Effects of sedation on intradermal skin testing in flea-allergic dogs

Effects of 4 commonly used sedatives on the wheal-and-flare response to histamine and flea antigen were evaluated in 8 flea-allergic Beagles. Skin testing was performed in 12 separate occasions, 3 to 4 days apart. Twelve intradermal injections were given during each skin test: 5 doubling dilutions of histamine phosphate, 6 doubling dilutions of flea antigen, and a phosphate-buffered saline solution (negative control). Of the 12 intradermal skin tests, 8 were control tests performed on nonsedated dogs. The remaining 4 tests were performed on dogs sedated with xylazine, ketamine and valium combination, acepromazine, or oxymorphone. Oxymorphone had the most profound effect on skin test results, significantly (P less than 0.05) decreasing skin responsiveness in 8 of 11 test sites (by objective evaluation) and in 5 of 11 test sites (by subjective evaluation). Xylazine sedation enhanced skin test results in 4 of 11 test sites (by objective evaluation) and in 1 of 11 test sites (by subjective evaluation). In non instance did xylazine significantly decrease skin responsiveness to histamine or flea antigen. Xylazine is the recommended sedative in dogs when sedation is necessary for intradermal skin testing.     

Effects of acepromazine on the incidence of vomiting associated with opioid administration in dogs

Opioids used in the pre‐operative period may frequently induce vomiting. Acepromazine is commonly combined with opioids as a pre‐anesthetic drug, and has antiemetic properties. The purpose of this study was to evaluate the antiemetic properties of acepromazine in dogs receiving opioids as a pre‐anesthetic. One hundred and sixteen dogs (ASA I or II), 58 males and 58 females; purebreds and mixed breeds; 3 months?13.4 years of age; weighing 1.8–57.7 kg admitted for elective surgical procedures, were randomly assigned to one of the three groups. All groups received acepromazine (0.05 mg kg^?1 IM). Group I (n = 40) received acepromazine 15 minutes prior to opioid administration. Group II (n = 38) received acepromazine in combination with the opioid. Group III (n = 38) received acepromazine 15 minutes after opioid administration. One of the three different opioids was administered IM to each dog: morphine at 0.5 mg kg^?1, hydromorphone at 0.1 mg kg^?1, or oxymorphone at 0.075 mg kg^?1. Statistical analysis included a χ²‐test for the incidence of vomiting and a Kruskal–Wallis nonparametric test for the sedation comparison between groups. The dogs receiving acepromazine before the opioid (Group I) had significantly lower incidence of vomiting (18%) than those in Groups II (45%) and III (55%). The degree of sedation assessed 15 minutes after administration of the last drug (s) in each group was significantly lower in the dogs receiving the combination of acepromazine and opioid (Group II) than in those receiving opioid as the first drug (Group III). Time to vomiting was less than 8 minutes in all groups. In conclusion, acepromazine administered 15 minutes before opioid reduces the incidence of vomiting induced by opioids.     

The use of intraoperative fentanyl in spontaneously breathing dogs undergoing orthopaedic surgery

Nineteen dogs were assigned randomly to one of three groups. Animals in Group 1 were pre-medicated with acepromazine, 50 μg/kg bodyweight (bwt) intramuscularly (im) and received 10 ml of 0.9 per cent saline intravenously (iv) at the time of skin incision. Dogs in Group 2 were pre-medicated with acepromazine, 50 μg/kg bwt im, and received fentanyl 2 μg/kg bwt iv at skin incision. Dogs in Group 3 were pre-medicated with acepromazine, 50 μg/kg bwt and atropine, 30 to 40 μg/kg bwt, im and received fentanyl, 2 μg/kg bwt iv at skin incision. Pulse rate, mean arterial blood pressure, respiratory rate and end tidal carbon dioxide were measured before and after fentanyl or saline injection. Fentanyl caused a short-lived fall in arterial blood pressure that was significant in dogs premedicated with acepromazine, but not in dogs pre-medicated with acepromazine and atropine. A significant bradycardia was evident for 5 mins in both fentanyl treated groups. The effect on respiratory rate was most pronounced in Group 3, in which four of seven dogs required intermittent positive pressure ventilation (IPPV) for up to 14 mins. Two of six dogs in Group 2 required IPPV, whereas respiratory rate remained unaltered in the saline controls. The quality of anaesthesia was excellent in the fentanyl treated groups; however, caution is urged with the use of even low doses of fentanyl in spontaneously breathing dogs under halothane-nitrous oxide anaesthesia.     

