Interactions between pipecuronium and suxamethonium in the dog

The depolarising muscle relaxant suxamethonium (0.3 mg kg-1) and the non-depolarising muscle relaxant pipecuronium (0.05 mg kg-1) were administered to four dogs. In the first series of experiments pipecuronium was administered intravenously, followed at 50 per cent of return of neuromuscular activity by suxamethonium. At 50 per cent return of activity atropine and neostigmine were administered to reverse the neuromuscular block. In the second series the sequence was reversed and pipecuronium was administered after suxamethonium. At 50 per cent recovery atropine and neostigmine were given. In the first series of experiments the time for the onset of suxamethonium block was significantly increased after prior administration of pipecuronium. However, in the second series of experiments the prior administration of suxamethonium had no significant effect on the duration of action of pipecuronium.     

Interactions between vecuronium and suxamethonium in the dog

The non-depolarising muscle relaxant vecuronium (0.2 mg kg-1) was administered to four dogs. At 50 per cent return of neuromuscular activity, as measured by the train-of-four technique, the depolarising muscle relaxant suxamethonium (0.3 mg kg-1) was injected intravenously. At 50 per cent return of neuromuscular activity reversal of the block was achieved with atropine and neostigmine. The duration of action of suxamethonium was reduced by the prior administration of vecuronium. In the second series of experiments the order of administration of the suxamethonium and vecuronium was reversed. Suxamethonium (0.3 mg kg-1) was administered first and at 50 per cent recovery vecuronium (0.2 mg kg-1) was given. At 50 per cent recovery of the twitch response after vecuronium administration the block was reversed with atropine and neostigmine. The previous administration of suxamethonium prolonged the duration of the vecuronium induced neuromuscular block.     

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.     

Cardiovascular and pulmonary effects of atropine reversal of oxymorphone-induced bradycardia in dogs.

Oxymorphone was administered intravenously (IV) to 10 dogs (0.4 mg/kg initial dose followed by 0.2 mg/kg three times at 20-minute intervals). Four hours after the last dose of oxymorphone, heart rates were less than 60 bpm in six dogs. After atropine (0.01 mg/kg IV) was administered, heart rate decreased in five dogs and sinus arrhythmia or second degree heart block occurred in four of them. A second injection of atropine (0.01 mg/kg IV) was administered 5 minutes after the first and the heart rates increased to more than 100 bpm in all six dogs. Ten minutes after the second dose of atropine, heart rate, cardiac output, left ventricular minute work, venous admixture, and oxygen transport were significantly increased, whereas stroke volume, central venous pressure, systemic vascular resistance, and oxygen extraction ratio were significantly decreased from pre-atropine values. The PaCO2 increased and the PaO2 decreased but not significantly. The oxymorphone-induced bradycardia did not produce any overtly detrimental effects in these healthy dogs. Atropine reversed the bradycardia and improved measured cardiovascular parameters.     

Autonomic and Cardiovascular Effects of Neuromuscular Blockade Antagonism in the Dog

Autonomic and cardiovascular changes were studied when neuromuscular blockade was antagonized in 96 dogs with one of eight anticholinesterase-antimuscarinic drug combinations. Neostigmine (50 or 100 micrograms/kg) was administered before or after atropine (40 micrograms/kg) or glycopyrrolate (10 micrograms/kg). The high dose of neostigmine (100 micrograms/kg) caused bradyarrhythmias, salivation, and signs of bronchosecretion when used with either antimuscarinic agent and irrespective of the administration sequence. The heart rate increased, but not significantly, when atropine was injected before either dose of neostigmine. This did not occur when this administration sequence was reversed. Arrhythmias and cardiovascular and autonomic changes did not occur when glycopyrrolate was injected before or after neostigmine at 50 micrograms/kg.     

Observations on the neuromuscular blocking action of alcuronium in the dog and its reversal by neostigmine.

The action of alcuronium chloride on neuromuscular transmission in the dogs was investigated by electrical and mechanical methods. The mean duration of action was 70 min. Reversal of its action was produced with atropine and neostigmine.     

