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Abstract

Objective—To assess duration of actions of butorphanol, medetomidine, and a butorphanol-medetomidine combination in dogs given subanesthetic doses of isoflurane (ISO).

Animals—6 healthy dogs.

Procedure—Minimum alveolar concentration (MAC) values for ISO were determined. for each dog. Subsequently, 4 treatments were administered to each dog (saline [0.9% NaCl] solution, butorphanol [0.2 mg/kg of body weight], medetomidine [5.0 mg/kg], and a combination of butorphanol [0.2 mg/kg] and medetomidine [5.0 mg/kg]). All treatments were administered IM to dogs concurrent with isoflurane; treatment order was determined, using a randomized crossover design. Treatments were given at 7-day intervals. After mask induction with ISO and instrumentation with a rectal temperature probe, endtidal CO2 and anesthetic gas concentrations were analyzed. End-tidal ISO concentration was reduced to 90% MAC for each dog. A tail clamp was applied 15 minutes later. After a positive response, 1 of the treatments was administered. Response to application of the tail clamp was assessed at 15-minute intervals until a positive response again was detected.

Results—Duration of nonresponse after administration of saline solution, butorphanol, medetomidine, and butorphanol-medetomidine (mean ± SD) was 0.0 ± 0.0, 1.5 ± 1.5, 2.63 ± 0.49, and 5.58 ± 2.28 hours, respectively. Medetomidine effects were evident significantly longer than those for saline solution, whereas effects for butorphanol-medetomidine were evident significantly longer than for each agent administered alone.

Conclusion and Clinical Relevance—During ISOinduced anesthesia, administration of medetomidine, but not butorphanol, provides longer and more consistent analgesia than does saline solution, and the combination of butorphanol-medetomidine appears superior to the use of medetomidine or butorphanol alone. (Am J Vet Res 2000;61:42–47)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To determine the relationship between bispectral index (BIS) and minimum alveolar concentration (MAC) multiples of isoflurane after IM injection of medetomidine or saline (0.9% NaCl) solution in anesthetized dogs.

Animals—6 dogs.

Procedure—Each dog was anesthetized 3 times with isoflurane. First, the MAC of isoflurane for each dog was determined by use of the tail clamp method. Second, anesthetized dogs were randomly assigned to receive an IM injection of medetomidine (8 µg · kg–1) or an equal volume of isotonic saline (0.9% NaCl) solution 30 minutes prior to beginning BIS measurements. Last, anesthetized dogs received the remaining treatment (medetomidine or isotonic saline solution). Dogs were anesthetized at each of 4 MAC multiples of isoflurane. Ventilation was controlled and atracurium (0.2 mg/kg followed by 6 µg/kg/min as a continuous infusion, IV) administered. After a 20-minute equilibration period at each MAC multiple of isoflurane, BIS data were collected for 5 minutes and median values of BIS calculated.

Results—BIS significantly decreased with increasing MAC multiples of isoflurane over the range of 0.8 to 2.0 MAC. Mean (± SD) MAC of isoflurane was 1.3 ± 0.2%. During isoflurane-saline anesthesia, mean BIS measurements at 0.8, 1.0, 1.5, and 2.0 MAC were 65 ± 8, 60 ± 7, 52 ± 3, and 31 ± 28, respectively. During isoflurane-medetomidine anesthesia, mean BIS measurements at 0.8, 1.0, 1.5, and 2.0 MAC were 77 ± 4, 53 ± 7, 31 ± 24, and 9 ± 20, respectively.

Conclusions and Clinical Relevance—BIS monitoring in dogs anesthetized with isoflurane has a predictive value in regard to degree of CNS depression. During isoflurane anesthesia, our results support a MAC-reducing effect of medetomidine. (Am J Vet Res 2003;64:316–320)

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in American Journal of Veterinary Research