Sedative and cardiorespiratory effects of acepromazine or atropine given before dexmedetomidine in dogs

To test the hypothesis that acepromazine could potentiate the sedative actions and attenuate the pressor response induced by dexmedetomidine, the effects of acepromazine or atropine were compared in six healthy adult dogs treated with this alpha2-agonist. In a randomised block design, the dogs received intravenous doses of either physiological saline, 0.05 mg/kg acepromazine or 0.04 mg/kg atropine, 15 minutes before an intravenous dose of 5 microg/kg dexmedetomidine. The dogs' heart rate was reduced by 50 to 63 per cent from baseline and their mean arterial blood pressure was increased transiently from baseline for 20 minutes after the dexmedetomidine. Atropine prevented the alpha2-agonist-induced bradycardia and increased the severity and duration of the hypertension, but acepromazine did not substantially modify the cardiovascular effects of the alpha2-agonist, except for a slight reduction in the magnitude and duration of its pressor effects. The dexmedetomidine induced moderate to intense sedation in all the treatments, but the dogs' sedation scores did not differ among treatments. The combination of acepromazine with dexmedetomidine had no obvious advantages in comparison with dexmedetomidine alone, but the administration of atropine before dexmedetomidine is contraindicated because of a severe hypertensive response.     

Hemodynamic,respiratory and sedative effects of progressively increasing doses of acepromazine in conscious dogs

ObjectiveTo evaluate the effects of progressively increasing doses of acepromazine on cardiopulmonary variables and sedation in conscious dogs.Study designProspective, experimental study.AnimalsA group of six healthy, adult, mixed-breed dogs weighing 16.5 ± 5.0 kg (mean ± standard deviation).MethodsDogs were instrumented with thermodilution and arterial catheters for evaluation of hemodynamics and arterial blood gases. On a single occasion, acepromazine was administered intravenously to each dog at 10, 15, 25 and 50 μg kg^–1 at 20 minute intervals, resulting in cumulative acepromazine doses of 10 μg kg^–1 (ACP₁₀), 25 μg kg^–1 (ACP₂₅), 50 μg kg^–1 (ACP₅₀) and 100 μg kg^–1 (ACP₁₀₀). Hemodynamic data and sedation scores were recorded before (baseline) and 20 minutes after each acepromazine dose.ResultsCompared with baseline, all acepromazine doses significantly decreased stroke index (SI), mean arterial pressure (MAP) and arterial oxygen content (CaO₂) with maximum decreases of 16%, 17% and 21%, respectively. Cardiac index (CI) decreased by up to 19% but not significantly. Decreases of 26–38% were recorded for oxygen delivery index (DO₂I), with significant differences for ACP₅₀ and ACP₁₀₀. Systemic vascular resistance index (SVRI) and heart rate did not change significantly. No significant difference was found among acepromazine doses for hemodynamic data. After ACP₁₀, mild sedation was observed in five/six dogs and moderate sedation in one/six dogs, whereas after ACP₂₅, ACP₅₀ and ACP₁₀₀, moderate sedation was observed in five/six or six/six dogs.Conclusions and clinical relevanceIn conscious dogs, acepromazine decreased MAP, SI, CaO₂ and DO₂I, but no significant dose effect was detected. SVRI was not significantly changed, suggesting that the reduction in MAP resulted from decreased CI. The ACP₂₅, ACP₅₀ and ACP₁₀₀ doses resulted in moderate sedation in most dogs; ACP₁₀ resulted in only mild sedation.     

Effects of acepromazine on the incidence of vomiting associated with opioid administration in dogs

Objective To evaluate the anti‐emetic properties of acepromazine in dogs receiving opioids as pre‐anesthetic medication. Study design Randomized prospective clinical study. Animals One hundred and sixteen dogs (ASA I or II), admitted for elective surgical procedures. The dogs were a mixed population of males and females, purebreds and mixed breeds, 0.25–13.4 years of age, weighing 1.8–57.7 kg. Methods A prospective clinical trial in which the dogs were randomly assigned to one of three groups. All groups received acepromazine (0.05 mg kg^?1 intramuscularly (IM)). Group I received acepromazine 15 minutes prior to opioid administration. Group II received acepromazine in combination with the opioid. Group III received acepromazine 15 minutes after opioid administration. One of three different opioids was administered IM to each dog: morphine sulfate at 0.5 mg kg^?1; hydromorphone hydrochloride at 0.1 mg kg^?1; or oxymorphone hydrochloride at 0.075 mg kg^?1. Results Dogs receiving acepromazine before the opioid (group I) had a significantly lower incidence of vomiting (18%) than dogs in groups II (45%) and III (55%). The degree of sedation was significantly lower in the dogs receiving the combination of acepromazine and the opioid (group II) than in dogs receiving the opioid as the first drug (group III). Conclusions and clinical relevance Acepromazine administered 15 minutes before the opioid lowers the incidence of vomiting induced by opioids.     

