Association of acepromazine with propofol in giant amazon turtles Podocnemis expansa reared in captivity

PURPOSE: To evaluate the effects of different concentrations of an anesthetic association in giant amazon turtles (Podocnemis expansa).METHODS: Twenty healthy P. expansa of both sexes weighing between 1.0 and 1.5kg commercially bred in the Araguaia River Valley, Goias, Brazil, were separated into two groups (G1 n=10 and G2 n=10). Each group received a respective protocol: P1=acepromazine (0.5 mg/kg IM) and propofol (5 mg/kg IV) and P2=acepromazine (0.5 mg/kg IM) and propofol (10 mg/kg IV). The acepromazine was administered in the left thoracic member and the propofol in the cervical vertebral sinus. Assessments were made of the anesthetic parameters of locomotion, muscle relaxation, response to pain stimuli in the right thoracic and pelvic members and heartbeat.RESULTS: The anesthetic induction time was the same for both protocols (P1 and P2); however the P2 effects were of a longer duration.CONCLUSION: The sedation achieved with both protocols (P1 and P2) were satisfactory for the biological sample collection, physical examinations and minor surgeries on this species.

Comparative study on the sedative effects of morphine, methadone, butorphanol or tramadol, in combination with acepromazine, in dogs

To compare the effects of morphine (MOR), methadone (MET), butorphanol (BUT) and tramadol (TRA), in combination with acepromazine, on sedation, cardiorespiratory variables, body temperature and incidence of emesis in dogs.Prospective randomized, blinded, experimental trial.Six adult mixed-breed male dogs weighing 12.0 +/- 4.3 kg.Dogs received intravenous administration (IV) of acepromazine (0.05 mg kg(-1)) and 15 minutes later, one of four opioids was randomly administered IV in a cross-over design, with at least 1-week intervals. Dogs then received MOR 0.5 mg kg(-1); MET 0.5 mg kg(-1); BUT 0.15 mg kg(-1); or TRA 2.0 mg kg(-1). Indirect systolic arterial pressure (SAP), heart rate (HR), respiratory rate (f(R)), rectal temperature, pedal withdrawal reflex and sedation were evaluated at regular intervals for 90 minutes.Acepromazine administration decreased SAP, HR and temperature and produced mild sedation. All opioids further decreased temperature and MOR, BUT and TRA were associated with further decreases in HR. Tramadol decreased SAP whereas BUT decreased f(R) compared with values before opioid administration. Retching was observed in five of six dogs and vomiting occurred in one dog in MOR, but not in any dog in the remaining treatments. Sedation scores were greater in MET followed by MOR and BUT. Tramadol was associated with minor changes in sedation produced by acepromazine alone.When used with acepromazine, MET appears to provide better sedation than MOR, BUT and TRA. If vomiting is to be avoided, MET, BUT and TRA may be better options than MOR.

Effects of methadone, alone or in combination with acepromazine or xylazine, on sedation and physiologic values in dogs

Objective To evaluate the effects of methadone, administered alone or in combination with acepromazine or xylazine, on sedation and on physiologic values in dogs.Study design Randomized cross-over design.Animals Six adult healthy mixed-breed dogs weighing 13.5 +/- 4.9 kg.Methods Dogs were injected intramuscularly with physiologic saline (Control), or methadone (0.5mg kg(-1)) or acepromazine (0.1 mg kg(-1)) or xylazine (1.0 mg kg(-1)), or acepromazine (0.05 mg kg(-1)) plus methadone (0.5 mg kg(-1)) or xylazine (0.5 mg kg(-1)) plus methadone (0.5 mg kg(-1)) in a randomized cross-over design, with at least 1-week intervals. Sedation, pulse rate, indirect systolic arterial pressure, respiratory rate (RR), body temperature and pedal withdrawal reflex were evaluated before and at 15-minute intervals for 90 minutes after treatment.Results Sedation was greater in dogs receiving xylazine alone, xylazine plus methadone and acepromazine plus methadone. Peak sedative effect occurred within 30 minutes of treatment administration. Pulse rate was lower in dogs that received xylazine either alone or with methadone during most of the study. Systolic arterial pressure decreased only in dogs receiving acepromazine alone. When methadone was administered alone, RR was higher than in other treatments during most of the study and a high prevalence of panting was observed. In all treatments body temperature decreased, this effect being more pronounced in dogs receiving methadone alone or in combination with acepromazine. Pedal withdrawal reflex was absent in four dogs receiving methadone plus xylazine but not in any dog in the remaining treatments.Conclusions Methadone alone produces mild sedation and a high prevalence of panting. Greater sedation was achieved when methadone was used in combination with acepromazine or xylazine. The combination xylazine-methadone appears to result in better analgesia than xylazine administered alone. Both combinations of methadone/sedative were considered effective for premedication in dogs.