Summary

Eight dogs (body weight, 12.5 to 21.5 kg) were assigned at random to each of 3 treatment groups (is, ix, im) that were not given glycopyrrolate and to each of 3 groups that were given glycopyrrolate (igs, igx, igm). Dogs were anesthetized with isoflurane (1.95% end-tidal concentration), and ventilation was controlled (PCO2 , 35 to 40 mm of Hg end-tidal concentration). Glycopyrrolate was administered iv and im at a dosage of 11 μg/kg of body weight, each. Saline solution, xylazine (1.1 mg/kg, im), or medetomidine (15 μg/kg, im) was administered 10 minutes after baseline ade determination. Redetermination of the ade at the same infusion rate was started 10 minutes after drug administration. Arrhythmogenic dose was determined by constant infusion of epinephrine at rates of 1.0, 2.5, and 5.0 μg/kg/min. The ade was defined as the total dose of epinephrine that induced at least 4 ectopic ventricular depolarizations within 15 seconds during a 3-minute infusion, or within 1 minute after the end of the infusion. Total dose was calculated as the product of infusion rate and time to arrhythmia. Statistical analysis of the differences between baseline and treatment ade values was performed by use of one-way anova. Mean ± sem baseline ade values for groups is, ix, and im were 1.55 ± 0.23, 161 ± 0.28, and 1.95 ± 0.65 μg/kg, respectively. Differences for groups is, ix, and im were – 0.12 ± 0.05, – O.31 ± 0.40, and – 0.17 ± 0.26, respectively. Differences for groups igs, igx, and igm could not be calculated because arrhythmias satisfying the ade criteria were not observed at the maximal infusion rate of 5.0 μg/kg/min. Differences among groups is, ix, and im were not significant. We conclude that in isoflurane-anesthetized dogs: preanesthetic dosages of xylazine (1.1 mg/kg, im) or medetomidine (15 μg/kg, im) do not enhance arrhythmogenicity, and at these dosages, there is no difference in the arrhythmogenic potential of either α2-adrenergic receptor agonist.

Free access
in American Journal of Veterinary Research

Summary

Eight dogs (12.5 to 21.5 kg) were assigned at random to each of 3 groups that were not given glycopyrrolate (hs, hx, hm) and to each of 3 groups that were given glycopyrrolate (hgs, hgx, hgm). Dogs were anesthetized with halothane (1.31% end-tidal concentration), and ventilation was controlled (PCO2 35 to 40 mm of Hg end-tidal concentration). Glycopyrrolate was administered iv and im at a dosage of 11 μg/kg of body weight, each. Saline solution, xylazine (1.1 mg/kg, im, or medetomidine (15 μg/ kg, im) was administered 10 minutes after baseline arrhythmogenic dose of epinephrine (ade) determination. Redetermination of the ade at the same infusion rate was started 10 minutes after drug administration. Arrhythmogenic dose was determined by constant infusion of epinephrine at rates of 1.0 and 2.5 μg/kg/min. The ade was defined as the total dose of epinephrine inducing at least 4 ectopic ventricular depolarizations within 15 seconds during a 3-minute infusion or within 1 minute after the end of the infusion. Total dose was calculated as the product of infusion rate and time to arrhythmia. Statistical analysis of the differences between baseline ade and posttreatment ade for groups hs, hx, and hm was performed by use of one-way anova. Mean ± sem baseline ade values for groups hs, hx, and hm were 1.50 ± 0.11, 1.49 ± 0.10, and 1.57 ± 0.22 pg/kg, respectively, and for groups hgs, hgx, and hgm were 3.37 ± 0.61, 3.10 ± 0.75, and 3.04 ± 0.94 pg/kg, respectively. Differences for groups hs, hx, and hm were – 0.02 ± 0.15, – 0.00 ± 0.14, and – 0.21 ± 0.17 μg/kg, respectively, and for groups hgs, hgx, and hgm, were – 0.59 ± 0.26, – 0.41 ± 0.15, and – 0.58 ± 0.20 μg/kg, respectively. Differences among groups hs, hx, and hm, or among groups hgs, hgx, and hgm were not significant. We conclude that without and with cholinergic blockade in halothane-anesthetized dogs: preanesthetic dosages of xylazine (1.1 mg/kg, im) or medetomidine (15 μg/kg, im) do not enhance arrhythmogenicity, and at these dosages, there is no difference in the arrhythmogenic potential of either α2-adrenoceptor agonist.

Free access
in American Journal of Veterinary Research

Summary

Hemodynamic and analgesic effects of medetomidine (30 μg/kg of body weight, im), atropine (0.044 mg/kg, im), and propofol (2 mg/kg, IV, as a bolus, and 165 μg/kg/min, Iv, for 60 minutes, as an infusion) were evaluated in 6 healthy adult Beagles. Catheters were placed while the dogs were anesthetized with isoflurane in oxygen. Administration of isoflurane was then discontinued, and dogs were allowed to breath oxygen until end-tidal isoflurane concentration was ≤ 0.5%. At this time, baseline measurements were recorded and medetomidine and atropine were administered. Ten minutes later, the bolus of propofol was given and the infusion was begun. Analgesia was evaluated with a tail clamp test and by use of a direct-current nerve stimulator. Sinoatrial and atrioventricular blockade developed in all 6 dogs within 2 minutes of administration of medetomidine and atropine, but disappeared within 10 minutes. Apnea did not develop after administration of propofol. Analgesia was strong and consistent throughout the entire 60-minute period of propofol infusion. Medetomidine significantly (P < 0.05) increased systemic vascular resistance and decreased cardiac output, compared with baseline values. Propofol infusion appeared to alleviate medetomidine induced vasoconstriction. Recovery was smooth and uncomplicated. All dogs were able to walk normally at a mean time (± sem) of 88.2 ± 20.6 minutes after termination of propofol infusion. It was concluded that medetomidine, atropine, and propofol, as given in the present study, is a safe combination of anesthetic drugs for use in healthy Beagles.