Incisional block with bupivacaine for analgesia after celiotomy in dogs

A blind, placebo-controlled clinical trial was performed to evaluate the postoperative analgesic effect of preoperative infiltration of the incision site with bupivacaine in dogs undergoing celiotomy. Sixty dogs were randomly allocated into four groups: preoperative bupivacaine, postoperative bupivacaine, preoperative saline, and postoperative saline. All dogs were premedicated with acepromazine and meperidine; then they were anesthetized with thiopentone and isoflurane. Each group received either bupivacaine or normal saline before midline incision or just before skin closure. After surgery, pain scores were assigned using a numerical rating scale. Preoperative bupivacaine was associated with significantly lower pain scores and a significantly lower need for opioid administration. The authors conclude that a preoperative incisional block with bupivacaine seems to be a useful adjunct for controlling pain after celiotomy in dogs.     

Double‐blinded cross‐over study on the efficacy of pentoxifylline for canine atopy

The pathogenesis of canine atopy has not been established completely. Recent studies have shown that tumour necrosis factor alpha and Interleukin‐6 play a role in allergic reactions in humans and mice. Pentoxifylline (PTX) suppresses synthesis of these cytokines and may be a useful therapy for modulating the symptoms of canine atopy. The objectives of this study were to investigate the effects of PTX (10mg kg^?1 twice daily for 4 weeks) on clinical signs (erythema and pruritus) and intradermal skin test reactivity in atopic dogs (n = 10). The study was a double‐blinded, placebo controlled, crossover clinical trial with a washout period of 2 weeks between treatments. Clinical signs were evaluated and scored by the investigator and owners. During PTX treatment, scores of pruritus and erythema decreased significantly. PTX did not affect intradermal skin test reactivity to house dust mite at 15 min (allergen of reference for this study).     

Evaluation of the arrhythmogenicity of a low dose of acepromazine: comparison with xylazine.

Alteration in the arrhythmogenic dose of epinephrine (ADE) was determined in 6 healthy dogs under halothane anesthesia following the administration of xylazine at 1.1 mg/kg i.v. and acepromazine at 0.025 mg/kg i.v. The order of treatment was randomly assigned with each dog receiving both treatments and testing was carried out on 2 separate occasions with at least a 1 wk interval. The ADE determinations were made prior to drug administration during halothane anesthesia (CNTL) and then 20 min and 4 h following drug treatment. Epinephrine was infused for 3 min at increasing dose rates (2.5, 5.0, 10.0 micrograms/kg/min) until the arrhythmia criterion (4 or more intermittent or continuous premature ventricular contractions) was reached within the 3 min of infusion or the 1 min following cessation. The interinfusion interval was 20 min. There was a significant difference (P = 0.0001) in the ADE determined following acepromazine administration at 20 min (20.95 micrograms/kg +/- 2.28 SEM) compared to CNTL (6.64 micrograms/kg +/- 1.09), xylazine at 20 min (5.82 micrograms/kg +/- 0.95) and 4 h (6.13 micrograms/kg +/- 1.05), and acepromazine at 4 h (7.32 micrograms/kg +/- 0.34). No other significant differences existed (P < 0.05). In this study we were unable to show any sensitization to epinephrine following xylazine administration during halothane anesthesia, while a protective effect was shown with a low dose of acepromazine.     

Evaluation of the analgesic properties of acepromazine maleate, oxymorphone, medetomidine and a combination of acepromazine-oxymorphone

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.     

Atopic dermatitis in Norwegian dogs

Of 122 dogs showing clinical symptoms of atopic dermatitis, 65.6% exhibited immediate skin test reactivity to one or more well defined allergen extracts, when intradermal skin tests were performed. The Prausnitz-Küstner test performed on two non-atopic recipient dogs, with serum from affected dogs, showed that "reaginic" antibodies transferred in serum from all affected dogs remained bound within the skin of the recipient dogs for 192 hours. House dust, house dust mite (D. farinae) and human dander were the allergens which most commonly caused immediate skin reactions and West Highland White Terriers and Boxers were the most affected breeds. Age at onset of clinical symptoms proved to be 1-4 year in 72.2% of the dogs.     