Effect of intravenous propofol and remifentanil on heart rate, blood pressure and nociceptive response in acepromazine premedicated dogs

ObjectiveTo investigate the cardiorespiratory, nociceptive and endocrine effects of the combination of propofol and remifentanil, in dogs sedated with acepromazine.Study designProspective randomized, blinded, cross-over experimental trial.AnimalsTwelve healthy adult female cross-breed dogs, mean weight 18.4 +/- 2.3 kg.MethodsDogs were sedated with intravenous (IV) acepromazine (0.05 mg kg-1) followed by induction of anesthesia with IV propofol (5 mg kg-1). Anesthesia was maintained with IV propofol (0.2 mg kg-1 minute-1) and remifentanil, infused as follows: R1, 0.125 mu g kg-1 minute-1; R2, 0.25 mu g kg-1 minute-1; and R3, 0.5 mu g kg-1 minute-1. The same dogs were administered each dose of remifentanil at 1-week intervals. Heart rate (HR), mean arterial pressure (MAP), respiratory rate (f(R)), end tidal CO(2) (Pe'CO(2)), arterial hemoglobin O(2) saturation, blood gases, and rectal temperature were measured before induction, and 5, 15, 30, 45, 60, 75, 90, and 120 minutes after beginning the infusion. Nociceptive response was investigated by electrical stimulus (50 V, 5 Hz and 10 ms). Blood samples were collected for plasma cortisol measurements. Statistical analysis was performed by anova (p < 0.05).ResultsIn all treatments, HR decreased during anesthesia with increasing doses of remifentanil, and increased significantly immediately after the end of infusion. MAP remained stable during anesthesia (72-98 mmHg). Antinociception was proportional to the remifentanil infusion dose, and was considered satisfactory only with R2 and R3. Plasma cortisol concentration decreased during anesthesia in all treatments. Recovery was smooth and fast in all dogs.Conclusions and clinical relevanceInfusion of 0.25-0.5 mu g kg-1 minute-1 remifentanil combined with 0.2 mg kg-1 minute-1 propofol produced little effect on arterial blood pressure and led to a good recovery. The analgesia produced was sufficient to control the nociceptive response applied by electrical stimulation, suggesting that it may be appropriate for performing surgery.

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 alpha(2)-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 mu g/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 alpha(2)-agonist-induced bradycardia and increased the severity and duration of the hypertension, but acepromazine did not substantially modify the cardiovascular effects of the a2-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.

Antinociceptive effects of tramadol and acepromazine in cats

Effects of tramadol and acepromazine on pressure and thermal thresholds were examined in eight cats. After baseline measurements, subcutaneous (SC) tramadol 1 mg/kg, acepromazine 0.1 mg/kg, tramadol 1 mg/kg with acepromazine 0.1 mg/kg, or saline 0.3 ml were given. Serial measurements were made for 24 h. Mean thermal thresholds did not change significantly [analysis of variance (ANOVA)] from baseline. The maximum thermal threshold increase above baseline was 2.8 +/- 2.8 degrees C at 6 h (P > 0.05) after tramadol; it was above the 95% confidence interval (0) at 0.75, 3 and 6 h. Pressure thresholds increased above baseline from 0.25 to 2 h after acepromazine (P < 0.05) and from 0.5 to 3 h after the combination (P < 0.05), with a maximum increase of 132 +/- 156 mmHg 0.25 h after acepromazine and 197 129 mmHg 0.5 h after the combination. Pressure thresholds were above the 95% Cl from 0.25 to 2 h after acepromazine and from 0.5 to 3 h after the combination. SC tramadol at 1 mg/kg in cats had limited effect on thermal and pressure nociception, but this was enhanced by acepromazine. Acepromazine alone had pressure antinociceptive effects. (c) 2007 ESFM and AAFR Published by Elsevier Ltd. All rights reserved.

