Objective-To evaluate the effects of subarachnoidally administered hyperbaric morphine, buprenorphine, and methadone on avoidance threshold to noxious electrical stimulation of the perineal, sacral, lumbar, and thoracic regions in horses. Animals-6 healthy adult horses. Procedures-Horses were assigned to receive subarachnoid administration of hyperbaric morphine (0.01 mg/kg), buprenorphine (0.001 mg/kg), methadone (0.01mg/kg), or 10% dextrose solution in equal volumes (5 mL). Electrical stimulation was applied every 10 minutes for 60 minutes and every 30 minutes for 120 minutes after subarachnoid injection over the dermatomes of the perineal, sacral, lumbar, and thoracic regions, and the avoidance threshold voltage was recorded. Heart and respiratory rate, blood gas tensions, serum electrolyte concentrations, and sedative effects were also evaluated. Results-Administration of 10% dextrose solution did not change the avoidance threshold. Morphine and methadone significantly increased the avoidance threshold by 10 minutes after injection, which lasted until 120 minutes after subarachnoid administration in the perineal, sacral, lumbar, and thoracic regions. Profound analgesia (avoidance threshold > 40 V) was achieved in all regions. Buprenorphine also significantly increased the avoidance threshold by 10 minutes (36 V) after injection, which lasted 60 minutes and was considered moderate. Heart rate, blood pressure, respiratory rate, and blood gas tensions stayed within reference range. No ataxia, signs of sedation, or CNS excitement were observed. Conclusions and Clinical Relevance-Subarachnoid administration of hyperbaric morphine or methadone produces intense analgesia for 120 minutes over the dermatomes of the perineal, sacral, lumbar, and thoracic areas without cardiorespiratory depression, ataxia, or CNS excitement in horses.

Objective-To evaluate the effects of metabolic acidosis and changes in ionized calcium (Ca(2+)) concentration on Pao2 in dogs. Animals-33 anesthetized dogs receiving assisted ventilation. Procedure-Normal acid-base status was maintained in 8 dogs (group I), and metabolic acidosis was induced in 25 dogs. For 60 minutes, normocalcemia was maintained in group I and 10 other dogs (group II), and 10 dogs were allowed to become hypercalcemic (group III); hypocalcemia was then induced in groups I and II. Groups II and IV (5 dogs) were treated identically except that, at 90 minutes, the latter underwent parathyroidectomy. At intervals, variables including Pao2, Ca(2+) concentration, arterial blood pH (pHa), and systolic blood pressure were assessed. Results-In group II, Pao2 increased from baseline value (96 +/- 2 mm Hg) within 10 minutes (pHa, 7.33 +/- 0.001); at 60 minutes (pHa, 7.21 +/- 0.02), Pao2 was 108 +/- 2 mm Hg. For the same pHa decrease, the Pao2 increase was less in group III. In group I, hypocalcemia caused Pao2 to progressively increase (from 95 +/- 2 mm Hg to 104 +/- 3 mm Hg), which correlated (r = -0.66) significantly with a decrease in systolic blood pressure (from 156 +/- 9 mm Hg to 118 +/- 10 mm Hg). Parathyroidectomy did not alter Pao2 values. Conclusions and Clinical Relevance-Induction of hypocalcemia and metabolic acidosis each increased Pao2 in anesthetized dogs, whereas acidosis-induced hypercalcemia attenuated that increase. In anesthetized dogs, development of metabolic acidosis or hypocalcemia is likely to affect ventilatory control.

Objective-To determine the effects of meloxicam and butorphanol on minimum alveolar concentration of isoflurane (MAC(ISO)) in rabbits. Animals-10 healthy young adult female rabbits. Procedure-Rabbits were anesthetized with isoflurane on 3 occasions in a blinded, randomized complete block design to determine the MAC(ISO) associated with administration of meloxicam (0, 0.3, or 1.5 mg/kg, PO) and butorphanol (0.4 mg/kg, IV). The MAC(ISO) was determined by use of a paw clamp technique as the end-tidal concentration of isoflurane halfway between the values that allowed or inhibited purposeful movement. Rectal temperature, end-tidal CO2 concentration, heart rate, oxygen saturation, and arterial blood pressure were measured to evaluate cardiopulmonary function. Results-Mean +/- SE MAC(ISO) in saline (0.9% NaCl) solution-treated rabbits was 2.49 +/- 0.07% and was not significantly different from that associated with administration of meloxicam at 0.3 mg/kg (2.56 +/- 0.07%) or 1.5 mg/kg (2.66 +/- 0.07%). Butorphanol significantly reduced the MAC(ISO) to 2.30 +/- 0.07% when administered with saline solution alone, 2.27 +/- 0.07% when administered with 0.3 mg of meloxicam/kg, and 2.33 +/- 0.07% when administered with 1.5 mg of meloxicam/kg. The percentage reduction in MAC(ISO) was significantly greater for rabbits that received butorphanol and meloxicam at either dose, compared with butorphanol and saline solution. Conclusions and Clinical Relevance-Results indicated that meloxicam does not have a direct isoflurane-sparing effect and does not interfere with the anesthetic-sparing effect of butorphanol in rabbits.