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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

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

Summary

The cardiorespiratory effects of thiamylal (10 mg/kg of body weight, iv) and the effects of preanesthetic medication with diazepam, acepromazine, detomidine, or xylazine administered prior to a thiamylal dosage of 6 mg/kg, iv, were evaluated in 6 adult horses. The quality of recovery from thiamylal anesthesia also was evaluated. Intravenous administration of thiamylal at a dosage of 10 mg/kg increased heart rate, systemic arterial, pulmonary artery, and central venous blood pressures, as well as cardiac output and arterial partial pressure of CO2 (PaCO2 ). The maximal rate of right ventricular pressure increase (RVdP/ dtmax), respiratory rate, and arterial partial pressure of Ο2 (PaO2 ) decreased, whereas arterial pH and systemic vascular resistance remained unchanged. Preanesthetic medication with diazepam prior to iv administration of thiamylal (6 mg/kg) did not change the pattern of this response, but diazepam did increase heart rate, cardiac output, and respiratory rate during the recovery period. Administration of acepromazine (0.1 mg/kg, iv) prior to administration of thiamylal increased heart rate and decreased systemic arterial and central venous blood pressures and systemic vascular resistance. Detomidine (10 μg/kg, iv), administered prior to thiamylal, decreased heart rate, cardiac output, and respiratory rate, and increased right atrial blood pressure. Administration of xylazine (0.5 and 1.0 mg/kg, iv) prior to thiamylal induced effects qualitatively similar to detomidine. Thiamylal decreased RVdP/dtmax and PaO2 in horses that received diazepam, acepromazine, detomidine, or xylazine.

Horses receiving 10 mg of thiamylal/kg, iv, or 0.1 mg of diazepam/kg, iv, prior to thiamylal (6 mg/kg, iv) had the most difficulty in attaining a standing position. Horses receiving 10 mg of thiamylal/kg, iv, or acepromazine, detomidine, or xylazine (1 mg/kg, iv) prior to thiamylal (6 mg/kg, iv) had the longest anesthesia time. Results indicated that bolus injections of thiamylal used to induce short-term anesthesia in horses increase heart rate, systemic arterial, pulmonary artery, and central venous pressures, as well as PacO2 , but decrease RVdP/dtmax, respiratory rate, and PaO2 . Further, the recovery process was improved by administration of acepromazine, detomidine, or xylazine, but not diazepam, as preanesthetic medication.

Free access
in Journal of the American Veterinary Medical Association

SUMMARY

The effects of iv administered amiodarone, a class-III antiarrhythmic agent, on myocardial contractility, early myocardial relaxation, and hemodynamic variables were evaluated in normal canine hearts and those with infarcts. In the normal canine heart, amiodarone had important, but relatively mild, depressant effects on left ventricular contractility (assessed by maximal positive first derivative of left ventricular pressure (+ dP/dtmax) and maximal elastance (Emax)) and heart rate when given iv at a dose of 10 mg/kg of body weight. An effect on contractility or active relaxation (assessed by maximal negative first derivative of left ventricular pressure (— dP/dtmax) and the time constant of isovolumic pressure decrease) was not identified with smaller doses. Myocardial infarction itself caused a predictable and marked depressant effect on myocardial contractility, as indicated by decreases in + dP/dtmax, ejection fraction, Emax, and — dP/dtmax, and elevation in end diastolic pressure. Additional depressive effects on contractility and active relaxation resulted when 10 mg of amiodarone/kg was administered to dogs with myocardial infarction and these effects were sufficient to worsen acute myocardial infarction-induced heart failure. Significant changes attributable to heart rate alone could not be identified. On the basis of our findings, we suggest that amiodarone administered iv should be used with caution in dogs with compromised ventricular function.

Free access
in American Journal of Veterinary Research

SUMMARY

The effects of single iv injections of sodium bicarbonate (0.5 mEq/kg of body weight, 1 mEq/kg, 2 mEq/kg, and 4 mEq/kg) on serum osmolality, serum sodium, chloride, and potassium concentrations, and venous blood gas tensions in 6 healthy cats were monitored for 180 minutes.

Serum osmolality increased and remained significantly (P < 0.05) increased for 120 minutes in cats given 4 mEq of sodium bicarbonate/kg. Serum sodium was increased significantly (P < 0.05) for 30 minutes in cats given 4 mEq of sodium bicarbonate/kg. Serum sodium decreased and remained significantly (P < 0.05) decreased for 120 minutes in cats given 1 g of 20% mannitol/kg, and serum osmolality was significantly (P < 0.05) decreased at 30 and 60 minutes. Serum chloride decreased significantly (P < 0.05) for 10 minutes in cats given 1 mEq of sodium bicarbonate/kg, and was significantly decreased for 30 minutes in cats given 2 mEq and 4 mEq of sodium bicarbonate/kg. Serum chloride decreased and remained significantly (P < 0.05) decreased for 30 minutes in cats given 1 g of 20% mannitol/kg. Serum sodium and serum osmolality did not change significantly (P < 0.05) in cats given 4 ml of 0.9% sodium chloride/kg.

Serum potassium decreased significantly (P < 0.05) for 10 minutes in cats given 1 mEq of sodium bicarbonate/kg, and for 120 minutes in cats given 2 mEq/kg or 4 mEq/kg. There was a significantly (P < 0.05) greater decrease in serum potassium that lasted for 30 minutes after giving sodium bicarbonate at the dosage of 4 mEq/kg, compared with other dosages given. Serum potassium did not change significantly in cats given 1 g of 20% mannitol/kg, but was significantly (P < 0.05) decreased 10 minutes following 4 ml of 0.9% sodium chloride/kg.