Comparison of pharmacopuncture, aquapuncture and acepromazine for sedation of horses

Pharmacopuncture, the injection of subclinical doses of drugs into acupoints reduces drug undesirable side effects, residues in animal consumption products and treatment costs in large animals. Acepromazine (Acp) produces several undesirable effects, such as hypotension. Previous studies with the injection of 1/10 of Acp dose in dog acupoints showed its advantage for sedation, minimizing undesirable effects. Eight horses were randomly submitted to four different treatment protocols according to a Latin Square double-blind design: (i) 0.1 ml kg(1) of saline subcutaneously injected at the cervical region, (ii) 0.1 mg kg(1) of Acp injected subcutaneously at the cervical region, (iii) 0.01 ml kg(1) of saline injected into GV1 acupoint (aquapuncture) and (iv) 0.01 mg kg(1) of Acp injected into GV1 acupoint (pharmacopuncture). Heart rate, respiratory rate, head height and degree of sedation were measured before and at 30, 60 and 90 min after treatments. Signs of sedation were observed in all treated groups at 30 min and only in 1/10Acp-GV1 at 60 min after the treatments. Only the group treated with 0.1 mg kg(1) of Acp s.c. had significantly lower values of head height at 30 min. Respiratory rate tended to reduce in all groups but was significantly lower only in horses treated with 0.1 mg kg(1) of Acp s.c. Heart rate remained unchanged in all groups. Acp-pharmacopuncture on GV1 in horses produced a mild sedation when compared with the conventional dose of Acp. More investigations are necessary to determine the optimal dosage of Acp-pharmacopuncture for sedation in horses.

Antinociceptive effects of methadone combined with detomidine or acepromazine in horses

To investigate two protocols to provide antinociception in horses. To evaluate the antinociceptive effects of intravenous methadone combined with detomidine or acepromazine in adult horses. Randomised, blinded, crossover study. Mechanical, thermal and electrical stimuli were applied to the dorsal left and right metacarpus and coronary band of the left thoracic limb, respectively. A thermal stimulus was applied caudal to the withers. The horses were treated with saline (C), a combination of methadone (0.2 mg/kg bwt) and detomidine (10 μg/kg bwt) (MD) or methadone (0.2 mg/kg bwt) and acepromazine (0.05 mg/kg bwt) (MA) at 1 week intervals. Nociceptive thresholds were measured before and at 15 min intervals until 150 min after treatment. Wilcoxon rank-sum and Wilcoxon signed rank tests were used to compare data between groups at each time point and over time within each group, followed by the Bonferroni method to adjust the P value. The mechanical stimulus was the most sensitive test to differentiate the antinociceptive effects of the treatments. Mechanical thresholds were greater after MD than MA between 15 and 30 min and with both MD and MA these thresholds were greater than C from 15 to 60 min. Electrical and thermal limb thresholds were greater after MD than C at 15 and 45 min and at 15, 30, 45, 75 and 105 min, respectively. Thermal limb thresholds were greater with MA than C at 30 min. Thoracic thermal threshold in MD and MA were higher than C at 45, 75, 90 and 120 min and from 30 to 75 min, respectively. Methadone and acepromazine produced less pronounced mechanical antinociception than MD.

Splenic congestion associated with acepromazine administration in dogs

The effects splenic dilatation induced by acepromazine in a prospective, randomized study. Thirtythree adult mongrel dogs were divided into two groups designated as AG (acepromazine 0.05 mg/kg, i.v., n = 23) and CG (0.9% sodium chloride administered at a similar volume, n = 10). In both groups underwent sonographic examinations before (T0) and fifteen minutes (T15) after drug injection. The thickness spleen and splenic vein width were measured. Higher thickness was found in the AG group at T15 (2.47 cm) when compared to that at T0 (2.06 cm, p = 0.016), while the T0 (2.33 cm) and T15 (2.39 cm) measures did not differ within the CG group. Moreover, the splenic vein width was higher (p = 0.013) at T15 than at T0 in the AG group. Based on results of this study, we concluded that acepromazine, in doses of 0.05 mg/kg, promotes splenomegaly in dogs after fifteen minutes of the injection.

Modulation of nociceptive withdrawal reflexes evoked by single and repeated nociceptive stimuli in conscious dogs by low-dose acepromazine

