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Abstract

Objective—To determine the analgesic, hemodynamic, and respiratory effects induced by caudal epidural administration of meperidine hydrochloride in mares.

Animals—7 healthy mares.

Procedure—Each mare received meperidine (5%; 0.8 mg/kg of body weight) or saline (0.9% NaCl) solution via caudal epidural injection on 2 occasions. At least 2 weeks elapsed between treatments. Degree of analgesia in response to noxious electrical, thermal, and skin and muscle prick stimuli was determined before and for 5 hours after treatment. In addition, cardiovascular and respiratory variables were measured and degree of sedation (head position) and ataxia (pelvic limb position) evaluated.

Results—Caudal epidural administration of meperidine induced bilateral analgesia extending from the coccygeal to S1 dermatomes in standing mares; degree of sedation and ataxia was minimal. Mean (± SD) onset of analgesia was 12 ± 4 minutes after meperidine administration, and duration of analgesia ranged from 240 minutes to the entire 300-minute testing period. Heart and respiratory rates, rectal temperature, arterial blood pressures, Hct, PaO2, PaCO2, pHa, total solids and bicarbonate concentrations, and base excess were not significantly different from baseline values after caudal epidural administration of either meperidine or saline solution.

Conclusions and Clinical Relevance—Caudal epidural administration of meperidine induced prolonged perineal analgesia in healthy mares. Degree of sedation and ataxia was minimal, and adverse cardiorespiratory effects were not detected. Meperidine may be a useful agent for induction of caudal epidural analgesia in mares undergoing prolonged diagnostic, obstetric, or surgical procedures in the anal and perineal regions. (Am J Vet Res 2001;62:1001–1007)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To compare the cardiorespiratory, gastrointestinal, analgesic, and behavioral effects between IV and IM administration of morphine in conscious horses with no signs of pain.

Animals—6 healthy adult horses.

Procedures—Horses received saline (0.9% NaCl) solution (IM or IV) or morphine sulfate (0.05 and 0.1 mg/kg, IM or IV) in a randomized, masked crossover study design. The following variables were measured before and for 360 minutes after drug administration: heart and respiratory rates; systolic, diastolic, and mean arterial blood pressures; rectal temperature; arterial pH and blood gas variables; intestinal motility; and response to thermal and electrical noxious stimuli. Adverse effects and horse behavior were also recorded. Plasma concentrations of morphine, morphine-3-glucuronide, and morphine-6-glucuronide were measured via liquid chromatography–mass spectrometry.

Results—No significant differences in any variable were evident after saline solution administration. Intravenous and IM administration of morphine resulted in minimal and short-term cardiorespiratory, intestinal motility, and behavioral changes. A decrease in gastrointestinal motility was detected 1 to 2 hours after IM administration of morphine at doses of 0.05 and 0.1 mg/kg and after IV administration of morphine at a dose of 0.1 mg/kg. Morphine administration yielded no change in any horse's response to noxious stimuli. Both morphine-3-glucuronide and morphine-6-glucuronide were detected in plasma after IV and IM administration of morphine.

Conclusions and Clinical Relevance—Clinically relevant doses of morphine sulfate yielded minimal and short-term behavioral and intestinal motility effects in healthy horses with no signs of pain. Neither dose of morphine affected their response to a noxious stimulus.

Full access
in American Journal of Veterinary Research

Abstract

Objective—To compare the minimum alveolar concentration (MAC) of isoflurane required to prevent corticocerebral activation, autonomic responses, and purposeful movements after somatic or visceral stimulation in cats anesthetized with isoflurane.

Animals—17 healthy spayed female cats.

Procedure—Bispectral index (BIS), autonomic parameters, and purposeful movements were monitored before and after somatic or visceral stimuli in cats anesthetized with isoflurane. End-tidal (ET) isoflurane concentration was varied to determine MAC values for cortical arousal (MACBIS), autonomic responsiveness (MACBAR), and purposeful movement (MAC). Bispectral index values ≥ 60 were considered to represent corticocerebral activation.

