed possuem validade de critério, conteúdo e construto, são confiáveis e possuem boa consistência interna. Sedation in horses is the target of studies evaluating sedative effects of drugs in experimental and clinical situations. There are different descriptions to estimate sedation in horses, but without standardization and validation, which makes reproducibility difficult. The objective was to validate an Equine composite numerical sedation scale (EquiSed) and Equine numerical facial sedation scale (FaceSed). Seven animals were submitted to a study with six different protocols: Detomidine in low dose isolated (DL, 2,5 μg/kg + 6,25 μg/kg/h for 120 min) or associated with methadone (DLM, 0,2 mg/kg of methadone + 0,05 mg/kg/h for 120 min), detomidine in high dose isolated (DH, 5 μg/kg + 12,5 μg/kg/h for 120 min) or associated with methadone (DHM, 0,2 mg/kg de methadone + 0,05mg/kg/h for 120 min), acepromazine in bolus in low dose (ACPL 0,02 mg/kg) and high dose (ACPH 0,09 mg/kg). When submitted to continuous rate infusion, the animals were evaluated for 240 minutes and when submitted to bolus, evaluated for 120 minutes. A photograph was taken of the horse´s faces and was subsequently they were filmed while the auditory, visual and pressure stimuli were applied by touching the ears, the thoracic and pelvic limbs and postural instability. The videos and photos were randomized and evaluated twice by four evaluators with and interval of one month. The responsiveness of both scales was verified over time (p0,70) in animals treated with detomidina at high dose. The head height above the ground (HHAG) presented average results (-0,69). Good and very good reliability of the sum of EquiSed were identified for intraobserver (0,89 – 0,91) and interobserver agreement matrix was 0,53 – 0,86. The sensitivity was >78 for touch the ears, auditory, visual and postural instability. Specificity for the pressure on the limbs (>74) was detected. FaceSed showed high internal consistency (Cronbach´s α = 0,83) and item-total correlation between 0,60 – 0,73. The Spearman correlation of the sum of FaceSed versus NRS was high (>0,85) and ACAC% was average (-0,38 to -0,56). The intraobserver correlation range between 0,82 to 0,91 and interobservers 0,64 to 0,84. Sensitivity was >84 to touch the ears, auditory and visual. for all items and specificity ranged from 44 to 82. The conclusions is that EquiSed and FaceSed have validity of criterion, content and construct, reliable and with good internal consistency. FAPESP: 2017/16208-0 FAPESP: projeto temático 2017/12815-0 CAPES: 001

OBJECTIVE To evaluate the effects of lidocaine as a coinduction agent with propofol on cardiopulmonary variables and administered propofol doses in healthy dogs premedicated with hydromorphone hydrochloride and acepromazine maleate and anesthetized with isoflurane. ANIMALS 40 client-owned dogs (American Society of Anesthesiologists physical status classification I or II and age ≥ 6 months) scheduled to undergo anesthesia for elective procedures. PROCEDURES In a randomized, blinded, controlled clinical trial, dogs received 2% lidocaine hydrochloride solution (2.0 mg/kg [0.9 mg/lb], IV; n = 20) or buffered crystalloid solution (0.1 mL/kg [0.05 mL/lb], IV; 20; control treatment) after premedication with acepromazine (0.005 mg/kg [0.002 mg/lb], IM) and hydromorphone (0.1 mg/kg, IM). Anesthesia was induced with propofol (1 mg/kg [0.45 mg/lb], IV, with additional doses administered as needed) and maintained with isoflurane. Sedation was assessed, and anesthetic and cardiopulmonary variables were measured at various points; values were compared between treatment groups. RESULTS Propofol doses, total sedation scores, and anesthetic and most cardiopulmonary measurements did not differ significantly between treatment groups over the monitoring period; only oxygen saturation as measured by pulse oximetry differed significantly (lower in the lidocaine group). Mean ± SD propofol dose required for endotracheal intubation was 1.30 ± 0.68 mg/kg (0.59 ± 0.31 mg/lb) and 1.41 ± 0.40 mg/kg (0.64 ± 0.18 mg/lb) for the lidocaine and control groups, respectively. CONCLUSIONS AND CLINICAL RELEVANCE No propofol-sparing effect was observed with administration of lidocaine as a coinduction agent for the premedicated dogs of this study. Mean propofol doses required for endotracheal intubation were considerably lower than currently recommended doses for premedicated dogs. (J Am Vet Med Assoc 2020;256:93–101)