Antagonism of pancuronium neuromuscular blockade in halothane-anesthetized ponies using neostigmine and edrophonium

Efficacy of neostigmine (0.04 mg/kg of body weight) and edrophonium (1 mg/kg), as antagonists for pancuronium neuromuscular blockade in halothane-anesthetized ponies, was evaluated. Neostigmine and edrophonium were satisfactory antagonists, with edrophonium having a significantly (P less than 0.01) more rapid onset of action than did neostigmine. Muscarinic activity of neostigmine and edrophonium was also evaluated. Neither antagonist was administered with atropine. Gastrointestinal effects, increased salivation, and increased airway secretions were minimal with edrophonium, but were marked after neostigmine. Blood pressure increased within 1 to 2 minutes of antagonist administration. Heart rate decreased after edrophonium injection, but this occurred after blood pressure increase. Heart rate increased or did not change after neostigmine administration.     

Cardiopulmonary effects of fentanyl-droperidol, nitrous oxide, and atropine sulfate in dogs.

The cardiopulmonary effects of droperidol-fentanyl, nitrous oxide, and atropine were evaluated in 12 adult male Beagle dogs. All dogs were surgically instrumented with a cardiac output thermistor and arterial and venous catheters and were prepared with a chronic tracheostomy. Each dog was used as its own control, and data obtained when dogs were nonanesthetized and nonmedicated were compared with data recorded after the test drugs were administered. The dogs were randomly allotted to 3 groups of 4 dogs each. Group I dogs were given droperidol-fentanyl alone intravenously (IV); group II dogs were given droperidol-fentanyl IV with 67% nitrous oxide; and group III dogs were given atropine sulfate intramuscularly followed by droperidol-fentanyl IV with 67% nitrous oxide. Minute volume was decreased in the 3 groups of dogs for 3 to 5 minutes after droperidol-fentanyl was injected. This resulted in respiratory and metabolic acidosis in all dogs, as indicated by increased arterial carbon dioxide tension, decreased pH, and increased base deficit. In addition, droperidol-fentanyl given alone caused a decrease in systolic pressure and a slight decrease in heart rate. Group 1 dogs were sensitive to auditory stimulation. Cardiovascular changes were not seen when nitrous oxide was added; however, analgesia and muscle relaxation were improved. Premedication with atropine sulfate resulted in increased cardiac output, heart rate, and diastolic pressure, and subsequent administration of droperidol-fentanyl with nitrous oxide caused a transient increase in mean arterial and systolic pressure. This last anesthetic regimen, along with assisted or controlled respiration, seems to provide an excellent anesthetic state with minimal cardiopulmonary depression.     

Interaction between atracurium and suxamethonium in the dog

The depolarising muscle relaxant suxamethonium (0.3 mg kg-1) and the non-depolarising relaxant atracurium (0.6 mg kg-1) were administered to four dogs. In the first series of experiments atracurium was administered, followed at 50 per cent return of neuromuscular activity by suxamethonium. At 50 per cent return of activity atropine and neostigmine were administered to reverse the block. In the second series of experiments the sequence was reversed and atracurium was administered after suxamethonium. At 50 per cent recovery atropine and neostigmine were given. In the first series of experiments it was demonstrated that the prior administration of atracurium reduced the duration of action of suxamethonium. However, in the second series it was shown that the prior administration of suxamethonium had no significant effect on the duration of action of atracurium.     

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.     

Cardiac arrhythmias associated with multiple trauma in dogs

Premature ventricular contractions and ventricular tachycardia were detected in 10 dogs 1 to 48 hours after trauma. All dogs were treated aggressively if the arrhythmias became severe. One dog died, 8 were discharged with stable cardiac rhythm, and 1 was euthanatized. Necropsy revealed gross and microscopic lesions of acute myocardial necrosis, probably of ischemic origin. Cardiac arrhythmias were associated with thoracic trauma, neurologic injury, severe shock, and/or extensive tissue trauma.     

Effects of thiopentone and propofol on lower oesophageal sphincter and barrier pressure in the dog

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).     

