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At least 19 recordsLinked to original sources
PubMed1999

A previously unidentified acepromazine metabolite in humans: implications for the measurement of acepromazine in blood.

High-performance liquid chromatography-diode-array detection results obtained during the investigation of two cases involving acepromazine prompted us to study the stability of the drug in blood. It was found that acepromazine can undergo in vitro conversion by human red blood cells to 2-(1-hydroxyethyl)promazine, a product that has been reported as a minor urinary metabolite in horse urine but not previously identified in humans. Further, our analytical findings in the two cases examined suggest that 2-(1-hydroxyethyl)promazine may be the major unconjugated metabolite of acepromazine in humans. These findings have important implications for the analytical toxicology of acepromazine.

Acepromazine↗
PubMed1997

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.

Journal Article↗
PubMed1992

Analgesia and behavioral responses of dogs given oxymorphone-acepromazine and meperidine-acepromazine after methoxyflurane and halothane anesthesia.

This study was designed to test analgesia, duration, and cardiovascular changes induced by meperidine (MEP) and oxymorphone (OXY) following methoxyflurane (MOF) and halothane (HAL) anesthesia. Eight healthy dogs were given atropine and acepromazine, and anesthesia was induced with thiamylal and maintained with 1.5 minimal alveolar concentration of MOF or HAL for 1 hour during controlled ventilation. Eight treatments were given with each anesthetic: 3 with MEP (0.5, 1.0, and 2.0 mg/kg, IV), 3 with oxymorphone (OXY; 0.05, 0.1, and 0.2 mg/kg, IV), and 2 placebos with sterile water. Test drugs were given at the end of anesthesia when early signs of recovery were evident. Minimal threshold stimulus/response nociception was assessed by use of an inflatable soft plastic colonic balloon. Blood pressures and pulse rate were measured with a noninvasive monitor. Meperidine and OXY were found to be effective analgesics and could be reversed with naloxone. Intravenous administration of 2.0 mg of MEP/kg provided analgesia for 36 +/- 6 minutes and 39 +/- 15 minutes after MOF and HAL, respectively. In contrast, OXY was effective at all 3 doses with effects of IV administration of 0.2 mg of OXY/kg lasting 154 +/- 13 minutes and 152 +/- 12 minutes, after MOF and HAL, respectively. Analgesia could not be demonstrated after anesthesia for acepromazine, MOF, or HAL. Blood pressure was not changed by either anesthetic nor was it influenced by MEP or OXY. Pulse rate was significantly depressed by the higher doses of OXY following HAL, but was not changed by MEP following either anesthetic.(ABSTRACT TRUNCATED AT 250 WORDS)

Acepromazine↗
PubMedDate not supplied

A clinical comparison of oxymorphone-acepromazine and butorphanol-acepromazine sedation in dogs.

Oxymorphone (0.2 mg/kg, maximum 4.5 mg) or butorphanol (0.2 mg/kg, maximum 4.5 mg), with acepromazine (0.05 mg/kg) and atropine (0.02 mg/kg), was administered intravenously to 106 healthy dogs undergoing radiographic examination of the pelvis. The dogs were returned to their owners after the examination and opioid reversal with naloxone (0.02 mg/kg intravenously, maximum 0.4 mg). Questionnaires were completed by the radiology staff and owners of the dogs, and results were coded by one person, all of whom were unaware of the treatment used. There was a lower incidence of temporary excitement upon injection and less panting in dogs sedated with butorphanol than with oxymorphone. There were no significant differences in degree of sedation, response to noise or manipulation, vocalization, defecation, heart rate, reversibility, sedation after reversal, or personality. Both forms of chemical restraint were satisfactory for radiographic examination of the pelvis, with no significant side effects in healthy dogs.

Acepromazine↗
PubMed1988

Immunoassay detection of drugs in racing horses. VII. Detection of acepromazine in equine urine and blood by ELISA and PCFIA.