Several tests have been devised in an attempt to detect behaviour modification due to training, supplements or diet in horses. These tests rely on subjective observations in combination with physiological measures, such as heart rate (HR) and plasma cortisol concentrations, but these measures do not definitively identify behavioural changes. The aim of the present studies was to develop an objective and relevant measure of horse reactivity. In Study 1, HR responses to auditory stimuli, delivered over 6 days, designed to safely startle six geldings confined to individual stalls was studied to determine if peak HR, unconfounded by physical exertion, was a reliable measure of reactivity. Both mean (±SEM) resting HR (39.5 ± 1.9 bpm) and peak HR (82 ± 5.5 bpm) in response to being startled in all horses were found to be consistent over the 6 days. In Study 2, HR, plasma cortisol concentrations and speed of departure from an enclosure (reaction speed (RS)) in response to a single stimulus of six mares were measured when presented daily over 6 days. Peak HR response (133 ± 4 bpm) was consistent over days for all horses, but RS increased (3.02 ± 0.72 m/s on Day 1 increasing to 4.45 ± 0.53 m/s on Day 6; P = 0.005). There was no effect on plasma cortisol, so this variable was not studied further. In Study 3, using the six geldings from Study 1, the RS test was refined and a different startle stimulus was used each day. Again, there was no change in peak HR (97.2 ± 5.8 bpm) or RS (2.9 ± 0.2 m/s on Day 1 versus 3.0 ± 0.7 m/s on Day 6) over time. In the final study, mild sedation using acepromazine maleate (0.04 mg/kg BW i.v.) decreased peak HR in response to a startle stimulus when the horses (n = 8) were confined to a stall (P = 0.006), but not in an outdoor environment when the RS test was performed. However, RS was reduced by the mild sedation (P = 0.02). In conclusion, RS may be used as a practical and objective test to measure both reactivity and changes in reactivity in horses.

Acepromazine maleate (Sedalin®) was administered orally to six thoroughbred horses at a dose of 0.15 mg kg−1. Urine and blood samples were collected up to 412 h post-administration. Plasma and urine were hydrolysed; plasma samples were then processed using liquid–liquid extraction and urine samples using solid-phase extraction. A sensitive tandem mass spectrometric method was developed in this study, achieving a lower limit of quantification for acepromazine of 10 pg mL−1 in plasma and 100 pg mL−1 in urine. Acepromazine, hydroxyethylpromazine, hydroxyacepromazine, hydroxyethylpromazine sulphoxide, hydroxyethylhydroxypromazine, dihydroxyacepromazine and dihydroxyhydroxyethylpromazine were detected in the post-administration samples. The parent drug and its metabolites were identified using a combination of UPLC–MS/MS and accurate mass measurement. Separation of the structural isomers hydroxyethylpromazine sulphoxide and hydroxyethylhydroxypromazine was another significant outcome of this work and demonstrated the advantages to be gained from investing in chromatographic method development.

Objective—To investigate the effects of acepromazine maleate and morphine on aqueous tear production before, during, and after sevoflurane anesthesia in dogs. Animals—6 mixed-breed dogs. Procedures—In a Latin square study design, dogs underwent IM administration of morphine (1 mg/kg), acepromazine (0.05 mg/kg), or saline (0.9% NaCl) solution (0.05 mL/kg), followed by induction and maintenance of anesthesia with sevoflurane for 30 minutes. The protocol was repeated until all dogs had received all treatments, with a minimum of 7 days between anesthetic episodes. Aqueous tear production was measured via Schirmer tear test I before treatment (baseline); before anesthetic induction; 5, 10, 20, and 30 minutes after anesthetic induction; immediately once dogs recovered from anesthesia; and 2 and 10 hours after recovery. Results—Aqueous tear production for all treatments was significantly lower 10, 20, and 30 minutes (but not 5 minutes) after anesthetic induction than at baseline, before anesthetic induction, at recovery, and 2 and 10 hours after recovery. Aqueous tear production was significantly higher after saline solution administration than after morphine administration at the preinduction measurement point and 2 hours after recovery. No other differences were detected among the 3 treatments. Conclusions and Clinical Relevance—Aqueous tear production after anesthesia did not differ significantly from baseline values after any treatment following 30 minutes of sevoflurane anesthesia, suggesting premedication with morphine or acepromazine does not contribute to a decrease in lacrimation in these circumstances.

