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Abstract

Objective

To examine effects of atipamezole on detomidine midsacral subarachnoidally-induced analgesia, cardiovascular and respiratory activity, head ptosis, and position of pelvic limbs in healthy mares.

Animals

10 healthy mares.

Procedure

Using a randomized, blinded, crossover study design, mares received detomidine (0.03 mg/kg of body weight, diluted in 3 ml of CSF) midsacral subarachnoidally, followed by atipamezole (0.1 mg/kg [test]) or sterile saline (0.9% NaCl) solution (control), IV 61 minutes later and saline solution (3 ml, midsacral subarachnoidally) on a separate occasion, at least 2 weeks later. Analgesia was determined by lack of sensory perception to electrical stimulation at the perineal dermatome and no response to needle-prick stimulation extending from the coccygeal to T15 dermatomes. Arterial acid-base (pH, standard bicarbonate, and base excess values), gas tensions (PO2 , PCO2 ), PCV, total solids concentration, heart and respiratory rates, rectal temperature, and arterial blood pressure were determined, and mares were observed for sweating and urination. Mean scores of perineal analgesia, head ptosis, position of pelvic limbs, and cardiovascular and respiratory data were compared for the 3-hour test period.

Results

Subarachnoidally administered detomidine induced perineal analgesia (mean ± SD onset, 9.0 ± 4.6 minutes; duration, 130 ± 26 minutes), marked head ptosis, moderate changes in pelvic limb position, cardiovascular and respiratory depression, sweating in analgesic zones, and diuresis. Intravenously administered atipamezole significantly reduced mean scores of detomidine-induced perineal analgesia, head ptosis, pelvic limb position, sweating and diuresis; partially antagonized detomidine-induced bradycardia; and did not effect detomidine-induced bradypnea.

Conclusions and Clinical Relevance

Most effects of midsacral subarachnoidally administered detomidine, except bradycardia and bradypnea, were reversed by atipamezole (0.1 mg/kg, IV), indicating that most of the actions of detomidine were mediated via activation of α2-adrenergic receptors. (Am J Vet Res 1998;59:468–477)

Free access
in American Journal of Veterinary Research

Abstract

Objective

To examine and compare effects of 2α2 - adrenergic receptor agonists, xylazine and detomidine, administered into the sacrococcygeal epidural space to induce safe and effective perineal analgesia on cardio-vascular and respiratory functions, head ptosis, and po-sition of pelvic limbs in healthy mares.

Animals

8 healthy mares.

Procedure

Blood samples were drawn and systemic hemodynamics were determined, including cardiac output and pulmonary arterial, systemic arterial, and right atrial pressures. Two-way ANOVA with repeated measures was used to detect significant (P < 0.05) differences between mean scores of perineal analgesia, cardiorespiratory variables, head ptosis, and position of pelvic limbs in mares before and during a 3-hour testing period. Analgesia was determined by lack of sensory perception to electrical stimulation at the perineal dermatome and no response to needle prick stimulation in dermatomes extending from the coccyx to T15. Avoidance responses to electrical current and needle prick stimulation and behavioral changes (head ptosis, position of pelvic limbs) were quantitatively assessed by use of a scoring system.

Results

Epidurally administered xylazine induced perineal analgesia and variable bilateral caudal analgesia extending from the coccyx to S3 dermatome, with minimal cardiovascular and respiratory depression, head ptosis, changes in position of pelvic limbs, and no urination in standing mares. Epidurally administered detomidine in-duced perineal analgesia, variable bilateral analgesia with dermatomal spread ranging from coccyx to S3 and coccyx to T15, with cardiovascular depression, marked head ptosis, changes in position of pelvic limbs, and diuresis in standing mares. Onset of perineal analgesia after xylazine and detomidine administrations was 13.1 ± 3.7 and 12.5 ± 2.7 minutes (mean ± SD), respectively. The period of perineal analgesia was significantly (P < 0.05) longer in mares after epidural xylazine administration than after epidural detomidine administration (165 to > 180 minutes vs 160 ± 8 minutes).

Conclusions

Caudal epidurally administered xylazine (0.25 mg/kg of body weight in 8 ml of 0.9% NaCI) offers the most desirable conditions in mares: long-term perineal analgesia (> 2.5 hours), with minimal cardiopulmonary depression, head ptosis, changes in pelvic limb position, and no urination in standing mares during a 3- hour test period. (Am J Vet Res 1996;57:1338-1345)

Free access
in American Journal of Veterinary Research

Abstract

Objective

To examine effects of 0.25 mg of xylazine/kg of body weight diluted to a total volume of 6 ml/450 kg with sterile 0.9% NaCl, administered into the epidural space of the sacrococcygeal joint on perineal analgesia, sedation, ataxia, and respiratory and cardiovascular function in standing mares:

Design

Randomized, blinded study, using xylazine (treatment) and 0.9% NaCl (controls). At least 2 weeks elapsed between the treatments.

