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- Author or Editor: William W. Muir III x
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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)
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.
Summary
Six nontrained mares were subjected to steady-state, submaximal treadmill exercise to examine the effect of exercise on the plasma concentration of atrial natriuretic peptide (anp) in arterial, compared with mixed venous, blood. Horses ran on a treadmill up a 6° grade for 20 minutes at a speed calculated to require a power equivalent to 80% of maximal oxygen uptake (Vo 2MAX). Arterial and mixed venous blood samples were collected simultaneously from the carotid and pulmonary arteries of horses at rest and at 10 and 20 minutes of exercise. Plasma was stored at − 80 C and was later thawed; anp was extracted, and its concentration was determined by radioimmunoassay. Exercise caused significant (P < 0.05) increases in arterial and venous plasma anp concentrations. Mean ± sem arterial anp concentration increased from 25.2 ± 4.4 pg/ml at rest to 52.7 ± 5.2 pg/ml at 10 minutes of exercise and 62.5 ± 5.2 pg/ml at 20 minutes of exercise. Mean venous anp concentration increased from 24.8 ± 4.3 pg/ml at rest to 67.2 ± 14.5 pg/ml at 10 minutes of exercise and 65.3 ± 13.5 pg/ml at 20 minutes of exercise. Significant differences were not evident between arterial or mixed venous anp concentration at rest or during exercise, indicating that anp either is not metabolized in the lungs or is released from the left atrium at a rate matching that of pulmonary metabolism.
SUMMARY
Programmed electrical stimulation techniques were used to evaluate the effects of halothane and isoflurane on induction of atrial fibrillation in anesthetized dogs. Experiments were performed in 16 dogs anesthetized with α-chloralose. Critically timed premature stimuli were applied to the right atrial appendage and Bachmann bundle to determine the atrial fibrillation threshold, defined as the minimal current required to induce rapid, irregular atrial electrical activity of at least 8 seconds' duration, Atrial fibrillation thresholds were determined at baseline (0.0% inhalational anesthetic), 0.5 minimal alveolar concentration (mac), and 1.0 mac of halothane (n = 8) and isoflurane (n = 8).
In the absence of inhalation anesthetic, it was significantly (P < 0.01) easier to induce atrial fibrillation at the Bachmann bundle vs the right atrial appendage. Atrial fibrillation threshold at the Bachmann bundle was not affected by increasing concentrations of halothane, but was increased by 1.0 mac of isoflurane (P < 0.05). It was concluded that at 1.0 mac isoflurane, but not halothane, has antifibrillatory effects in atrial tissue.
SUMMARY
The cardiopulmonary effects of 4 positions (standing, right lateral, left lateral, and dorsal recumbency) were evaluated in conscious cattle in which no sedatives or anesthetic drugs were given. Each position was maintained for 30 minutes, during which time there were no significant changes in heart rate, respiratory rate, mean arterial blood pressure, arterial pH, PaCO2 , arterial base excess, or venous blood gas values. Significant decreases in PaO2 developed when cattle were in lateral positions and dorsal recumbency. Cardiac index was unchanged in all positions, except in dorsal recumbency at 30 minutes, when it was significantly decreased.
Abstract
Objective
To determine sedative, cardiorespiratory and metabolic effects of xylazine hydrochloride, detomidine hydrochloride, and a combination of xylazine and acepromazine administered IV at twice the standard doses in Thoroughbred horses recuperating from a brief period of maximal exercise.
Animals
6 adult Thoroughbreds,
Procedure
Horses were preconditioned by exercising them on a treadmill to establish a uniform level of fitness. Each horse ran 4 simulated races, with a minimum of 14 days between races. Simulated races were run at a treadmill speed that caused horses to exercise at 120% of their maximal oxygen consumption. Horses ran until they were fatigued or for a maximum of 2 minutes. One minute after the end of exercise, horses were treated IV with xylazine (2.2 mg/kg of body weight), detomidine (0.04 mg/kg), a combination of xylazine (2.2 mg/kg) and acepromazine (0.04 mg/kg), or saline (0.9% NaCl) solution. Treatments were randomized so that each horse received each treatment once, in random order. Cardiopulmonary indices were measured, and samples of arterial and venous blood were collected immediately before and at specific times for 90 minutes after the end of each race.