OBJECTIVES: To investigate the modulation of the nociceptive withdrawal reflex (NWR) and temporal summation (TS) by low-dose acepromazine (ACP) in conscious dogs. To assess the short- and long-term stability of the reflex thresholds. STUDY DESIGN: Randomized, blinded, placebo-controlled cross-over experimental study. ANIMALS: Eight adult male Beagles. METHODS: The NWR was elicited using single transcutaneous electrical stimulation of the ulnar nerve. Repeated stimuli (10 pulses, 5 Hz) were applied to evoke TS. The responses of the deltoideus muscle were recorded and quantified by surface electromyography and the behavioural reactions were scored. Each dog received 0.01 mg kg(-1) ACP or an equal volume saline intravenously (IV) at 1 week intervals. Measurements were performed before (baseline) and 20, 60 and 100 minutes after drug administration. Sedation was scored before drug administration and then at 10 minutes intervals. Data were analyzed with Friedman repeated measures analysis of variance on ranks and Wilcoxon signed rank tests. RESULTS: Acepromazine resulted in a mild tranquilization becoming obvious at 20 minutes and peaking 30 minutes after injection. Single (I(t)) and repeated stimuli (TS(t)) threshold intensities, NWR and TS characteristics and behavioural responses were not affected by the ACP at any time point. Both I(t) and TS(t) were stable over time. CONCLUSIONS AND CLINICAL RELEVANCE: In dogs, 0.01 mg kg(-1) ACP IV had no modulatory action on the NWR evoked by single or repeated stimuli, suggesting no antinociceptive activity on phasic nociceptive stimuli. The evidence of the stability of the NWR thresholds supports the use of the model as an objective tool to investigate nociception in conscious dogs. A low dose of ACP administered as the sole drug, can be used to facilitate the recordings in anxious subjects without altering the validity of this model.

Safety, tolerability, and efficacy of fixed combination therapy with dorzolamide hydrochloride 2% and timolol maleate 0.5% in glaucoma and ocular hypertension.

Glaucoma is a collection of diseases characterized by multifactorial progressive changes leading to visual field loss and optic neuropathy most frequently due to elevated intraocular pressure (IOP). The goal of treatment is the lowering of the IOP to prevent additional optic nerve damage. Treatment usually begins with topical pharmacological agents as monotherapy, progresses to combination therapy with agents from up to 4 different classes of IOP-lowering medications, and then proceeds to laser or incisional surgical modalities for refractory cases. The fixed combination therapy with the carbonic anhydrase inhibitor dorzolamide hydrochloride 2% and the beta blocker timolol maleate 0.5% is now available in a generic formulation for the treatment of patients who have not responded sufficiently to monotherapy with beta adrenergic blockers. In pre- and postmarketing clinical studies, the fixed combination dorzolamide-timolol has been shown to be safe and efficacious, and well tolerated by patients. The fixed combination dorzolamide-timolol is convenient for patients, reduces their dosing regimen with the goal of increasing their compliance, reduces the effects of "washout" when instilling multiple drops, and reduces the preservative burden by reducing the number of drops administered per day.

Perioperative use of crystalloids in patients undergoing open radical cystectomy: balanced Ringer's maleate versus a glucose 5%/potassium-based balanced solution: study protocol for a randomized controlled trial

BACKGROUND The optimal crystalloid solution to use perioperatively in patients undergoing open radical cystectomy remains unclear. Many of the fluids used for intravenous hydration contain supraphysiologic concentrations of chloride, which can induce hyperchloremia and metabolic acidosis, resulting in renal vasoconstriction and decreased renal function. In addition, patients receiving less fluid and less sodium show faster recovery of gastrointestinal (GI) function after colonic surgery. METHODS AND DESIGN This is an investigator-initiated, single-center, randomized, controlled, parallel group trial with assessor-blinded outcome assessment, in the Department of Urology, University Hospital Bern, Switzerland. The study will involve 44 patients with bladder cancer scheduled for radical cystectomy and urinary diversion. The primary outcome is the duration between the end of surgery and the return of the GI function (first defecation). Secondary outcomes are fluid balance (body weight difference postoperatively versus preoperatively) and the incidence of kidney function disorders according to the Risk-Injury-Failure-Loss-End Stage Renal Disease (RIFLE classification). An equal number of patients are allocated to receive Ringerfundin® solution or a glucose/potassium-based balanced crystalloid solution as baseline infusion during the entire time that intravenous administration of fluid is necessary during the perioperative period. The randomized crystalloid solution is infused at a rate of 1 ml/kg/h until the bladder has been removed, followed by 3 ml/kg/h until the end of surgery. Postoperative hydration is identical in both groups and consists of 1,500 ml of the randomized crystalloid solution per 24 hours. Postoperative patient care is identical in both groups; patients are allowed to drink clear fluids immediately after surgery, and liquid diet is started on postoperative day 1, as well as active mobilization and the use of chewing gum. Body weight is measured daily in the morning. Time of first flatus and first defecation are recorded. DISCUSSION This trial assesses the benefits and harms of two different balanced crystalloid solutions for perioperative fluid management in patients undergoing open radical cystectomy with urinary diversion, with regard to return of GI function and effects on postoperative renal function. TRIAL REGISTRATION Current Controlled Trials ISRCTN32976792 (registered on November 21 2013).