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  • Author or Editor: Sophie G. Cuvelliez x
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Abstract

Objective

To determine variations in minimal alveolar concentration (MAC) of isoflurane and analgesic and cardiorespiratory effects of lumbosacral epidural administration of 0.25 mg of butorphanol/kg of body weight in dogs.

Animals

16 healthy male dogs.

Procedure

Dogs were anesthetized with isoflurane alone. Eight dogs received butorphanol (group B) and the others an equal volume of isotonic saline solution (group S) administered by a catheter inserted in the lumbosacral epidural space. Isoflurane MAC was determined before and 30 minutes after the epidural injection, along with noxious stimulation to the fore- and hind limbs. Cardiorespiratory variables were recorded prior to and until 120 minutes after epidural administration. At that time, isoflurane anesthesia was ended, and nociception (toe pinch and pin-prick responses) was evaluated for 7 hours. Dogs were observed for 3 days to determine presence of neurologic side effects.

Results

For group-B dogs, isoflurane MAC decreased by 31 ± 8.6% after butorphanol was administered. Cutaneous insensitivity (to pin-prick nociceptive test) persisted for 3 hours after the end of isoflurane anesthesia in group-B dogs. No response was observed to toe pinch stimulation for 80 minutes after anesthesia.

Conclusions

Epidural administration of 0.25 mg of butorphanol/kg in dogs was safe; minimal cardiorespiratory and no neurologic side effects were observed, and analgesia and an isoflurane-sparing effect were apparent.

Clinical Relevance

The short duration of action of epidurally administered butorphanol limits its value for clinical practice. (Am J Vet Res 1996;57:1478-1482)

Free access
in American Journal of Veterinary Research

Abstract

Objectives

To evaluate the cardiovascular and respiratory effects of buprenorphine administered intravenously in clinically normal horses and horses with chronic obstructive pulmonary disease (COPD).

Animals

5 clinically normal horses and 5 horses with COPD that were in partial clinical remission (period A) or were having an acute attack of airway obstruction (period B).

Procedures

Pulmonary function testing, arterial blood gas analysis, and arterial blood pressure measurements were performed before and after a single intravenous bolus of buprenorphine (3 μg/kg of body weight). Respiratory rate (f), tidal volume (VT), expiratory-to-inspiratory time ratio (TE/TI), minute expiratory ventilation (VE), maximal change in transpulmonary pressure (ΔPL), dynamic compliance (Cdyn), and pulmonary resistance (RL) were calculated with a pulmonary function computer. Heart rate (HR) and systolic (SABP), diastolic (DABP), and mean arterial blood pressures (MABP) were measured.

Results

At baseline, COPD horses in period A had decreased Cdyn and increased f, VE, PL, and HR, whereas COPD horses in period B had decreased TE/TI and Cdyn, arterial blood pH, and Po2, and increased f, vE, ΔPL, and RL, compared with clinically normal horses. After drug administration, SABP, DABP, and MABP increased in all horses, f and VE increased in clinically normal horses, and Pao2 decreased within 60 minutes in horses with COPD.

Conclusion and Clinical Relevance

Buprenorphine can induce excitement in unsedated horses or horses that do not have signs of pain, but does not seem to induce severe respiratory depression or adverse cardiovascular effects in clinically normal horses or those with COPD. (Am J Vet Res 1998;59:1287–1291)

Free access
in American Journal of Veterinary Research

SUMMARY

Anesthesia of equids is associated with pulmonary dysfunction. Cardiovascular and respiratory effects of inhalation anesthetic agents and duration of anesthesia have been studied, using oxygen as the carrier gas. To our knowledge, the effects of inspired oxygen have not been determined. We studied the cardiovascular and respiratory effects of 2 inspired oxygen fractions (0.30 and > 0.85) in 5 laterally recumbent, halothane-anesthetized horses. Mean systemic arterial blood pressure, cardiac output, central venous pressure, pulmonary arterial pressure, arterial pH, and arterial base excess were similar in horses of the 2 groups during 4 hours of anesthesia at constant end-tidal halothane concentration. End-tidal partial pressure of CO2, arterial partial pressure of CO2 and O2, and alveolar-to-arterial O2 tension difference were greater in horses exposed to the higher oxygen concentration. On the basis of the data obtained, we suggest that greater hypoventilation and ventilation/perfusion mismatch occur when horses are breathing high-oxygen fraction. Arterial partial pressure of O2 was not different between the 2 groups of horses after they were disconnected from the anesthesia circuit and allowed to breathe room air. Horses recovered from anesthesia without complications.

Free access
in American Journal of Veterinary Research