Animals

Eight healthy mares.

Procedure

Blood samples were drawn. Systemic hemodynamics were determined, including cardiac output and pulmonary arterial, systemic arterial, and right atrial pressures. Two-way ANOVA with repeated measures was used to detect significant (P < 0.05) differences between mean scores of analgesia, sedation, ataxia, and cardiorespiratory variables before and during a 3-hour testing period. Analgesia was determined by lack of sensory perception to electrical stimulation at the perineal dermatome and no response to needle prick stimulation extending from coccyx to S3 dermatomes. Sedation was determined by head ptosis.

Results

Epidurally administered xylazine induced variable bilateral caudal analgesia extending from coccyx to S3, with minimal sedation, ataxia, and cardiovascular and respiratory depression in standing mares. Analgesia was attained at 15 ± 6 minutes and lasted for 165 to over 180 minutes. Heart and respiratory rates, systolic, diastolic, and mean arterial blood pressure, PCV, hemoglobin concentration, arterial oxygen content, and oxygen transport were decreased after xylazine, but not 0.9% NaCl, treatment. Cardiac output, stroke volume, mean right atrial pressure, mean pulmonary artery pressure, systemic vascular resistance, pulmonary vascular resistance, arterial and mixed venous pH and gas tensions (Po2 and Pco2 ), oxygen consumption, blood temperature, and rectal temperature did not change significantly (P < 0.05) after epidural administration of xylazine or 0.9% NaCl.

Conclusions

Caudal epidurally administered xylazine (0.25 mg/kg in 6 ml of 0.9% NaCl) can be given safely to induce prolonged (> 2 hours) caudal analgesia with minimal sedation, ataxia, and circulatory and respiratory disturbances in conscious, standing mares.

Free access
in American Journal of Veterinary Research

Summary

Seven adult mares were used to determine the analgesic, cns, and cardiopulmonary effects of detomidine hydrochloride solution after epidural or subarachnoid administration, using both regimens in random sequence. At least 1 week elapsed between experiments.

A 17-gauge Huber point (Tuohy) directional needle was used to place a catheter with stylet into either the epidural space at the first coccygeal interspace or the subarachnoid space at the lumbosacral intervertebral junction. Catheters were advanced so that the tips lay at the caudal sacral (S5 to S4) epidural space or at the midsacral (S3 to S2) subarachnoid space. Position of the catheter was confirmed radiographically. A 1% solution of detomidine HCl was injected into the epidural catheter at a dosage of 60 µg/kg of body weight, and was expanded to a 10-ml volume with sterile water to induce selective caudal epidural analgesia (cea). A dose of 30 µg of detomidine HCl/kg expanded to a 3-ml volume with spinal fluid was injected into the subarachnoid catheter to induce caudal subarachnoid analgesia (csa). Analgesia was determined by lack of sensory perception to electrical stimulation (avoidance threshold > 40 V, 0.5-ms duration) at the perineal dermatomes and no response to superficial and deep muscular pinprick stimulation at the pelvic limb and lumbar and thoracic dermatomes. Maximal cea and csa extended from the coccyx to spinal cord segments T15 and T14 at 10 to 25 minutes after epidural and subarachnoid drug administrations in 2 mares. Analgesia at the perineal area lasted longer after epidural than after subarachnoid administration (142.8 ± 28.8 minutes vs 127.1 ± 27.7 minutes). All mares remained standing. Both cea and csa induced marked sedation, moderate ataxia, minimal cardiopulmonary depression, increased frequency of second-degree atrioventricular heart block, and renal diuresis. All treatments resulted in significantly (P < 0.05) decreased heart rate, respiratory rate, systemic arterial blood pressure, pcv, and plasma total solids concentration. To the contrary, arterial carbon dioxide tension, plasma bicarbonate, and standard base excess concentrations were significantly (P < 0.05) increased. Arterial oxygen tension, pH, and rectal temperature did not change significantly from baseline values.

Results indicate that use of detomidine for cea and csa in mares probably induces local spinal and cns effects, marked sedation, moderate ataxia, mild cardiopulmonary depression, and renal diuresis.

Free access
in American Journal of Veterinary Research