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.

Naloxone reversal of oxymorphone effects in dogs.

Oxymorphone was administered IV to dogs 4 times at 20-minute intervals (total dosage, 1 mg/kg of body weight, IV) on 2 separate occasions. Minute ventilation, mixed-expired carbon dioxide concentration, arterial and mixed-venous pH and blood gas tensions, arterial, central venous, pulmonary arterial, and pulmonary wedge pressures, and cardiac output were measured. Physiologic dead space, base deficit, oxygen transport, and vascular resistance were calculated before and at 5 minutes after the first dose of oxymorphone (0.4 mg/kg) and at 15 minutes after the first and the 3 subsequent doses of oxymorphone (0.2 mg/kg). During 1 of the 2 experiments in each dog, naloxone was administered 20 minutes after the last dose of oxymorphone; during the alternate experiment, naloxone was not administered. In 5 dogs, naloxone was administered IV in titrated dosages (0.005 mg/kg) at 1-minute intervals until the dogs were able to maintain sternal recumbency, and in the other 5 dogs, naloxone was administered IM as a single dose (0.04 mg/kg). Naloxone (0.01 mg/kg, IV or 0.04 mg/kg, IM) transiently reversed most of the effects of oxymorphone. Within 20 to 40 minutes after IV naloxone administration and within 40 to 70 minutes after IM naloxone administration, most variables returned to the approximate values measured before naloxone administration. The effects of oxymorphone outlasted the effects of naloxone; cardiovascular and pulmonary depression and sedation recurred in all dogs. Four hours and 20 minutes after the last dose of oxymorphone, alertness, responsiveness, and coordination improved in all dogs after IM administration of naloxone. Cardiac arrhythmia, hypertension, or excitement was not observed after naloxone administration.

Blood pressure response to tourniquet use in anesthetized horses.

Blood pressure during anesthesia and surgery was compared for 2 groups of horses. Group A, consisting of 23 horses, had a tourniquet placed on the distal portion of a limb. The other group of 20 horses (group B) had surgery of comparable nature and duration as did group-A horses, but a tourniquet was not used. There was a statistical difference (P less than 0.05) in the peak systolic arterial blood pressure between the groups; group-A horses had a mean (+/- SEM) peak of 151 +/- 6 mm of Hg and group-B horses had a peak of 118 +/- 4 mm of Hg. In addition, group-A horses had immediate decrease in blood pressure, coincident with tourniquet deflation. The blood pressure decrease of 23 +/- 3 mm of Hg represented 16% of immediate predeflation blood pressure. Comparable blood pressure decrease was not observed at the end of surgery in group-B horses. Significant difference was not found when other factors that could affect blood pressure were considered. These factors included preanesthetic medication, anesthetic agents, mode of ventilation, pretourniquet inflation blood pressure, and duration of tourniquet inflation. Significant (P less than 0.05) difference in peak blood pressure was observed when the tourniquet was placed on the dependent, compared with the uppermost, limb, with changes more pronounced when the tourniquet was placed on the dependent limb. Tourniquet placement was associated with hypertension, and tourniquet deflation was associated with blood pressure decrease in these anesthetized horses.

Clinical use of the neuromuscular blocking agents atracurium and pancuronium for equine anesthesia.

Neuromuscular blocking agents (muscle relaxants) are useful and common adjuncts to general anesthesia for human beings, but have not been used extensively during anesthesia of large animal species. Over a 3-year period, atracurium or pancuronium were used as adjuncts to general anesthesia for 89 anesthetic procedures in 88 equids (of 18 breeds and age ranging in age from 5 weeks to 25 years) at the teaching hospital. Forty-one of the anesthetic procedures were for abdominal surgery, and orthopedic (n = 19), ophthalmologic (n = 17), thoracotomy (n = 1), and soft tissue (n = 14) procedures composed the rest. Most equids were given atracurium because it was less expensive than pancuronium. Initial dosage of either relaxant ranged from 0.12 to 0.2 mg/kg of body weight IV, and repeat doses ranged from 10 to 30 mg. Relaxants were used for as long as 205 minutes. Muscles of the face or hind limb digital extensor muscles were used to monitor relaxation. Muscles of the hind limb were more sensitive to the effects of relaxants than were muscles of the face. At the end of a surgical procedure, just prior to being taken to the recovery stall, a relaxant antagonist, edrophonium (0.5 to 1 mg/kg), was administered IV to each equid. Edrophonium caused blood pressure to increase in most of the equids. Heart rate change was variable, with approximately half the equids having no change or increased heart rate and the remainder having decreased heart rate. Recovery to standing after anesthesia was rated excellent or good for 72 equids, fair for 11, and poor for 2.(ABSTRACT TRUNCATED AT 250 WORDS)

Oxymorphone: cardiovascular, pulmonary, and behavioral effects in dogs.

Cardiovascular, pulmonary, and behavioral effects of multiple doses of oxymorphone in 10 nonanesthetized, spontaneously breathing, healthy dogs were studied. Oxymorphone (0.4 mg/kg of body weight) was administered IV, and at 20, 40, and 60 minutes after the first injection was given, 0.2 mg of oxymorphone/kg was administered. Cardiovascular and pulmonary variables were measured before (base line) and at 5, 15, 35, 55, 75, 100, 120, 150, 180, 210, 240, 270, and 300 minutes after the first oxymorphone injection. Degree of sedation and behavioral effects also were recorded. Naloxone (0.04 mg/kg, IV) was administered 4.5 hours after the 4th oxymorphone injection, and behavioral changes were recorded. Oxymorphone induced mild respiratory depression. After transient apnea developed, respiratory rate increased to a pant, tidal volume decreased, and minute ventilation increased, but these values were not significantly (P = 0.05) different from base line. The PaCO2, physiologic dead space, and base deficit increased; alveolar tidal volume decreased; and alveolar minute ventilation did not change. The PaO2 decreased, hemoglobin and arterial O2 content increased, and O2 transport did not change. Venous admixture transiently increased. Oxymorphone induced minimal cardiovascular depression. Mean arterial blood pressure, stroke volume, central venous pressure, pulmonary artery pressure, and pulmonary wedge pressure increased. Heart rate decreased, systemic vascular resistance transiently increased, and cardiac output transiently decreased. Because the dogs moved spontaneously, responded to sound with sudden, vigorous movements, and breathed with excessive effort, oxymorphone alone was considered inadequate as a general anesthetic.