We have developed and evaluated a one step enzyme-linked immunosorbent assay (ELISA) test and a particle concentration fluorescence immunoassay (PCFIA) test for acepromazine as part of a panel of pre- and post-race tests for illegal medications in racing horses. These tests are rapid, sensitive and economical and development of the tests occurred in less than seven months. The ELISA test detects acepromazine with an I-50 of about 150 pg/ml. In vivo, it readily detects the presence of acepromazine or its metabolites in equine blood and urine from 8 to 72 hours or longer, respectively, after administration of sub-therapeutic doses. In vitro, the ELISA test cross-reacts with analogs of acepromazine, suggesting that it will also detect the use of other phenothiazine tranquilizers. The PCFIA test detects acepromazine with an I-50 of about 10 ng/ml. When applied to pre-race screening of serum samples as part of the pre-race testing program at a midwestern racetrack, the PCFIA test detected a number of cases of acepromazine abuse. Screening of stored post-race urine samples from associated horses by the ELISA test 'flagged' numerous samples for acepromazine, suggesting a pattern of acepromazine abuse. To date about twenty of these acepromazine flagged samples have been confirmed positive on mass spectrometry. As such the ELISA and PCFIA tests described in this communication are capable of substantially improving the quality of pre- and post-race testing programs for phenothiazine tranquilizers in racing horses.

Acepromazine↗
PubMed2004

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 (i.m.)). 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 i.m. 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.

Acepromazine↗
PubMedDate not supplied

Effects of acepromazine on three-phase 99mTc-MDP bone imaging in 11 horses.

Horses undergoing skeletal scintigraphy can have decreased radiopharmaceutical bone uptake in the limbs. This reduces the diagnostic value of the scan. The aim of the present study was to measure the changes in count density caused by vasodilatation and increased blood flow associated with intravenous injection of acepromazine during bone scintigraphy in normal horses. A three-phase bone scan was performed twice in 11 adult horses to study the effects of acepromazine on the count density of the resultant scintigrams. With acepromazine, there was a statistically significant mean difference of 12 s for initial blood flow and 21 s for peak flow. The time to initial blood flow and time to peak flow occurred earlier for the scans in which acepromazine was used. There were no significant differences in the bone to soft tissue ratios during the soft tissue and bone phases of the scan between procedures. Intravenous administration of acepromazine increases peripheral blood flow causing an earlier onset of the vascular phase during the three-phase bone scan. Acepromazine did not increase the count density of the bone phase scintigrams. As expected, the vasodilatation and increased blood flow associated with intravenous injection of acepromazine affected the count density of the vascular phase of the bone scan.

Acepromazine↗
PubMed1982

The pharmacokinetics, pharmacological responses and behavioral effects of acepromazine in the horse.

After intravenous (i.v.) injection, acepromazine was distributed widely in the horse (Vd = 6.6 litres/kg) and bound extensively (greater than 99%) plasma proteins. Plasma levels of drug declined with an alpha half-life of 4.2 min, while the beta phase or elimination half-life was 184.8 min. At a dosage level of 0.3 mg/kg acepromazine was detectable in the plasma for 8 h post dosing. The whole blood partitioning of acepromazine was 46% in the plasma phase and 54% in the erythrocyte phase. Penile prolapse was clearly evident at doses from 0.01 mg/kg to 0.4 mg/kg i.v., and the duration and extent of protrusion were dose related. Hematocrit levels were significantly lowered by administration of 0.002 mg/kg i.v. (about 1 mg to a 500 kg horse) and increasing dosages resulted in greater than 20% lowering of the hematocrit from control levels. Pretreatment of horses with acepromazine also reduced the variable interval (VI 60) responding rate in all horses tested. These data show that hematocrit changes are the most sensitive pharmacological responses to acepromazine, followed by changes in penile extension, respiratory rate, VI responding and locomotor responses. Acepromazine is difficult to detect in plasma at normal clinical doses. However, because of its large volume of distribution, its urinary elimination is likely prolonged, and further work on its elimination in equine urine is required.

Acepromazine↗
PubMed2005

Effects of acepromazine on pulmonary gas exchange and circulation during sedation and dissociative anaesthesia in horses.