Results
All sedatives produced effective sedation. The cardiopulmonary depression that was induced was qualitatively similar to that induced by administration of these sedatives to resting horses and was not severe. Sedative administration after exercise prolonged the exercise-induced increase in body temperature.
Conclusions and Clinical Relevance
Administration of xylazine, detomidine, or a combination of xylazine-acepromazine at twice the standard doses produced safe and effective sedation in horses that had just undergone a brief, intense bout of exercise. (Am J Vet Res 1999;60:1271–1279)
Abstract
Objective
To determine cardiorespiratory effects of a tiletamine/zolazepam-ketamine-detomidine (TZKD) combination in horses.
Animals
8 healthy adult horses.
Procedure
Horses were instrumented for measurement of cardiorespiratory, acid-base, and electrolyte values. Each horse was given xylazine (0.44 mg/kg of body weight, IV) 10 to 15 minutes prior to induction of recumbency by administration of the TZKD combination. Cardiorespiratory, acid-base, and electrolyte values were measured at 5-minute intervals for ≥ 30 minutes.
Results
All horses became recumbent within 1 minute after IV administration of TZKD. Mean ± SD duration of recumbency was 40 ± 8 minutes. All horses regained standing position after ≤ 2 attempts. Quality of anesthesia and analgesia was determined to be satisfactory in all horses. Xylazine induced decreases in respiratory rate, heart rate, cardiac output, maximum rate of increase of right ventricular pressure, and rate pressure product. The PaCO2, right atrial pressure, and peripheral vascular resistance increased, whereas blood temperature, PO2, pHa, HCO3 −, PCV, total solids, Na, and K values remained unchanged. Subsequent administration of TZKD caused right atrial pressure and PaCO2 to increase and PaO2 to decrease, compared with values obtained after xylazine administration. Remaining cardiorespiratory, acid-base, hematologic, and electrolyte values did not differ from those obtained after xylazine administration.
Conclusion
IV administration of TZKD induces short-term anesthesia in horses. Potential advantages of this drug combination are the small volume of drug administered; minimal cardiorespiratory depression; quality of induction and maintenance of, and recovery from, anesthesia; and duration of drug effects. (Am J Vet Fles 1999;60:770–774)
SUMMARY
Cardiorespiratory effects of the combination of acepromazine maleate (acp) and buprenorphine hydrochloride (bpn) were studied in 11 healthy, conscious dogs. Values for systemic and pulmonary artery blood pressure, cardiac output, arterial and venous pH and blood gas tensions, and invasive and noninvasive estimates of ventricular systolic function, preload, and afterload were obtained before sedation and after administration of each drug. Acepromazine maleate (0.1 mg/kg, iv) depressed cardiac function, compared with baseline values for unsedated dogs. Cardiac output decreased from a mean (± sd) value of 4.2 (± 1.5) L/min to 3.1 (± 0.8) L/min (P < 0.001), a change not attributed to heart rate. Pulmonary capillary wedge pressure decreased from 8.3 (± 4.2) mm of Hg to 6.5 (± 4.3) mm of Hg (P < 0.01), but mean right atrial pressure did not change. Left ventricular measurement of the maximal positive rate of pressure change (dP/dtmax) decreased from 2,668 (± 356)/mm of Hg/s to 2,145 (± 463) mm of Hg/s (P < 0.001), and ventricular stroke volume decreased from 43.2 (± 15.2) ml/beat to 32.3 (± 8.6) ml/beat. Noninvasive indices of left ventricular function, ventricular shortening fraction, peak aortic velocity, and aortic average acceleration were decreased after acp administration, but were not statistically different from baseline values. Mean systemic arterial blood pressure decreased from 121 ± 12 mm of Hg to 96 ± 13 mm of Hg 15 minutes after acp administration (P < 0.001). Total systemic vascular resistance was not significantly different from the baseline value. Sequential administration of cumulative doses of bpn (0.005, 0.01, and 0.1 mg/kg of body weight, iv), initiated 15 minutes after administration of acp, did not cause statistically significant depression of hemodynamic variables, except for heart rate, which decreased after bpn, and left ventricular dP/dtmax, which decreased slightly at the highest dose of bpn. Small, clinically insignificant changes in blood pH, venous bicarbonate concentration, and Paco2 were observed after administration of acp and bpn. Respiratory rate decreased from 60 ± 48 breaths/min to 24 ± 12 breaths/min, and sedation level was significantly (P < 0.05) increased from baseline values by administration of acp. Sedation level was further increased by administration of bpn at the lowest dose (P < 0.05). The combination of acp and bpn resulted in good to excellent sedation, but depressed ventricular function; however, most of the hemodynamic effects could be attributed to administration of acp and withdrawal of sympathetic activity.