A 10-year-old 45-kg (99-lb) castrated male English Pointer with body condition score of 5 of 6 was evaluated for removal of a subcutaneous mass in the left thoracic wall diagnosed as a mast cell tumor on the basis of results of ex-amination of fine-needle aspirates. Additionally, the dog had an 8-week history of reverse sneezing, coughing, and puru-lent nasal discharge with episodes of dyspnea and cyanosis.On physical examination, the patient was bright, alert, and responsive but appeared stressed and was panting heav-ily; therefore, thoracic auscultation and body temperature measurement were not performed. Heart rate was 120 beats/min; mucous membranes were pink and moist. The dog was premedicated with acepromazine maleate

Objective: To retrospectively evaluate the incidence of seizures in dogs presenting with a history of seizures that were treated with acepromazine (ACE) during hospitalization. Design: Retrospective study. Setting: Privately owned emergency and referral hospital. Animals: Thirty-one client-owned dogs. Interventions: Administration of ACE. Measurements and main results: The medical records from dogs with an acute or chronic seizure history that received ACE were reviewed. Factors evaluated included presenting complaint, seizure history, ACE dosage, duration of observation, seizure activity, and other medications used. Thirty-one dogs qualified for the study: 20 males and 11 females. Age range was 3 months to 14.9 years. Presenting complaint was seizure in 28/31 dogs. There was a prior history of seizures in 22/31 dogs, and 15/22 were currently on antiseizure medication. ACE was given 1–5 times per dog. Mean ACE dose was 0.029 mg/kg IV (range: 0.008–0.057 mg/kg; n=46), 0.036 mg/kg IM (range: 0.017–0.059 mg/kg; n=14), 0.53 mg/kg PO (n=2). Twenty-seven dogs did not seizure after administration of ACE within the observation period (mean: 16.4 hours, range: 0.25–66 hours). Twenty-five dogs received antiseizure medication before ACE. Eight seizure episodes occurred in 4 dogs (all of whom presented for seizures) within 0.3–10 hours after ACE administration. Conclusions: There was no observed correlation between ACE administration in dogs with a seizure history and the recurrence of seizure activity during hospitalization. The time from ACE administration to seizure activity was greater than expected for measurable effects to be seen in 1 dog (10 hour). Further studies with a larger group and alternative ACE doses are needed to more thoroughly evaluate the safety of short-term ACE use in dogs with a seizure history.

Perphenazine enanthate was used to allow adaptation to captivity in 11 Pyrenean chamois (Rupicapra pyrenaica). At the time of capture, all animals received 0.10 mg/kg of acepromazine maleate and 2.5 mg/kg of perphenazine enanthate intramuscularly. The effect was evaluated by means of three behaviors: alertness, defecation, and flight distance. The tranquilization and lack of fear of humans of all animals were determined and the usefulness of this long-acting tranquilizer for chamois adaptation to captivity was confirmed.

We opportunistically evaluated a combination of acepromazine maleate and medetomidine HCl for use in sedating Rocky Mountain elk (Cervus elaphus nelsoni) and black bears (Ursus americanus) as an alternative to scheduled drug combinations. This combination was safe and effective with limitations inherent in its sedative rather than anesthetic properties.

Objective To determine the presence and duration of analgesia after oxymorphone, acepromazine maleate, acepromazine-oxymorphone combination and medetomidine administration in dogs. Study design Blinded, controlled study. Animals Six adult beagle dogs. Methods Each dog participated in five trials receiving acepromazine maleate (0.2 mg kg−1 IM), oxymorphone (0.2 mg kg−1 IM), acepromazine-oxymorphone drug combination (0.2 mg kg−1 each IM), medetomidine (20 μg kg−1 IM) and sterile saline (control). Two specially designed instruments were used for analgesia determination: a heat device (HD) utilized a linear ramped intensity incandescent bulb and a pressure device (PD) consisted of a pneumatic cylinder that protruded a 2.5-cm bolt. The minimum pressure and heat necessary to produce an avoidance response were determined. Analgesia testing was performed prior to and at 30-minute intervals for six hours after drug administration. Results Oxymorphone, acepromazine-oxymorphone and medetomidine significantly elevated both pressure and heat response thresholds compared to controls and acepromazine. Both medetomidine and acepromazine-oxymorphone provided a significantly longer duration of analgesia than oxymorphone. No adverse effects were observed at any of the thermal or pressure application sites. Conclusions Oxymorphone, medetomidine and acepromazine-oxymorphone produced significant analgesia with medetomidine and acepromazine-oxymorphone providing the longest duration of analgesia.