OBJECTIVE: To study pulmonary gas exchange and cardiovascular responses to sedation achieved with romifidine and butorphanol (RB) alone, or combined with acepromazine, and during subsequent tiletamine-zolazepam anaesthesia in horses. ANIMALS: Six (four males and two females) healthy Standardbred trotters aged 3-12 years; mass 423-520 kg. STUDY DESIGN: Randomized, cross-over, experimental study. MATERIALS AND METHODS: Horses were anaesthetized on two occasions (with a minimum interval of 1 week) with intravenous (IV) tiletamine-zolazepam (Z; 1.4 mg kg(-1)) after pre-anaesthetic medication with IV romifidine (R; 0.1 mg kg(-1)) and butorphanol (B; 25 microg kg(-1) IV). At the first trial, horses were randomly allocated to receive (protocol ARBZ) or not to receive (protocol RBZ) acepromazine (A; 35 microg kg(-1)) intramuscularly (IM) 35 minutes before induction of anaesthesia. Each horse was placed in left lateral recumbency and, after tracheal intubation, allowed to breathe room air spontaneously. Respiratory and haemodynamic variables and ventilation-perfusion (; multiple inert gas elimination technique) ratios were determined in the conscious horse, after sedation and during anaesthesia. One- and two-way repeated-measures anova were used to identify within- and between-technique differences, respectively. RESULTS: During sedation with RB, arterial oxygen tension (PaO(2)) decreased compared to baseline and increased mismatch was evident; there was no O(2) diffusion limitation or increase in intrapulmonary shunt fraction identified. With ARB, PaO(2) and remained unaffected. During anaesthesia, intrapulmonary shunt occurred to the same extent in both protocols, and mismatching increased. This was less in the ARBZ group. Arterial O(2) tension decreased in both protocols, but was lower at 25 and 35 minutes of anaesthesia in RBZ than in ARBZ. During sedation, heart rate (HR) and cardiac output (Qt) were lower while arterial-mixed venous oxygen content differences and haemoglobin concentrations were higher in RBZ compared with ARBZ. Total systemic vascular resistance, mean systemic, and mean pulmonary arterial pressures were higher during anaesthesia with RBZ compared to ARBZ. CONCLUSIONS AND CLINICAL RELEVANCE: Acepromazine added to RB generally improved haemodynamic variables and arterial oxygenation during sedation and anaesthesia. Arterial oxygenation was impaired as a result of increased shunt and mismatch during anaesthesia, although acepromazine treatment reduced disturbances and falls in PaO(2) to some extent. Haemodynamic variables were closer to baseline during sedation and anaesthesia when horses received acepromazine. Acepromazine may confer advantages in healthy normovolaemic horses.

Acepromazine↗
PubMed2002

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.

Acepromazine↗
PubMed2004

Investigation of the effect of acepromazine on intravenous glucose tolerance tests in dogs.

OBJECTIVE: To investigate the effects of administration of acepromazine on IV glucose tolerance tests (IVGTTs) in dogs. ANIMALS: 8 male mixed-breed dogs. PROCEDURE: With a 1-week interval between tests, each dog underwent (in random order) an IVGTT with or without pretest administration of acepromazine maleate (0.1 mg/kg, SC, 30 minutes prior to the start of the IVGTT). Food was withheld from the dogs for 14 hours prior to each test. Blood samples were obtained at 20, 10, and 1 minute prior to and at 2, 3, 4, 5, 6, 8, 10, 12, 14, 16, 19, 22, 25, 30, 40, 50, 60, 70, 80, 90, 100, 120, 140, 160, and 180 minutes after administration of glucose. RESULTS: There were no significant differences in the baseline (ie, after food was withheld) plasma glucose, lactate, and insulin concentrations between dogs undergoing the IVGTT and acepromazine-IVGTT; however, lower baseline free fatty acid concentration was observed in acepromazine-treated dogs. Analysis of data via the application of Bergman's minimal model of glucose kinetics revealed no differences in insulin sensitivity, acute insulin response to glucose, disposition index, or glucose effectiveness between dogs treated or not treated with acepromazine before testing. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicated that in dogs undergoing IV glucose tolerance testing, pretest administration of small doses of acepromazine can be used as a means of chemical restraint without interfering with results of the glucose metabolism assessment.

Acepromazine↗
PubMed1984

Reversal of pentobarbital anesthesia with 4-aminopyridine and yohimbine in cats pretreated with acepromazine and xylazine.

