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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

Summary

Opsonized Rhodococcus equi activated the respiratory burst of resident alveolar macrophages (am) from adult horses in a logarithmic-linear, mass-related manner. The effect of R equi was not significantly different from that of equal masses of opsonized zymosan A. Therefore, R equi does not appear to attenuate the respiratory burst of equine am. The stimulatory effect of R equi was not reflected by increased production of superoxide anion (O2 -), but increased activity of the hexose monophosphate shunt was observed. These results suggest a similarity between the respiratory burst of am from horses and that of am from rabbits. We concluded that resident am from adult horses do not produce O2 - concurrently with an increase in activity of the hexose monophosphate shunt when stimulated with either opsonized zymosan A or opsonized R equi. This suggests that O2 - is not an important component of the antibacterial defenses of equine am. Whether equine am are incapable of producing O2 - or require different stimuli to produce it was not determined.

Free access
in American Journal of Veterinary Research

Abstract

Objective

To determine effectiveness of a new and practical method for fluid resuscitation of dehydrated diarrheic calves.

Design

Animals randomly allocated to 4 groups with appropriate controls.

Animals

16 healthy male dairy calves, 3 to 6 days old.

Procedure

After instrumentation and recording baseline data, diarrhea and hypovolemia were induced by administering milk replacer (33 ml/kg of body weight) and isotonic sucrose solution (2 g of sucrose in 19.5 ml of water/kg, PO) every 8 hours, and furosemide (2 mg/kg, IM) every 4 to 8 hours. Administration of milk replacer and furosemide was discontinued when calves became 6% dehydrated. Calves were then randomly allocated as: control (no treatment); hypertonic saline-dextran (HSD) solution (4 ml/kg, 2,400 mOsm/L NaCl in 6% dextran-70, administered once over 4 minutes, IV); isotonic alkalinizing oral electrolyte solution (55 ml/kg, PO, q 8 h); and HSD-oral electrolyte solution (combination of HSD and oral treatments). Calves were monitored for 24 hours after treatment.

Results

Significant changes included moderate dehydration (8% body weight), marked lethargy, decreased cardiac output and plasma volume, and increased blood lactate concentration, hematocrit, and serum concentrations of albumin, creatinine, sodium, and phosphate. Control calves continued to be lethargic and dehydrated, with significant increases in hematocrit and serum creatinine concentration. Increase in cardiac output and plasma volume was transient in the HSD group and waned by 2 to 8 hours after treatment. Oral electrolyte fluid administration caused slow and sustained increase in cardiac output and plasma volume, and decrease in heart rate, blood lactate concentration, and hematocrit. Combined administration of HSD-oral electrolyte solution caused immediate and sustained increase in cardiac output and plasma volume, and decrease in heart rate, blood lactate concentration, and hematocrit.

Conclusions and Clinical Relevance

Treatment of hypovolemic diarrheic calves with IV HSD and oral electrolyte solution is superior to administration of either solution alone. (Am J Vet Res 1996;57:97-104)

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

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

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

Objective

To investigate the relation between cardiac output (CO) and peripheral (fetlock) temperature (PT) and core-peripheral (rectal-fetlock) temperature difference (CPTD) in dehydrated calves housed in a thermoneutral environment.

Animals

28 male dairy calves 3 to 10 days old.

Procedure

Severe dehydration and watery diarrhea were induced by administering diuretics (furosemide, hydrohlorothiazide, spironolactone) and sucrose solution. Cardiac output was measured by means of thermodilution, core temperature was determined by placing a digital thermometer in the rectum, and PT was measured by taping a thermistor to the left hind fetlock and insulating the thermistor from ambient air.

Results

In thermoneutral ambient temperatures (10 to 24 C), PT and CPTD were constant and independent of CO at normal or high CO values but were linearly dependent on CO below a critical value (78% of normal CO output). Regression equations were developed that predicted CO from measured PT or CPTD. At ambient temperatures below the lower critical temperature for neonatal calves (8 to 10 C), normal values for PT and CPTD in healthy calves were significantly different from those at thermoneutral ambient temperatures.