Free access
in American Journal of Veterinary Research

Summary

Hemodynamic and analgesic effects of medetomidine (15 µg/kg of body weight, im) and etomidate (0.5 mg/kg, iv, loading dose; 50 µg/kg/min. constant infusion) were evaluated in 6 healthy adult Beagles. Instrumentation was performed during isoflurane/oxygen-maintained anesthesia. Before initiation of the study, isoflurane was allowed to reach end-tidal concentration ≤ 0.5%, when baseline measurements were recorded. Medetomidine and atropine (0.044 mg/kg) were given im after recording of baseline values. Ten minutes later, the loading dose of etomidate was given im, and constant infusion was begun and continued for 60 minutes. Oxygen was administered via endotracheal tube throughout the study. Analgesia was evaluated by use of the standard tail clamp technique and a direct-current nerve stimulator.

Sinoatrial and atrial-ventricular blocks occurred in 4 of 6 dogs within 2 minutes after administration of a medetomidine-atropine combination, but disappeared within 8 minutes. Apnea did not occur after administration of the etomidate loading dose. Analgesia was complete and consistent throughout 60 minutes of etomidate infusion. Medetomidine significantly (P < 0.05) increased systemic vascular resistance and decreased cardiac output. Etomidate infusion caused a decrease in respiratory function, but minimal changes in hemodynamic values. Time from termination of etomidate infusion to extubation, sternal recumbency, standing normally, and walking normally were 17.3 ± 9.4, 43.8 ± 14.2, 53.7 ± 11.9, and 61.0 ± 10.9 minutes, respectively. All recoveries were smooth and unremarkable. We concluded that this anesthetic drug combination, at the dosages used, is a safe technique in healthy Beagles.

Free access
in American Journal of Veterinary Research

Summary

The case records of 26 horses with ileocecal intussusception over a 7-year period were reviewed to determine clinical features of the disease and response to treatment. The median age of horses with ileocecal intussusception was 1 year and ranged from 2 weeks to 19 years. There was no apparent gender or breed predisposition to this disease.

An acute form of ileocecal intussusception was diagnosed in 19 horses with signs of moderate to severe abdominal pain of:$ 24 hours' duration, and a chronic form was diagnosed in 7 horses with signs of intermittent, mild to moderate abdominal pain of more than 3 days' duration. Horses with chronic ileocecal intussusception had a history of weight loss or failure to gain weight, slow growth, poor appetite, low-grade pyrexia, and postprandial signs of abdominal pain. At surgery, the involved segments of intestine (intussusceptum and intussuscipiens) in chronic cases were 2 to 10 cm long, and the ileum and much of the distal portion of the jejunum were flaccid, dilated, and thick walled. In the acute cases, the length of involved intestine ranged from 6 to 457 cm. Whereas only 1 of 7 chronic intussusceptions (14%) could be reduced, 9 of 19 (47%) acute intussusceptions were reducible.

Surgical treatment included resection and jejunocecostomy (6 horses), partial resection through a cecotomy and a side-to-side jejunocecostomy (2 horses), and a side-to-side ileocecostomy or jejunocecostomy without resection (12 horses, 7 of which had chronic intussusception). Six horses with acute intussusception were euthanatized before or during surgery. Four horses with acute intussusception died or were euthanatized between 2 and 9 months after surgery, 1 from unknown causes, 2 from impaction at the anastomosis, and 1 from small-intestinal strangulation. Two horses were lost to long-term follow-up. Horses with chronic intussusception survived, but some of these horses had a slow postoperative recovery.

Free access
in Journal of the American Veterinary Medical Association

Objective

To determine causes of tracheal rupture in cats and the mechanism of injury.