Vecuronium infusion in the dog

The non-depolarising muscle relaxant vecuronium bromide was administered to 20 dogs undergoing a variety of surgical procedures under general anaesthesia. An initial dose of 0–1 mg/kg was administered and followed by an infusion of 0–1 mg/kg/hour. Reversal of the neuromuscular block was carried out with neostigmine and atropine.     

Clinical observations on the use of the muscle relaxant atracurium in the dog

The use of the new neuromuscular blocking agent, atracurium besylate, is described in 22 dogs undergoing a variety of surgical procedures under general anaesthesia. An initial dose of 0.5 mg/kg proved effective and produced a block of 40 min duration. Incremental doses of 0.2 mg/kg were used. Reversal of the neuromuscular block by neostigmine preceded by atropine was rapid and effective. No untoward side-effects were observed with this drug.     

A case report of the treatment of an overdose of xylazine in a cow.

An adult Holstein cow was inadvertently administered an overdose of xylazine hydrochloride. The cow became weak, collapsed, and developed severe bradycardia and intermittent heart block. Initial therapy for cardiovascular collapse consisted of rapid infusion of large volumes of intravenous fluids and intravenous injection of atropine sulfate. Yohimbine, an alpha 2-adrenergic antagonist, and tolazoline hydrochloride, an alpha 1- and alpha 2-adrenergic antagonist, were administered intravenously as antidotes for xylazine overdose. The cow recovered but calved prematurely 4 days later.     

The effects of atropine and methotrimeprazine on the epinephrine-induced arrhythmias in halothane-anesthetized dogs.

The effects of atropine and methotrimeprazine on epinephrine-induced ventricular arrhythmias were evaluated in halothane-anesthetized dogs. Ten mixed-breed dogs were assigned to 3 treatments (saline, atropine, and methotrimeprazine) in a randomized complete block design. Anesthesia was induced and maintained with halothane (1.5 minimum alveolar concentration) in oxygen. Controlled ventilation was used throughout to maintain eucapnia. Saline, atropine (0.05 mg/kg, i.v.) or methotrimeprazine (0.5 mg/kg, i.v.) were administered and, 5 minutes later the arrhythmogenic dose of epinephrine (ADE) was measured by i.v. infusion of progressively increasing infusion rates of epinephrine, until the ventricular arrhythmia criterion was met (at least 4 ectopic ventricular contractions (EVCs) during a 15-second period). Data were analyzed using a student's t-test for ADE values and multivariate profile analysis for heart rate (HR), arterial blood pressure (ABP), and rate pressure product (RPP). The ADE increased in atropine- and methotrimeprazine-treated groups, whereas 1 and 4 animals from these groups did not develop any ventricular arrhythmia, respectively. Epinephrine induced multiform premature ventricular contractions (PVCs) in the atropine group, whereas ventricular escape beats were observed in the control and methotrimeprazine groups. Heart rate and RPP decreased, and ABP increased at the time of ADE observation in the control group. Epinephrine infusion in the atropine group caused marked increases in HR, ABP, and RPP, which were associated with pulsus alternans in 2 animals. It was concluded that 1) the presence of cholinergic blockade influences the type of ventricular arrhythmia induced by epinephrine; 2) increased ADE values recorded following atropine administration must be cautiously interpreted, since in this situation the PVCs were associated with signs of increased myocardial work and ventricular failure; and 3) the use of a broader arrhythmia criterion (EVCs instead of PVCs) may not allow a direct comparison between ADE values, since it includes ventricular arrhythmias mediated by different mechanisms.     