In 2 separate experiments, groups of atropinized cats (6 cats/group) were given acepromazine (0.25 mg/kg of body weight) or xylazine (2.2 mg/kg) IM and anesthetized with pentobarbital. The mean dose of pentobarbital was decreased approximately 36% by acepromazine, and approximately 80% by xylazine, compared with published doses. Anesthetized cats were given IV saline solution (control groups) or were given the antagonists 4-aminopyridine (4-AP; 0.5 mg/kg), yohimbine (0.4 mg/kg), or 4-AP + yohimbine (0.5 mg/kg and 0.4 mg/kg, respectively). In acepromazine-treated cats, 4-AP + yohimbine was the most effective antagonist; arousal and walking occurred in an average of 10.4 minutes and 91.7 minutes, respectively. Yohimbine enhanced the antagonistic effects of 4-AP. In xylazine-treated cats, yohimbine was an effective antagonist; arousal and walking occurred in an average of 2.8 minutes and 12.8 minutes, respectively. Yohimbine did not enhance the antagonistic effects of 4-AP. Mean respiratory rates were decreased by acepromazine, but were increased by xylazine. Thus, respiratory rate depression by pentobarbital was not as marked with xylazine as it was with acepromazine. Changes in mean heart rate were not remarkable with either sedative, and cardiac irregularities were not palpated or auscultated. In healthy cats, the duration of pentobarbital anesthesia can be controlled by 4-AP + yohimbine (acepromazine-pretreated cats) or by yohimbine alone (xylazine-pretreated cats).

4-Aminopyridine↗
PubMed2003

Changes in intraocular pressure and pupil size following intramuscular administration of hydromorphone hydrochloride and acepromazine in clinically normal dogs.

OBJECTIVE: To investigate the effects of intramuscularly administered hydromorphone hydrochloride and acepromazine on intraocular pressure (IOP) and pupil size (PS). ANIMALS STUDIED: Seventeen dogs free of clinically relevant ocular abnormalities. PROCEDURE: Measurements of IOP and PS were obtained and the dogs were injected intramuscularly with hydromorphone (0.04-0.08 mg/kg) and acepromazine (0.04 mg/kg). Measurements of IOP and PS were repeated 10 min and 25 min later. RESULTS: Though a decreasing trend in IOP values was demonstrated, no significant difference was noted in IOP from the initial examination to examination following intramuscular administration of hydromorphone and acepromazine. Significant miosis was present in 16 of 17 dogs at 10 min and 25 min following administration of hydromorphone and acepromazine. CONCLUSION: Hydromorphone (0.04-0.08 mg/kg) and acepromazine (0.04 mg/kg) cause significant miosis in dogs at 10 and 25 min following intramuscular administration.

Acepromazine↗
PubMedDate not supplied

Suicide with the veterinary drug acepromazine.

A suicide case involving the veterinary drug acepromazine is described. After a single-step liquid alkaline extraction, acepromazine was identified in a chest-cavity blood sample using gas chromatography (GC) with nitrogen-phosphorus (NPD) and mass selective detectors. Acepromazine was then quantitated in the blood and other postmortem tissues by GC with NPD using chlorpromazine as the internal standard. Acepromazine concentrations in the chest-cavity blood, liver, brain, and bile were 0.6, 3.0, 0.4, and 6.5 micrograms/mL, respectively. The stomach contents contained a total of 2.5 mg acepromazine.

Acepromazine↗
PubMed1979

Modification of the cardiotoxic effects of ouabain by acepromazine, tetrodotoxin and magnesium sulphate.

Acepromazine (500 microgram), tetrodotoxin (0.5 microgram) and magnesium sulfate (7.5 mg twice) given intracerebroventricularly increased the doses of ouabain given by continuous intravenous infusion, required to induce arrhythmias and death. Acepromazine (150 microgram kg-1) was also effective when administered intravenously. Acepromazine (1.5 mg kg-1) and tetrodotoxin (4-6 microgram kg-1) given intravenously did not protect against, and even increased, the toxicity of ouabain. Both substances decreased blood pressure and increased heart rate. Tetrodotoxin, but neither acepromazine nor magnesium sulphate given intracerebroventricularly, induced a decrease in the heart rate before ouabain infusion. Acepromazine (500 microgram) and tetrodotoxin (0.5 microgram), but not magnesium sulphate, given intracerebroventricularly, decreased the blood pressure before ouabain infusion. The results are discussed in relation to the effects of those substances and ouabain on the circulation, and to the fact that the cardiac arrhythmias induced by high doses of ouabain and the protection obtained with tetrodotoxin and magnesium sulphate are, at least in part, mediated by the central nervous system.