Results—Minimum alveolar concentration for purposeful movement was significantly less than MACBIS and MACBAR for both somatic and visceral stimulation. Individual MAC values for somatic stimulation were not significantly different from respective MAC values for visceral stimulation. The percentage of cats that had a BIS response ≥ 60 was inversely related to the end-tidal isoflurane concentration.

Conclusions and Clinical Relevance—Corticocerebral arousal and subcortical autonomic reflexes occured at isoflurane anesthetic concentrations at which reflexive or purposeful movements were absent. These results suggested that isoflurane had a preferential effect on voluntary motor output at low end-tidal isoflurane concentrations, and that sensory pathways, subcortical sympathetic output, and cortical responsiveness are less susceptible to the anesthetic effects of isoflurane. Bispectral index values obtained after somatic or visceral stimulation were sensitive for the detection of early changes in cortical excitability. (Am J Vet Res 2003; 64:1528–1533)

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in American Journal of Veterinary Research

Abstract

Objective—To determine whether the prestimulation bispectral index (BIS) value or relative change in BIS after noxious stimulation can be used to assess the depth of isoflurane anesthesia in cats.

Animals—17 healthy female cats.

Procedure—Electroencephalogram (EEG) patterns and BIS values were examined in cats that received increasing end-tidal (ET) isoflurane concentrations. Subsequently, BIS values were determined before and after either a noxious somatic or visceral stimulus in cats that received ET isoflurane concentrations ranging from 1.8% to 2.4%. Electrical stimuli of the tail base and bladder distension to 50 cm of water were the somatic and visceral stimuli, respectively.

Results—The resting BIS at ET isoflurane concentrations from 1.4% to 1.9% steadily decreased concurrently with increasing degrees of EEG suppression. Prestimulation BIS values, however, were not related to 1.8% to 2.4% ET isoflurane concentrations and not useful for prediction of BIS values or hemodynamic and movement responses after a noxious stimulus. The poststimulation BIS value and the difference between mean BIS values before and after stimulation were inversely correlated with increasing ET isoflurane concentrations. Poststimulation BIS values > 60 were observed at ET isoflurane concentrations greater than those associated with a movement response after a stimulus.

Conclusions and Clinical Relevance—The prestimulation BIS value has limited use in assessing anesthetic depth in cats during isoflurane anesthesia. The change in BIS values after a noxious somatic or visceral stimulus was a reliable measure of anesthetic depth and may be a useful measure of early arousal from the hypnotic state. (Am J Vet Res 2003;64:1534–1541)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To compare effects of electroacupuncture and butorphanol on hemodynamic and respiratory variables and rectal analgesia in mares after controlled rectal distention.

Animals—8 healthy mares.

Procedure—Each horse received saline (0.9% NaCl) solution (0.01 mL/kg, IV; control treatment), butorphanol tartrate (0.1 mg/kg, IV), or 2 hours of electroacupuncture (EA) at acupoints Bladder 21, 25, and 27 on both sides of the vertebral column, Bai hui, and Stomach 36 (right side only). Order of treatments in each mare was randomized. At least 7 days elapsed between treatments. A balloon was inserted in the rectum of each mare, and controlled distention of the balloon (pressures of ≤ 220 mm Hg) was used to measure nociceptive rectal pain threshold. Rectal temperature and cardiovascular and respiratory variables were measured before (baseline) and 5, 15, 30, 60, 90, and 120 minutes after onset of each treatment.

Results—Butorphanol produced greater increases in rectal pain threshold, compared with EA (mean ± SD, 214 ± 24 vs 174 ± 35 mm Hg of balloon pressure). Electroacupuncture produced minimal cardiovascular and respiratory changes. Although clinically not important, butorphanol produced moderate significant increases in heart and respiratory rates, arterial blood pressure, and rectal temperature and decreases in arterial oxygen tension. Arterial pH, carbon dioxide tension, bicarbonate concentrations, base excess, Hct, and concentration of total solids were not significantly different from baseline values after EA, butorphanol, and control treatments.