Effects of atropine on xylazine-pentobarbital anesthesia in dogs: preliminary study

The influence of atropine on anesthesia induced by xylazine-pentobarbital administration was studied in 5 dogs. The combination of xylazine (2.2 mg/kg of body weight, IM) and pentobarbital (14.0 mg/kg, IV) caused anesthesia with the duration of absence of the pedal reflex, duration of anesthesia, and the time from return of consciousness to ambulation to be 107.4, 123.4, and 59.2 minutes, respectively. Bradycardia and short-term respiratory depression were observed. An IM injection of atropine sulfate (0.045 mg/kg) did not significantly change the durations of absence of the pedal reflex and of anesthesia, the time from return of consciousness to ambulation, or the pattern of respiration in the anesthetized dogs. The PaO2 increased gradually in both groups; however, atropine caused a marked tachycardia and increased the PaCO2. Fifteen minutes after pentobarbital injection, administration of atropine sulfate caused a slight but significant (P less than 0.01) decrease in arterial pH. Although atropine sulfate antagonized xylazine bradycardia, the data indicated that it may have caused increased respiratory depression in dogs anesthetized with xylazine and pentobarbital.     

THE EFFECT OF A COMBINATION OF MEDETOMIDINE-BUTORPHANOL AND MEDETOMIDINE, BUTORPHANOL, ATROPINE ON GLOMERULAR FILTRATION RATE IN DOGS

The effects of intramuscularly administered medetomidine and butorphanol (MB), and medetomidine, butorphanol, atropine (MBA) on glomerular filtration rate (GFR) were determined in six dogs as measured by 99m-Tc-labeled diethylenetriaminepentaacetic acid (99mTc-DTPA) nuclear scintigraphy. Direct systolic, diastolic, and mean arterial blood pressures and heart rate were measured at regular time intervals before, during, and after GFR calculations. The mean GFR measurement following MB was significantly greater (4.44 ml/min/kg) than following MBA (3.82 ml/min/kg) or saline treatment (3.41 ml/min/kg). There was no significant difference between the mean GFR measurements following MBA injection and following saline injection. Diastolic and mean arterial pressures following MBA injection were significantly higher than the values recorded after either MB or saline alone. Heart rate following MB administration was significantly lower than that recorded for dogs receiving MBA or saline alone. The results of this study indicate that the administration of medetomidine in combination with butorphanol significantly increases total GFR in healthy dogs, while the administration of the combination of medetomidine, butorphanol, and atropine does not.     

Atracurium infusion in the dog

The non-depolarizing muscle relaxant atracurium was administered to 25 dogs undergoing a variety of surgical procedures under general anaesthesia. An initial dose of 0–5 mg/kg was administered and when the block began to wear off an infusion was begun. A dose of 0–5 mg/kg/hr was administered by a simple infusion technique. Reversal of the neuromuscular block was carried out with either neostigmine or edrophonium preceded by atropine.     

Butorphanol Tartrate for Partial Reversal of Oxymorphone-Induced Postoperative Respiratory Depression in the Dog

A randomized, blinded, crossover study was designed to evaluate the respiratory, cardiovascular, and behavioral effects of butorphanol given postoperatively to oxymorphone-premedicated and surgically stimulated dogs. Nine healthy adult dogs were premedicated intramuscularly with atropine (0.04 mg/kg), acepromazine (0.10 mg/kg), and oxymorphone (0.2 mg/kg). Anesthesia was induced with thiamylal (12 mg/kg) and maintained with halothane in oxygen. According to the protocol of a concurrent study, all dogs had percutaneous endoscopic gastrostomy (PEG) feeding tubes placed during the first anesthetic episode and removed during the second anesthetic episode. All dogs received postoperatively either butorphanol tartrate (0.2 mg/kg) or an isovol-umetric dose of saline placebo, both given intravenously. Respiratory rate (RR), tidal volume (TV), minute ventilation (MV), end-tidal CO₂ concentration (ET_CO2). heart rate (HR), and indirect diastolic (DP), systolic (SP) and mean arterial (MAP) blood pressures were measured at times 0, 2, 5, 10, 20, 40, 80, and 120 minutes after injection. The time from injection of the test drug until extubation was recorded. RR, MV, HR, and DP were significantly ( P < .05) increased, while ET_co2 was significantly decreased, for a minimum of 30 minutes in butorphanol-treated dogs compared with saline controls. TV, SP, and MAP were transiently (≤15 minutes) increased in butorphanol-treated dogs compared with saline controls. There was no significant difference between the times to extubation in the butorphanol-treated dogs versus the saline control dogs.