Abstract
Objectives
To determine the concentrations of sevoflurane and compound A (a degradation product of sevoflurane) in the anesthetic circuit when sevoflurane was delivered with an in-circuit vaporizer, and to determine the cardiorespiratory effects of sevoflurane in dogs.
Animals
6 mixed-breed dogs.
Procedure
In-circuit vaporizers were connected to the inspiratory limb of a circle rebreathing system connected to a ventilator. A reservoir bag was attached to the Y-piece connector to act as an artificial lung, and sevoflurane concentrations in the anesthetic circuit were measured at vaporizer settings of 1, 3, 5, 7, and 10 and oxygen flow rates of 250 and 500 ml/min. Cardiorespiratory effects of sevoflurane were determined in dogs while they were breathing spontaneously, during controlled ventilation, and during closed circuit anesthesia. Concentrations of compound A were determined by means of gas chromatography with flame ionization.
Results
The concentration of sevoflurane in the anesthetic circuit increased with vaporizer setting and time. For oxygen flow rates of 250 and 500 ml/min, vaporizer settings between 5 and 7 and between 7 and 10, respectively, produced sevoflurane concentrations closest to values reported to produce surgical anesthesia in dogs. Significant differences were not observed in cardiorespiratory variables with time or among anesthetic conditions. Concentrations of compound A in the anesthetic circuit were less than values reported to produce renal toxicoses and death in rats.
Conclusion
Results suggested that sevoflurane can be administered to nonsurgically stimulated dogs, using an in-circuit vaporizer and low (< 15 ml/kg/min) oxygen flow rates, without causing significant cardiorespiratory depression or clinically important concentrations of compound A. (Am J Vet Res 1998;59:603–608)
Abstract
Objective— To determine the hemodynamic effects of IM administration of romifidine hydrochloride in propofol-anesthetized cats.
Animals—15 adult domestic shorthair cats.
Procedure—Cats were randomly assigned to receive romifidine (0, 400, or 2,000 µg/kg, IM). Cats were anesthetized with propofol and mechanically ventilated with oxygen. The right jugular vein, left carotid artery, and right femoral artery and vein were surgically isolated and catheterized. Heart rate; duration of the PR, QRS, and QT intervals; mean pulmonary artery pressure; mean right atrial pressure; systolic, diastolic, and mean arterial pressures; left ventricular systolic pressure; left ventricular end-diastolic pressure; and cardiac output were monitored. Systemic vascular resistance, rate of change of left ventricular pressure, and rate pressure product were calculated. Arterial and venous blood samples were collected anaerobically for determination of pH and blood gas tensions (PO2 and PCO2).
Results—Administration of romifidine at 400 and 2,000 µg/kg, IM, decreased heart rate, cardiac output, rate of change of left ventricular pressure, rate pressure product, and pH. Arterial and pulmonary artery pressures, left ventricular pressure, left ventricular end-diastolic pressure, and right atrial pressure increased and then gradually returned to baseline values. Arterial blood gas values did not change, whereas venous PCO2 increased and venous PO2 decreased. Significant differences between low and high dosages were rare, suggesting that the dosages investigated produced maximal hemodynamic effects.
Conclusion and Clinical Relevance—Romifidine produces cardiovascular effects that are similar to those of other α2-agonists. High dosages of romifidine should be used with caution in cats with cardiovascular compromise. (Am J Vet Res 2002;63:1241–1246)