Conclusions and Clinical Relevance—Electroacupuncture and butorphanol (0.1 mg/kg, IV) may provide useful rectal analgesia in horses. (Am J Vet Res 2003;64:137–144)

Full access
in American Journal of Veterinary Research
in Journal of the American Veterinary Medical Association

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

Abstract

Objective

To determine effects of IV administered yohimbine on perineal analgesia, cardiovascular and respiratory activity, and head and pelvic limb position in healthy mares following epidural administration of detomidine hydrochloride solution.

Animals

8 healthy mares.

Procedure

Each mare received detomidine hydrochloride (0.06 mg/kg of body weight), administered in the caudal epidural space, followed 61 minutes later by yohimbine (0.05 mg/kg; test) or sterile saline (0.9% NaCl) solution (control), administered IV, in a randomized, crossover study design with ≥ 2 weeks between treatments. Analgesia was determined by lack of sensory perception to electrical stimulation of perineal dermatomes and needle-prick stimulation of coccygeal to 15th thoracic dermatomes. Arterial pH, Paco2, Pao2, heart and respiratory rates, rectal temperature, arterial blood pressure, and cardiac output were determined, and mares were observed for sweating and urination. Mean scores obtained for test and control groups were compared.

Results

Intravenously administered yohimbine significantly reduced mean scores of detomidine-induced perineal analgesia, head ptosis, changes in pelvic limb position, and sweating and diuresis; antagonized detomidine-induced decreases in heart rate and cardiac output; but did not affect detomidine-induced decrease in respiratory rate.

Conclusions and Clinical Relevance

Most effects of epidurally administered detomidine, except bradypnea, were antagonized by yohimbine, suggesting that detomidine may influence respiratory rate by mechanisms other than stimulation of α2-adrenoceptors, or that yohimbine induces respiratory depressant effects. Yohimbine may be an effective α2-adrenoceptor antagonist for all but respiratory depression following epidural administration of detomidine to mares. (Am J Vet Res 1999;60:1262–1270)

Free access
in American Journal of Veterinary Research

Abstract

Objectives

To determine oxygen metabolism, permeability, and blood flow in isolated joints in response to interleukin 1β (IL-1β) and contribution of innervation.

Sample Population

One metacarpophalangeal (MCP) joint of 24 adult horses.

Procedure

The MCP joint was isolated for 6 hours in a pump-perfused, auto-oxygenated, innervated or denervated preparation. Isolated joints were assigned to the following 4 groups: control, control-denervated, inflamed, and inflamed-denervated, and inflammation was induced by intra-articular injection of IL-1β. Circuit arterial and venous pressures, flows, and blood gas tensions, synovial fluid production, and intra-articular pressure were measured. Total vascular resistance; oxygen delivery, consumption, and extraction ratio (ER); and permeability surface area product were calculated. Synovial membrane blood flow was determined at 0, 60, and 330 minutes. Synovial membrane wet-to-dry ratio was obtained, and permeability to macromolecules was determined by intra-articular injection of Evans blue albumin and fluorescein isothiocyanate-conjugated dextran.

Results

Oxygen delivery and synovial membrane blood flow progressively increased but were not different among groups. Oxygen consumption and ER significantly increased in inflamed joints, as did intraarticular pressure and synovial fluid production. Inflamed joints had greater wet-to-dry ratio. Albumin permeability significantly increased in the villous synovial membrane of the inflamed groups, and dextran permeability was increased in the innervated groups, with a trend toward increased permeability in inflamed groups.

Conclusion

Inflammation significantly increased oxygen demand, which was initially met by increased ER. Permeability to small molecules was increased with inflammation; innervation increased permeability to large molecules. Use of an isolated joint model enabled documentation of the physiologic responses of the joint to acute inflammation. (Am J Vet Res 1998;59:1307–1316)

Free access
in American Journal of Veterinary Research

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