Tonometry was performed to estimate intraocular pressure (IOP) in 12 Nubian ibexes (Capra ibex nubiana), 10 Grant zebras (Equus burchelli ) and five Arabian oryxes (Oryx leucoryx), using both applanation (Tono-Pen) and/or indentation (Schiotz) tonometers. Animals were anesthetized with a mixture of etorphine hydrochloride and acepromazine maleate. Mean (+/- SD) IOP in the ibex was 17.95 +/- 4.78 mmHg (24 eyes, indentation tonometry). In the zebra, indentation tonometry (20 eyes) yielded a mean IOP of 25.30 +/- 3.06 mmHg, and applanation tonometry (six eyes) yielded a mean IOP of 29.47 +/- 3.43 mmHg. In the oryx, indentation tonometry (five eyes) yielded a mean IOP of 22.68 +/- 8.15 mmHg, and applanation tonometry (10 eyes) yielded a mean IOP of 11.76 +/- 3.43 mmHg. There were no significant effects of gender, age, weight, side or reading number on the IOP measured in any of the three species. No significant differences were found between the IOP of the three species, nor between the readings of the two instruments, although some of the P-values were close to the significance level.

Objective—To evaluate the effect of acepromazine maleate administered IV on platelet function assessed in healthy dogs by use of a modified thromboelastography assay. Animals—6 healthy adult mixed-breed dogs. Procedures—Dogs received each of 3 treatments (saline [0.9% NaCl] solution [1 to 2 mL, IV] and acepromazine maleate [0.05 and 0.1 mg/kg, IV]) in a randomized crossover study with a minimum 3-day washout period between treatments. From each dog, blood samples were collected via jugular venipuncture immediately before and 30 and 240 minutes after administration of each treatment. A modified thromboelastography assay, consisting of citrated kaolin–activated (baseline assessment), reptilase-ADP–activated (ADP-activated), and reptilase-arachidonic acid (AA)–activated (AA-activated) thromboelastography, was performed for each sample. Platelet inhibition was evaluated by assessing the percentage change in maximum amplitude for ADP-activated or AA-activated samples, compared with baseline values. Percentage change in maximum amplitude was analyzed by use of Skillings-Mack tests with significance accepted at a family-wise error rate of P < 0.05 by use of Bonferroni corrections for multiple comparisons. Results—No significant differences were found in the percentage change of maximum amplitude from baseline for ADP-activated or AA-activated samples among treatments at any time. Conclusions and Clinical Relevance—Platelet function in dogs, as assessed by use of a modified thromboelastography assay, was not inhibited by acepromazine at doses of 0.05 or 0.1 mg/kg, IV. This was in contrast to previous reports in which it was suggested that acepromazine may alter platelet function via inhibition of ADP and AA.

The current study was undertaken to develop a successful procedure for the nonsurgical transfer of pig embryos. A total of 663 embryos were surgically collected on Day 4 or 5 from 55 donors, of which 542 embryos of acceptable quality were nonsurgically transferred to 46 recipients. Nonsurgical recipient gilts were sedated 15 min prior to transfer with 20 mg im acepromazine maleate. A disposable insemination spirette with an attached 3-way stopcock was manipulated into the cervix of each gilt. Embryos were expelled from a tomcat catheter into the spirette, and 10 to 12 ml of Whitten's medium were used to flush embryos through the spirette into the reproductive tract. Sixteen (34.8%) recipient gilts did not return to estrus before Day 36, and 10 (21.7%) gilts farrowed with an average litter size of 4.3 ± 0.7. Embryos were collected from an additional 20 donors and were surgically transferred to an additional 19 recipients. Surgical transfers conducted at the same time as the nonsurgical transfers resulted in 12 (63.2%) gilts farrowing and 7.1 ± 0.6 pigs were born per litter. In conclusion, a procedure has been developed for nonsurgical transfer of swine embryos which simplifies the process of embryo transfer and which may increase the potential for utilization of embryo transfer technologies by swine producers.