Design

A retrospective study was conducted to identify cats with tracheal rupture. A second study was conducted to establish mechanism of injury, and a third study was conducted to determine volume of air needed to obtain an airtight seal when inflating the cuff of an endotracheal tube in a cat.

Animals

16 cats with clinical signs of tracheal rupture, 10 cat cadavers, and 20 clinically normal cats that were undergoing anesthesia.

Procedures

Details were extracted from medical records of 16 cats with tracheal rupture (9 treated surgically and 7 treated conservatively). For the cadaver study, the trachea of each cat cadaver was intubated and observed during overinflation of the endotracheal tube cuff. For clinically normal cats, volume of air needed to obtain an airtight seal for the endotracheal tube was recorded.

Results

Most ruptures were associated with cats anesthetized for dental procedures. Clinical signs associated with tracheal rupture included subcutaneous emphysema, coughing, gagging, dyspnea, anorexia, and fever. Tracheoscopy was the method of choice for documenting tracheal rupture. Surgical and conservative management were successfully used, unless the injury extended to the carina. In the cadaver study, overinflation of the endotracheal tube cuff with > 6 ml of air resulted in tracheal rupture in 7 of 10 cadavers. For clinically normal cats, the volume of air (mean ± SD) needed to obtain an airtight seal was 1.6 ± 0.7 ml.

Clinical Implications

Overinflation of an endotracheal tube cuff may result in tracheal rupture in cats. (J Am Vet Med Assoc 1999;214:508–512).

Free access
in Journal of the American Veterinary Medical Association

Abstract

Objective—To determine the hemodynamic consequences of the coadministration of a continuous rate infusion (CRI) of medetomidine with a fentanyl bolus in dogs.

Animals—12 healthy sexually intact male dogs weighing 30.3 ± 4.2 kg (mean ± SD).

Procedure—Dogs received either fentanyl alone (15.0 µg/kg, IV bolus) or the same dose of fentanyl during an 11-hour CRI of medetomidine (1.5 µg/kg/h, IV). Prior to drug administration, dogs were instrumented for measurement of cardiac output, left atrial pressure, and systemic arterial blood pressures. Additionally, blood samples were collected from the pulmonary artery and left atrium for blood gas analysis.

Results—Medetomidine infusion reduced the cardiac index, heart rate, and O2 delivery while increasing left atrial pressure. Subsequent fentanyl administration further decreased the cardiac index. The PaO2 was not significantly different between the 2 treatment groups; however, fentanyl transiently decreased PaO2 from baseline values in dogs receiving a CRI of medetomidine.

Conclusions and Clinical Relevance—Because of the prolonged hemodynamic changes associated with the CRI of medetomidine, its safety should be further evaluated before being clinically implemented in dogs. (Am J Vet Res 2005;66:1222–1226)

Full access
in American Journal of Veterinary Research

Abstract

Objective

To investigate hemodynamic effects of thyroidectomy in horses at rest.

Animals

6 healthy aged Quarter Horse mares.

Procedure

Horses were monitored for 5 months before and 4 weeks after thyroidectomy and for an additional 4 weeks after administration of thyroid hormone supplement (2.5 µg of thyroxine/kg of body weight, PO, q 12 h, and 0.6 µg of triiodothyronine/kg, PO, q 12 h). Responses to thyroid-stimulating hormone (TSH) were measured before and 4 weeks after thyroidectomy. Other variables monitored daily were resting rectal temperature (T), heart rate (HR), respiratory rate (RR), and body weight (BW), Monthly cardiac output (Q), blood volume (BV), plasma volume (PV), standard electrocardiographic measures, systolic and right ventricular blood pressure, and HR responses were determined after IV administration of isoproterenol and phenylephrine. Variables were analyzed by use of repeated-measures ANOVA.

Results

Complete thyroidectomy was confirmed by minimal response to TSH 4 weeks after surgery. Resting HR, RR, T, Q, and β-adrenergic responsiveness to isoproterenol decreased significantly after thyroidectomy. Resting T, Q, and β-adrenergic responsiveness increased after administration of supplement and was not significantly different from euthyroid values. Blood volume and PV increased significantly after thyroidectomy but did not return to euthyroid values despite administration of supplement. Response to phenylephrine was minimally different between treatments.

Conclusions and Clinical Relevance

Thyroidectomy in horses caused decreased resting HR, RR, T, Q, and isoproterenol responsiveness and increased BV, PV, PQ interval, and QT interval corrected for HR. Some of these surgically induced changes appeared to be partially reversed by administration of thyroid hormone supplement. (Am J Vet Res 1999;60:14–21)

Free access
in American Journal of Veterinary Research