Sodium bicarbonate infusion significantly (P < 0.05) increased venous blood pH and plasma bicarbonate concentration in all cats. The magnitude and duration of these changes were significantly greater following administration of sodium bicarbonate at dosages of 2 mEq/kg and 4 mEq/kg. Significant (P < 0.05) increases in Pco2 were associated only with the highest dosage of sodium bicarbonate (4 mEq/kg). Base excess increased significantly (P < 0.05) in all cats following sodium bicarbonate infusion. There were significantly (P < 0.05) greater increases in base excess lasting 30 minutes following administration of sodium bicarbonate at dosages of 2 mEq/kg and 4 mEq/kg. Significant (P < 0.05) changes in venous blood pH, Pco2 , or bicarbonate were not observed in cats given 4 ml of 0.9% sodium chloride/kg, or in cats given 1 g of 20% mannitol/kg. Base excess was significantly (P < 0.05) increased for 10 minutes in cats given 1 g of 20% mannitol/kg.

As expected, 4 mEq of sodium bicarbonate/kg induced the most time- and dosage-related effects. Caution should be used when administering sodium bicarbonate iv to cats at dosages > 2 mEq/kg, because of the potential for important acid-base and electrolyte changes.

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

SUMMARY

The ventricular arrhythmogenic dose of epinephrine (ade) was determined in 6 dogs anesthetized with halothane alone or with halothane after injection of tiletamine/zolazepam (tz). Respiratory rate and tidal volume were controlled and sodium bicarbonate was administered to maintain arterial pH and blood gas values within reference range. Heart rate and arterial blood pressure were recorded during determination of the ade. The ade (mean ± sd) was no different during anesthesia with use of halothane alone (8.9 ± 4.3) than it was when injections of tz preceded administration of halothane (6.7 ± 2.8). Tiletamine/zolazepam was also administered iv immediately after determination of the ade during halothane-induced anesthesia. The tz administered in this manner did not alter the ade. Blood pressure and heart rate were significantly greater during infusion of epinephrine than immediately prior to infusion. The administration of tz did not alter blood pressure response.

The ade was also determined in 6 cats anesthetized with halothane preceded by administration of tz. The ade (mean ± sd) was 0.7 ± 0.23 μg/kg, a value similar to that reported for cats during anesthesia with halothane alone.

Free access
in American Journal of Veterinary Research

SUMMARY

The cardiovascular effects of xylazine and detomidine in horses were studied. Six horses were given each of the following 5 treatments, at 1-week intervals: xylazine, 1.1 mg/kg, iv; xylazine, 2.2 mg/kg, im; detomidine, 0.01 mg/ kg, iv; detomidine, 0.02 mg/kg, iv; and detomidine, 0,04 mg/kg, im. All treatments resulted in significantly decreased heart rate, increased incidence of atrioventricular block, and decreased cardiac output and cardiac index; cardiac output and cardiac index were lowest following iv administration of 0.02 mg of detomidine/kg. Mean arterial pressure was significantly reduced for various periods with all treatments; however, iv administration of 0.02 nig of detomidine/kg caused hypertension initially. Systemic vascular resistance was increased by all treatments. Indices of ventricular contractility and relaxation, + dP/dt and − dP/dt, were significantly depressed by all treatments. Significant changes were not detected in stroke volume or ejection fraction. The pcv was significantly reduced by all treatments. Respiratoiy rate was significantly decreased with all treatments, but arterial carbon dioxide tension did not change. Arterial oxygen tension was significantly decreased briefly with the 3 iv treatments only.

Free access
in American Journal of Veterinary Research

Abstract

Objective—To evaluate the cardiovascular effects of total IV anesthesia with propofol (P-TIVA) or ketamine-medetomidine-propofol (KMP-TIVA) in horses.

Animals—5 Thoroughbreds.

Procedures—Horses were anesthetized twice for 4 hours, once with P-TIVA and once with KMP-TIVA. Horses were medicated with medetomidine (0.005 mg/kg, IV) and anesthetized with ketamine (2.5 mg/kg, IV) and midazolam (0.04 mg/kg, IV). After receiving a loading dose of propofol (0.5 mg/kg, IV), anesthesia was maintained with a constant rate infusion of propofol (0.22 mg/kg/min) for P-TIVA or with a constant rate infusion of propofol (0.14 mg/kg/min), ketamine (1 mg/kg/h), and medetomidine (0.00125 mg/kg/h) for KMP-TIVA. Ventilation was artificially controlled throughout anesthesia. Cardiovascular measurements were determined before medication and every 30 minutes during anesthesia, and recovery from anesthesia was scored.

Results—Cardiovascular function was maintained within acceptable limits during P-TIVA and KMP-TIVA. Heart rate ranged from 30 to 40 beats/min, and mean arterial blood pressure was > 90 mm Hg in all horses during anesthesia. Heart rate was lower in horses anesthetized with KMP-TIVA, compared with P-TIVA. Cardiac index decreased significantly, reaching minimum values (65% of baseline values) at 90 minutes during KMP-TIVA, whereas cardiac index was maintained between 80% and 90% of baseline values during P-TIVA. Stroke volume and systemic vascular resistance were similarly maintained during both methods of anesthesia. With P-TIVA, some spontaneous limb movements occurred, whereas with KMP-TIVA, no movements were observed.

Conclusions and Clinical Relevance—Cardiovascular measurements remained within acceptable values in artificially ventilated horses during P-TIVA or KMP-TIVA. Decreased cardiac output associated with KMP-TIVA was primarily the result of decreases in heart rate.

Full access
in American Journal of Veterinary Research