The effects of thiopentone and propofol on oesophageal pressures were examined in 39 bitches. The dogs were premedicated with either atropine (n = 13), acepromazine maleate (n = 13) or a combination of atropine and acepromazine. Anaesthesia was induced with either thiopentone (15 dogs) or propofol (24 dogs), both given intravenously. Immediately following the induction of anaesthesia, gastric pressure and lower oesophageal sphincter pressure (LOSP) were measured and oesophageal barrier pressure determined. There were no significant differences attributable to the premedication regimens used but both LOSP and barrier pressure were significantly lower in the dogs anaesthetised with propofol compared to the animals given thiopentone (LOSP 12-2 ± 4-2 cm H2O propofol group versus 26-8 ± 6-5 cm H2O thiopentone group).

Objective—To compare the time to desaturation in healthy dogs that breathed oxygen or room air for 3 minutes before induction of anesthesia. Animals—20 healthy dogs. Procedures—Dogs were sedated with morphine and acepromazine maleate. Dogs received a 3-minute treatment of room air or oxygen (100 mL/kg/min) via face mask. Arterial blood samples were collected before and after treatment to determine PaCO2, PaO2, pH, and SaO2; propofol (6 mg/kg, IV) was injected during a 7-second period, and the dogs were intubated. A lingual pulse oximeter probe was placed. Dogs remained disconnected from the breathing circuit until SpO2 equaled 90% (desaturation point) and then connected and ventilated until the SpO2 was ≥ 97%. Arterial blood samples were collected and SpO2 was recorded every 30 seconds for 4 minutes and then every minute until the desaturation point. Times to first breath and the desaturation point were recorded. Data were collected at 0, 5, 30, 60, 90, 120, and 150 seconds. Results—Mean ± SEM time to desaturation differed significantly between dogs treated with room air (69.6 ± 10.6 seconds) and oxygen (297.8 ± 42.0 seconds). Lowest mean PaO2 and SaO2 when dogs were breathing room air were 62 ± 6.3 mm Hg and 82.3 ± 4%, respectively, at 30 seconds. Conclusions and Clinical Relevance—Preoxygenation for 3 minutes increased the time to desaturation in healthy dogs sedated with acepromazine and morphine in which anesthesia was induced with propofol.

Twenty ewes were used as donors in a 2 x 2 factorial design experiment to investigate the effects of two different insemination times (48 vs 60 h after pessary withdrawal), with or without sedation, on the ovum recovery rate 5 d after insemination, the proportion of transferable embryos recovered, and the subsequent survival rate of embryos transferred to recipients. The ovum recovery rate following intrauterine insemination at 48 h after progestagen pessary withdrawal was 63.8 and 53.4% for sedated and nonsedated control ewes, respectively. Following intrauterine insemination at 60 h the corresponding values for sedated and control ewes were 72.6 and 73.9%, respectively. The proportion of transferable quality embryos recovered was not affected by sedation but was improved by insemination at 48 h rather than 60 h after pessary withdrawal (100 vs 35.4%). Embryo survival following laparoscopic transfer to recipients from donor ewes inseminated at 48 h, with or without sedation was 38.8% (7/18) and 50% (7/14), respectively. Following intrauterine insemination of the donors at 60 h, the survival rate in recipients was reduced for embryos transferred from both the sedated and control ewes to 6.25% (1/16) and 36.3% (4/11). It is concluded that delaying the timing of intrauterine insemination relative to pessary withdrawal and the use of acepromazine maleate as a sedative at the time of insemination are deleterious to embryo development and subsequent viability.

Use of acepromazine (i.e., acetylpromazine) maleate in dogs with a history of seizures is reportedly contraindicated because of the risk of decreasing the seizure threshold in these animals. In this retrospective study, acepromazine was administered for tranquilization to 36 dogs with a prior history of seizures and to decrease seizure activity in 11 dogs. No seizures were seen within 16 hours of acepromazine administration in the 36 dogs that received the drug for tranquilization during hospitalization. After acepromazine administration, seizures abated for 1.5 to 8 hours (n=6) or did not recur (n=2) in eight of 10 dogs that were actively seizing. Excitement-induced seizure frequency was reduced for 2 months in one dog.