Immediate intradermal flea antigen reactivity in clinically normal adult dogs from south Florida, USA

Eighty-six clinically normal adult dogs from southern Florida, USA, with no history of dermatitis, were intradermally skin tested with Greer flea antigen 1:1000 w/v to determine the prevalence of positive immediate intradermal reactivity. This study describes the test group of animals and reports the prevalence of sensitivity to the Greer whole-body flea antigen in normal dogs living in a flea-rich environment. Similar to previous research, the highest prevalence of reactivity to flea antigen occurred at 3–4 years of age. The results indicate that 24% of clinically normal dogs from a flea-rich environment exhibited positive immediate skin test reactivity. These dogs had no clinical signs of flea allergic dermatitis (FAD) in spite of ongoing flea exposure. A 2-year follow-up telephone call to the owners of these flea antigen intradermal skin test (IDST)-positive dogs indicated that only two of 21 dogs had developed clinical signs of FAD.     

Effects of propofol-induced sedation on intradermal test reactions in dogs with atopic dermatitis

We compared the effect of propofol and saline control on intradermal test reactions in dogs with atopic dermatitis undergoing outpatient intradermal testing (IDT). Nineteen dogs were used in this clinical study. Patients were randomly allocated to receive either intravenous (IV) propofol or IV 0.9% saline, and IDT was performed on the right or left (randomized) lateral thorax. One investigator, unaware of the treatments, interpreted all IDT results. Injection sites were analysed using a subjective and objective method. A value of P or= 1+ on all dogs, significantly more positive sites were apparent during propofol sedation than during saline administration. In addition, the greater number of individual dogs experiencing more positive reactions >or= 1+ during propofol sedation was significant. When subjectively analysing reactions >or= 2+, the greater number of positive reactions and the greater number of dogs with more positive reactions observed during propofol treatment was not significantly different from the saline control. When analysed objectively, the greater number of positive reactions observed during propofol sedation was not significant. A greater number of dogs had higher subjective scores and larger objective measurements during propofol sedation compared with saline administration. In summary, propofol sedation was associated with an overall greater number of positive IDT reactions compared with the saline control. Although not always significant, this difference should be considered when choosing propofol for skin testing dogs with atopic dermatitis.     

Evaluation of two sedation protocols for use before diagnostic intra-articular anaesthesia in lame dogs

Objectives : To assess the influence of two sedation protocols on the degree of lameness in dogs. Methods : Fifty lame dogs were allocated to one of two sedation protocols. Group ACPM (acepromazine + methadone; n=25) was sedated with acepromazine and methadone. Group MED (medetomidine antagonised with atipamezole; n=25) was sedated with medetomidine and reversed with atipamezole. Each dog was evaluated for lameness before and after sedation using videotapes. Four experienced clinicians allocated global lameness scores before and after sedation to each dog using a numerical rating scale. Results : In 80% of the dogs in group ACPM and in 72% in group MED lameness was not affected by the sedation. In 12% of the dogs in group ACPM and 20% of the dogs in group MED the observers noticed an increase of lameness of 1 or 2 degrees on a scale of 0 to 10. In 8% of the dogs in both groups lameness decreased with 1 degree. Clinical Relevance : A possible diagnostic test for investigation of obscure lameness is intra‐articular anaesthesia. Sedation is necessary to allow intra‐articular injection. This study provided evidence that the effect of sedation with the proposed protocols on the degree of lameness is negligible.     

Cardiopulmonary and behavioral effects of combinations of acepromazine/butorphanol and acepromazine/oxymorphone in dogs.

Cardiopulmonary and behavioral effects of the following tranquilizer-opioid drug combinations were compared in conscious dogs: acepromazine (0.22 mg/kg of body weight, IV) and butorphanol (0.22 mg/kg, IV); acepromazine (0.22 mg/kg, IM) and butorphanol (0.22 mg/kg, IM); and acepromazine (0.22 mg/kg, IV) and oxymorphone (0.22 mg/kg, IV). Marked sedation and lateral recumbency that required minimal or no restraint was achieved with every drug combination. Analgesia was significantly better in dogs receiving oxymorphone than in dogs receiving butorphanol, as evaluated by response to toe pinch. There were no significant differences between the effects of the 3 drug combinations on heart rate, respiratory rate, arterial blood pressure, body temperature, and arterial pH, PCO2, PO2, and bicarbonate concentration. Heart rate, respiratory rate, and systolic arterial pressure decreased significantly over time with all drug combinations. Total recovery time (minutes from the initial injection to standing) was significantly longer in the dogs given acepromazine and oxymorphone.     