Conclusions and Clinical Relevance

Peripheral temperature and CPTD are practical, noninvasive, and inexpensive but only moderately useful methods for predicting CO in hemodynamically stable calves housed in a thermoneutral environment. Thus, these parameters are of some value in daily monitoring of the response to treatment and in determining need for IV fluid administration in dehydrated calves housed at a dry still-air temperature of 10 to 24 C but are of minimal to no value in calves housed at < 10 C. (Am J Vet Res 1998;59:874–880)

Free access
in American Journal of Veterinary Research

Objective

To determine effectiveness of rapid IV administration of hypertonic saline-dextran (HSD) solution combined with oral administration of isotonic electrolyte solution for resuscitating severely dehydrated calves and to compare the resuscitative response with that of a conventional treatment of lactated Ringer's solution (LRS) IV and orally administered isotonic electrolyte solution.

Design

Prospective study.

Animals

15 male dairy calves 3 to 10 days old.

Procedure

Baseline data were obtained. Osmotic diarrhea and severe dehydration were induced for 48 hours. Calves were then allocated to 3 treatment groups. The control group (group C) did not receive fluids, a second group (group H) received hypertonic saline (7.2% NaCI) solution with 6% dextran 70 and isotonic electrolyte solution, and a third group (group L) received LRS and isotonic electrolyte solution. Physical examinations were performed every 8 hours.

Results

Calves developed diarrhea, lethargy, severe dehydration (mean, 14% of body weight), azotemia, hyperkalemia, and mild acidemia. Group-C calves remained lethargic and severely dehydrated during the 24-hour treatment phase. Calves treated with HSD and LRS were effectively resuscitated; however, response for most variables was more rapid and sustained for the HSD-treated group. Cardiac output was greater in LRS- than HSD-treated calves 1, 2, and 8 hours after initiation of treatment because of continued IV administration of fluids.

Clinical Implications

A combination of HSD and isotonic electrolyte solution was a rapid and effective method for resuscitation of severely dehydrated calves. It was similar in effectiveness to conventional treatment in which LRS and isotonic electrolyte solution were used for resuscitating calves with severe dehydration.(J Am Vet Med Accoc 1998;213:113-121)

Free access
in Journal of the American Veterinary Medical Association

Summary

Anesthesia was induced and maintained in 6 Suffolk wethers by continuous iv infusion of guaifenesin (50 mg/ml), ketamine (1 mg/ml), and xylazine (0.1 mg/ml) in 5% dextrose in water (triple drip) to assess the anesthetic and cardiopulmonary effects. All sheep were positioned in right lateral recumbency. Dosages of triple drip used for induction and maintenance of anesthesia were 1.2 ± 0.02 ml/kg and 2.6 ml/kg/h, respectively. Lack of gross purposeful movement of sheep to electrical stimulation indicated that analgesia and muscular relaxation induced by triple trip were adequate for surgical procedures. Heart rates and arterial blood pressure remained unchanged from baseline values during a 1-hour period of anesthesia. Arterial blood pressures were measured indirectly, using an inflation cuff placed over the metatarsal artery at the heart level. Significant decrease in arterial partial pressure of O2 (Pao2 ), coupled with an increase in arterial partial pressure of CO2 (Paco2 ), from baseline values was observed throughout the course of the study. Decrease in Pao2 was observed concomitantly with significant (P < 0.05) increase in respiration rate. Changes in arterial blood gas tensions observed in this study were attributed to respiratory depressant effect induced by anesthetic drugs and right-to-left shunting, perfusion/ventilation mismatch, or both caused by right lateral recumbency. Administration of 100% O2 via the endotracheal tube reduced the magnitude of the decrease in Pao2 . All sheep recovered smoothly and stood within 96.3 ± 48.9 minutes after termination of triple drip administration

Free access
in American Journal of Veterinary Research