To determine the plasma cortisol response to laparoscopy in ewes and investigate means of reducing it.Ewes without lambs at foot (n=40) were subjected to one of three control or one laparoscopy treatments (n=10 ewes/treatment), being: no restraint or drugs; acepromazine maleate (ACP) control and no restraint; ACP and restraint in a cradle for 5 min; and laparoscopy following ACP. Additional ewes with lambs at foot (n=30) were subjected to: laparoscopy following ACP; laparoscopy following ACP and ketoprofen; and laparoscopy following detomidine. Drugs were injected 20 min before treatment, after a first blood sample had been taken. Blood samples were taken by jugular venepuncture from the ewes 20 min before treatment and at 20, 40, 60, 90, 120, 150 and 180 min after treatment, while all ewes were held in a pen. Plasma was harvested and assayed for its concentration of cortisol.Plasma cortisol concentrations (PCC) remained constant in ewes in the control restraint group for 80 min. In ewes given ACP, PCC increased for the first 20 min after treatment but then returned to pre-treatment concentrations. PCC of ewes given ACP and restrained in a cradle were elevated above pre-treatment concentrations for 90 min. PCC in ewes subjected to laparoscopy following sedation with ACP increased to a peak at 40 min and returned to pre-treatment concentrations after 60 (with lambs) or 120 (without lambs) min. When ACP and ketoprofen were given before laparoscopy, PCC peaked at 20 min and returned to pre-treatment concentrations by 40 min. PCC of ewes given detomidine before laparoscopy remained at pre-treatment concentrations throughout. PCC of ewes subjected to laparoscopy with ACP sedation only were greater than those of control restraint, ACP control, and ewes subjected to laparoscopy after being given ketoprofen or detomidine between 20 and 60 min after treatment. PCC of ewes subjected to laparoscopy were greater than those of control ewes placed in a cradle at 20 and 40 min. PCC of ewes given ketoprofen were lower than those of ewes subject to laparoscopy following ACP.Laparoscopy, even after sedation with ACP, caused some distress in ewes, as evidenced by increased plasma cortisol levels. Plasma cortisol response was alleviated by the administration of ketoprofen and eliminated by detomidine, probably because of both analgesic and sedative effects of the latter drug.

Combinations of acepromazine maleate, pethidine hydrochloride and atropine sulphate (0.05 mg/kg) or acepromazine maleate and pethidine hydrochloride and acepromazine maleate alone or atropine sulphate (0.1 mg/kg) alone were used to premedicate cats before they were anaesthetised with thiopentone, to investigate their effects on gastric pressure, lower oesophageal sphincter pressure and barrier pressure under anaesthesia. Manometric measurements were made by using a non-perfused manometric technique. The lower oesophageal sphincter pressure was lowest in the cats premedicated with atropine sulphate alone. The difference in barrier pressure between the atropine (0.1 mg/kg) and acepromazine treated cats was highly significant. The risk of gastro-oesophageal reflux appeared to be highest with atropine (0.1 mg/kg) if barrier pressure is used as an indicator of the likelihood of reflux.

PURPOSE To establish a normal reference range of intraocular pressure estimates in Thomson gazelles (Gazella thomsoni). MATERIALS AND METHODS Applanation tonometry was conducted in 22 eyes of 11 gazelles anesthetized for transportation purposes with a mixture of etorphine hydrochloride and acepromazine maleate. Five sequential readings using a Tono-Pen XL (Mentor Ophthalmics, Inc., Norwell, MA) were obtained from each eye. Results were analyzed for the effect of age, weight, gender, side, and replicate readings and were compared with estimates in other species. RESULTS Mean (+/- standard deviation) intraocular pressure estimate in 22 eyes of 11 gazelles was 7.6 +/- 1.6 mm Hg. None of the variables tested had a significant effect on the results. CONCLUSIONS To date, the intraocular pressure estimates in the Thomson gazelle are the lowest reported in any species.

Propofol was administered to 49 cats to induce anaesthesia. The mean dose required was 6.8 mg/kg and this was not affected by prior administration of acepromazine maleate. In 27 cases, propofol was also used as the principal maintenance agent (mean dose rate 0.51 mg/kg/minute). Inductions were very smooth and problem free. Intubation was easily achieved in 15 cats with the aid of local desensitisation by lignocaine spray or neuromuscular relaxation by suxamethonium. Heart rate did not vary significantly during induction or maintenance of anaesthesia but respiratory rates did fall significantly. Recovery from anaesthesia was remarkably smooth in all cases and there was no significant difference in recovery times between the cats in which halothane was the principal maintenance agent and cats which received propofol alone. Side effects were seen during recovery in eight cats and included retching, sneezing and pawing of the face.