Evaluation of intraperitoneal and incisional lidocaine or bupivacaine for analgesia following ovariohysterectomy in the dog

Objective To determine if intraperitoneal (IP) and incisional (SC) lidocaine or bupivacaine provide analgesia following ovariohysterectomy (OHE). Study Design Prospective, randomized, controlled, blinded clinical trial. Animals Thirty dogs presenting to the Veterinary Teaching Hospital for elective OHE. Methods Dogs were pre‐medicated with acepromazine and butorphanol, induced with thiopental and maintained with isoflurane. They were randomly assigned to three groups: 10 received 8.8 mg kg^?1 2% lidocaine with epinephrine IP (LID); 10 received 4.4 mg kg^?1 0.75% bupivacaine IP (BUP); and 10 received 0.9% saline IP (SAL) upon completion of OHE. All IP doses were standardized to 0.88 mL kg^?1 with saline. An additional 2 mL of undiluted solution was placed SC prior to incisional closure. Dogs were scored at 0.5, 1, 2, 3, 6, 8 and 18 hours post‐extubation by one observer. Dogs were evaluated using a visual analogue scale (VAS) for pain and sedation, and a composite pain scale (CPS) that included physiologic and behavioral variables. Dogs were treated with 0.22 mg kg^?1 butorphanol + acepromazine if their VAS (pain) score was >50. Parametric variables were analyzed using Student's t‐test or repeated measures anova as appropriate. Non‐parametric variables were analyzed by χ²‐test. Results There were no significant differences in age, weight, incision length, surgery time, anesthesia time, or total thiopental dose among groups. Peak post‐surgical pain scores for all groups occurred at 0.5 hours and returned to baseline by 18 hours. Dogs in the BUP group had significantly lower VAS‐pain scores overall than dogs in the SAL group. Seven out of 10 dogs in the SAL group, 4/10 in the LID group and 2/10 in the BUP group were treated with supplemental acepromazine and butorphanol. No differences between groups were detected with the CPS. No adverse side‐effects were observed. Conclusions and clinical relevance Our findings support the use of IP and SC bupivacaine for post‐operative analgesia following OHE in the dog.     

A retrospective study on the use of acepromazine maleate in dogs with seizures

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.     

The use of propofol for induction of anaesthesia in dogs premedicated with acepromazine, butorphanol and acepromazine-butorphanol

Cardiovascular, pulmonary and anaesthetic-analgesic responses were evaluated in 18 male and female dogs to determine the effect of the injectable anaesthetic propofol used in conjuction with acepromazine and butorphanol. The dogs were randomly divided into three groups. Dogs in Group A were premeditated with 0.1 mg/kg of intramuscular acepromazine followed by an induction dose of 4.4 mg/kg of intravenous propofol; Group B received 0.2 mg/kg of intramuscular butorphanol and 4.4 mg/kg of intravenous propofol; dogs in Group AB were administered a premeditation combination of 0.1 mg/kg of intramuscular acepromazine and 0.2 mg/kg of intramuscular butorphanol, followed by induction with 3.3 mg/kg of intravenous propofol. The induction dose of propofol was given over a period of 30-60 seconds to determine responses and duration of anaesthesia. Observations recorded in the dogs included heart and respiratory rates, indirect arterial blood pressures (systolic, diastolic and mean), cardiac rhythm, end-tidal CO, tension, oxygen saturation, induction time, duration of anaesthesia, recovery time and adverse reactions. The depth of anaesthesia was assessed by the response to mechanical noxious stimuli (tail clamping), the degree of muscle relaxation and the strength of reflexes. Significant respiratory depression was seen after propofol induction in both groups receiving butorphanol with or without acepromazine. The incidence of apnea was 4/6 dogs in Group B, and 5/6 dogs in Group AB. The incidence of apnea was also correlated to the rate of propofol administration. Propofol-mediated decreases in arterial blood pressure were observed in all three groups. Moderate bradycardia (minimum value > 55 beats/min) was observed in both Groups B and AB. There were no cardiac dysrhythmias noted in any of the 18 dogs. The anaesthetic duration and recovery times were longer in dogs premeditated with acepromazine/butorphanol.