Acepromazine↗
PubMed1985

Premedication of dogs with acepromazine or pentazocine before euthanasia with carbon monoxide.

Euthanasia of unwanted or sick animals should always be done in a humane manner. This study involving two groups of 12 dogs evaluated a two step method of euthanasia using first acepromazine or pentazocine then inhalation of carbon monoxide. During the experiment, behavioral reactions (anxiety, agitation, vocalization and sphincter relaxation) and physiological parameters (electro-encephalogram, electrocardiogram, arterial blood pressure, respiratory and heart rates and serum cortisol) were monitored. The results showed that both drugs modified many behavioral reactions and physiological changes associated with administration of carbon monoxide. Acepromazine and pentazocine reduced by 25% and 20% respectively the number of dogs that showed vocalization and agitation. In acepromazine premedicated dogs, the duration of these signs was significantly diminished and sphincter relaxation did not occur in more than 50% of cases. Furthermore, with the use of acepromazine, no significant peaks or drastic drops were noticed in the heart and respiratory rates and in the arterial blood pressure. These manifestations are usually related to stress. In light of these results, it is recommended to premedicate dogs with acepromazine before submitting them to euthanasia by carbon monoxide inhalation.

Acepromazine↗
PubMed1994

Pharmacokinetics and pharmacodynamics of acepromazine in horses.

A specific, sensitive, reverse-phase high-performance liquid chromatographic assay for acepromazine, with analytic sensitivity as low as 5 ng/ml of plasma, and electrochemical detection with an oxidation potential of 0.7 V, was used to study the pharmacokinetics of acepromazine given at a dosage of 0.15 mg/kg of body weight in horses. The relation between effect and pharmacokinetics of the drug was examined. The effects studied included those on blood pressure, pulse, PCV, measures of respiration function, and sedation. Intravenously administered doses led to a biphasic concentration decay pattern with an alpha-phase distribution half-life of < 3 minutes. The beta-phase half-life was in the range of 50 to 150 minutes. The CNS effects peaked at 20 minutes after administration, and the hemodynamic effects peaked at 100 minutes. In all horses, the most sensitive variable was the PCV, which decreased by up to 20% (P < 0.0001). Systolic, diastolic, and mean blood pressures decreased (P < 0.0001); heart rate was unchanged (P > 0.05). Neither blood gas tensions nor blood pH changed noticeably (P > 0.05). In all horses studied, acepromazine had a significant (P < 0.0001) sedative effect, as observed by posture and alertness. None of the observed pharmacodynamic effects correlated well with plasma acepromazine concentration. These effects persisted beyond the time of detectable acepromazine concentration, indicating that they might be caused by active metabolites, or that their timing could result from complex pharmacokinetic compartment influences.

Acepromazine↗
PubMed1996

Effects of acepromazine maleate and phenoxybenzamine on urethral pressure profiles of anesthetized, healthy, sexually intact male cats.

OBJECTIVES: To evaluate the effects of 2 compounds with alpha adrenergic antagonist properties on the urethral pressures of anesthetized, healthy, sexually intact male cats, and to evaluate one of the compounds for effect on striated muscle. ANIMALS: 20 healthy, sexually intact male cats. PROCEDURE: Cats were anesthetized with halothane, and urethral pressure profilometry was performed before and after treatment. 125I-labeled alpha-bungarotoxin bound to nicotinic receptors of murine skeletal muscle was used in a competitive binding study with acepromazine maleate. RESULTS: Acepromazine maleate significantly decreased intraurethral pressures in the preprostatic (19%) and prostatic (21%) regions of the urethra. There was no effect on the postprostatic/penile segment. Acepromazine did not inhibit 125I-labeled alpha-bungarotoxin binding to nicotinic receptors in murine skeletal muscle. Phenoxybenzamine significantly decreased intraurethral pressures (14%) in the preprostatic region of the urethra only. CONCLUSIONS: Acepromazine maleate and phenoxybenzamine have effects on the smooth muscle of the urethra of healthy, male cats. Acepromazine has no effect on striated muscle. CLINICAL RELEVANCE: alpha-Adrenergic compounds may be used in the pharmacologic management of feline urinary tract disease.

Acepromazine↗