The effect of acepromazine maleate (ACP) on the equine venous haematocrit and total plasma protein concentration was studied in six clinically normal horses. Total plasma protein concentration was not appreciably influenced by ACP. However, the haematocrit decreased with the duration, but not the degree, of the decrease being dose-related. Mean haematocrit values returned to control levels by 12 h after 0.05 mg ACP/kg body weight and 21 h after 0.15 mg ACP/kg body weight.

Summary A total of 103 anaesthetic inductions were performed in horses for a variety of elective procedures. All cases were premedicated with acepromazine maleate (0.02 to 0.05 mg/kg body weight [bwt] intramuscularly [im]). In 50 cases (Group A) anaesthesia was induced by a single intravenous (iv) bolus of thiopentone sodium (11.1 mg/kg bwt or 1 g/90 kg bwt) followed immediately by a bolus of suxamethonium chloride (0.1 mg/kg bwt). In 53 cases (Group B) anaesthesia was induced using iv guaiacol glycerine ether (GGE) (approximately 50 mg/kg bwt) followed by a bolus of thiopentone at half the usual dose rate (5.6 mg/kg bwt or 1 g/180 kg bwt). Induction of anaesthesia was uneventful in both groups although in Group B it was particularly smooth. Following endotracheal intubation anaesthesia was maintained with halothane in oxygen administered via a circle system. The duration of anaesthesia was comparable between the two groups; however, the mean (± sd) time to standing in Group B, 35 ± 22 mins, was significantly shorter than in Group A, 48 ± 25 mins. The use of the GGE/thiopentone technique is discussed.

Summary Drugs and drug combinations currently in use for chemical restraint of the horse are discussed with a view to establishing their likely usefulness to the practising veterinary surgeon. Acepromazine maleate and xylazine hydrochloride are considered to be the most useful tranquillisers in spite of their limitations. A xylazine-methadone sequence is described for more profound chemical restraint and the possible future role of ketamine and glyceryl guaiacolate in combination with other agents to produce recumbency is discussed. Resume On discute des medicaments et des associations medicamenteuses utilises couramment pour la contention chimique du cheval, afin d'etablir leur valeur en pratique courante. Le maleate d'acepromazine et le chlorhydrate de xylazine paraissent etre les plus efficaces malgre leurs limits. Un couplage zylazine-methadone est indique pour obtenir une contention chimique plus profonde. L'emploi de la ketamine et de l'esther glycerique du gaiacol, combines a d'autres agents afin d'obtenir le decubitus, est evoque. Zusammenfassung Sedierende Medikamente oder Medikamentenkombinationen und ihre Anwendung werden im Hinblick auf ihre wahrscheinliche Nutzlichkeit fur den Praktiker besprochen. Acepromazin-Maleat und Xylazin Hydrochlorid werden trotz ihrer Grenzen als nutzlichste Tranquilliser angesehen. Eine Xylazin-Methadon Sequenz fur tiefe Sedation wird beschrieben und die mogliche zukunftige Rolle von Ketamin und Glycerin-Guaiacolaether in Kombination mit andern Mitteln zum Niederlegen der Pferde wird diskutiert.

The hypotensive effect of acepromazine maleate was related to both the dose and route of administration. The degree and duration of hypotension varied between individual horses. In general, intravenous administration produced a more rapid maximum effect than intramuscular injection and the larger the dose the longer blood pressure remained at low levels. Average systolic pressure (of 6 horses) remained significantly below control values for more than 6 h after an intramuscular injection of 0.05 mg acepromazine maleate/kg body weight. Respiratory rate was markedly decreased, with the duration, but not the degree of bradypnoea related to the dose administered. A slight, transient decrease in body temperature was observed. Heart rate was not significantly influenced by administration of acepromazine maleate.

Continuous monitoring of the foetal electrocorticogram, eye movements and heart rate in ewes during the last month of gestation showed rapid placental transfer from the mother to the foetus of phenothiazine derivatives (acepromazine maleate), short-acting barbiturates (thiopental sodium) and narcotic analgesics (meperidine). Acepromazine and thiopental partially disrupted the foetal sleep cycle by synchronization of the ECoG for 1–2 h but increased the heart rate for 2–3 h. The effects of meperidine were similar but lasted only 5–10 min for the ECoG and less than 0.5 h for the heart rate.

One hundred anaesthetics were administered in a clinical trial to 95 equine patients, ranging in age from nine months to 19 years and in weight from 140 to 1270 kg, undergoing a variety of surgical procedures. Acepromazine maleate premedication (0.01 to 0.03 mg per kg intramuscularly) was given to seven animals, the remainder were not premedicated. Xylazine (1.1 mg per kg) was injected intravenously over a two minute period and after a pause of two minutes ketamine (2.2 mg per kg) was injected rapidly by the same route. For 30 procedures no other anaesthetic was given but in 59 cases anaesthesia was prolonged with halothane-oxygen while in 11 additional intravenous agents were administered. Recumbency followed one-and-a-half to two minutes after completion of the ketamine injection and limb movements occurring immediately after the animal lay down gradually subsided over the next 30 to 60 seconds. On 26 occasions when no other agent was given satisfactory operating conditions were produced for a mean (+/- sd) of 20 +/- 7 minutes and on four occasions when absence of complete muscle relaxation was observed surgery was still possible. When no other agent was given the onset of recovery was abrupt but recovery was always extremely quiet; the animals stood 33 +/- 10 minutes after induction of anaesthesia and showed a remarkable absence of ataxia. A similar recovery was seen in the 56 animals receiving halothane-oxygen and all stood 28 +/- 14 minutes after disconnection from the anaesthetic system. Heart block was observed during induction of anaesthesia bu otherwise cardiovascular and respiratory parameters were well maintained. It was concluded that the xylazine-ketamine combination had advantages over other current techniques of inducing anaesthesia in horses.

Ketamine [dl-2-(o-chlorophenyl)-2-(methylamino)cyclohexanone] hydrochloride was used in conjunction with Acepromazine [10–3-(dimethylamino)-propyl]phenothiazin-2-yl-methyl ketone] Maleate to produce surgical depth anesthesia in guinea pigs. In tests with 97 animals, an intramuscular injection of 44 mg/kg ketamine hydrochloride plus 2 mg Acepromazine Maleate was found to be effective in producing a surgical level of anesthesia within 2 min after administration. The anesthetic state lasted for an average of 1.5 h and could be safely extended by supplemental administrations of the drugs. This anesthetic combination was found to be fast acting, safe, and easily controlled.

During the past decade etorphine and its antagonist, diprenorphine, have been successfully used to immobilize and revive, respectively, a number of North American cervids including white-tailed deer (Odocoileus virginianus) (Woolf 1970, Presnell et al. 1973); elk (Cervus elaphus) (Coggins 1975, Magonigle et al. 1977), and moose (Alces alces) (Houston 1970, Franzmann and Arneson 1974, Roussel and Patenaude 1975, Haigh et al. 1977, Gasaway et al. 1978). However, the use of etorphine to immobilize caribou (Rangifer tarandus) has not been reported. This paper reports on the use of etorphine hydrochloride in combination with acepromazine maleate to immobilize free-ranging caribou in Newfoundland, analyzes induction times relative to dosages, and provides information on drugrelated mortality.

Badgers (Taxidea taxus) were successfully immobilized using four different drugs under field conditions in central Colorado during an ecological investigation of an enzootic plague (Yersinia pestis) focus. A total of 33 individual doses of the drugs were administered to captured animals. Six badgers were immobilized using phencyclidine hydrochloride, acepromazine maleate was used on five, chlorpromazine hydrochloride was used on five, and succinylcholine chloride was used on 17 badgers. All of the drugs were successful in immobilizing the badgers, but succinylcholine chloride proved most useful in the present study because the animals recovered quickly from its effects. Dosages of phencyclidine hydrochloride and succinylcholine chloride were respectively higher and lower than those reported by other workers using these drugs on badgers. J. WILDL. MANAGE. 37(3):418-421 This paper compares the four immobilizing agents phencyclidine hydrochloride (Sernylan; Parke, Davis and Co.), acepromazine maleate (Ayerst Laboratories, Inc.), chlorpromazine hydrochloride (Thorazine; Pitman-Moore Laboratories), and succinylcholine chloride (Travenol Laboratories, Inc.) used on badgers under field conditions. The badgers were captured on a 3 square mile area in South Park, Park County, Colorado during 1967-72. Badgers were being investigated as a part of a plague ecology study in part financed by NIH grant 5-R01-A106196. With the exception of papers by Balser (1965), Bailey (1971), and Lindzey (1971) little data exist on the immobilization of badgers in the field. Seal and Erickson (1969) presented some data on immobilizing captive badgers.