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- Author or Editor: Jeff C. H. Ko x
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SUMMARY
We compared the ability of 2 α2-adrenergic receptor antagonists, atipamezole and yohimbine, to reverse medetomidine-induced CNS depression and cardiorespiratory changes in lambs. Twenty lambs (7.8 ± 2.6 kg) were randomly allotted to 4 treatment groups (n = 5). Each lamb was given medetomidine (30 μg/kg of body weight, IV), followed in 15 minutes by IV administration of atipamezole (30 or 60 μg/kg), yohimbine (1 mg/kg), or 0.9% NaCl (saline) solution. Medetomidine caused lateral recumbency in 1 to 2 minutes in all treated lambs. Medetomidine significantly (P < 0.05) decreased heart rate at 5 and 10 minutes after its administration. Heart rate remained above 120 beats/min, and severe bradycardia (≤ 70 beats/min) and other arrhythmias did riot occur throughout the study. Medetomidine also induced tachypnea in all treated lambs. The tachypnea was abolished by atipamezole and yohimbine, but not by saline solution administration. The medetomidine-induced tachypnea did not significantly affect arterial pH and Paco2. Arterial oxygen tension was within acceptable range (Pao2 , = 71 to 62 mm of Hg), but was lower than expected. Administration of atipamezole, yohimbine, or saline solution did not change Pao2, significantly. Lambs treated with 30 or 60 μg of atipa- mezole/kg were able to walk unassisted in 2.4 ± 0.4 and 2.3 ± 0.7 minutes, respectively, whereas yohimbine- and saline-treated lambs did not walk unassisted until 15.6 ± 2.7 and 73.0 ± 6.8 minutes later, respectively. Results of this study indicated that medetomidine is a potent CNS depressant in lambs. Atipamezole at dosage of 30 or 60 μg/kg was equally effective, and was more effective in antagonizing medetomidine-induced CNS depression than was yohimbine.
Abstract
Objective—To determine sedative and cardiorespiratory effects of IM administration of medetomidine alone and in combination with butorphanol or ketamine in dogs.
Design—Randomized, crossover study.
Animals—6 healthy adult dogs.
Procedure—Dogs were given medetomidine alone (30 µg/kg [13.6 µg/lb] of body weight, IM), a combination of medetomidine (30 µg/kg, IM) and butorphanol (0.2 mg/kg [0.09 mg/lb], IM), or a combination of medetomidine (30 µg/kg, IM) and ketamine (3 mg/kg [1.36 mg/lb], IM). Treatments were administered in random order with a minimum of 1 week between treatments. Glycopyrrolate was given at the same time. Atipamezole (150 µg/kg [68 µg/lb], IM) was given 40 minutes after administration of medetomidine.
Results—All but 1 dog (given medetomidine alone) assumed lateral recumbency within 6 minutes after drug administration. Endotracheal intubation was significantly more difficult when dogs were given medetomidine alone than when given medetomidine and butorphanol. At all evaluation times, percentages of dogs with positive responses to tail clamping or to needle pricks in the cervical region, shoulder region, abdominal region, or hindquarters were not significantly different among drug treatments. The PaCO2 was significantly higher and the arterial pH and PaO2 were significantly lower when dogs were given medetomidine and butorphanol or medetomidine and ketamine than when they were given medetomidine alone. Recovery quality following atipamezole administration was unsatisfactory in 1 dog when given medetomidine and ketamine.
Conclusion and Clinical Relevance—Results suggested that a combination of medetomidine with butorphanol or ketamine resulted in more reliable and uniform sedation in dogs than did medetomidine alone. (J Am Vet Med Assoc 2000;216:1578–1583)
Abstract
Objective—To determine the cardiorespiratory effects of preemptive atropine administration in dogs sedated with medetomidine.
Design—Randomized crossover trial.
Animals—12 healthy adult dogs.
Procedures—Dogs underwent 6 treatments. Each treatment consisted of administration of atropine (0.04 mg/kg [0.018 mg/lb] of body weight, IM) or saline solution (0.9% NaCl, 1 ml, IM) and administration of medetomidine (10, 20, or 40 µg/kg [4.5, 9.1, or 18.2µg/lb], IM) 10 minutes later. Treatments were administered in random order, with a minimum of 1 week between treatments. Cardiorespiratory effects before and after atropine and medetomidine administration were assessed. Duration of lateral recumbency and quality of sedation and recovery were assessed.
Results—Bradycardia (heart rate < 60 beats/min) was seen in all dogs when saline solution was administered followed by medetomidine, and the dose of medetomidine was not associated with severity or frequency of bradycardia or second-degree heart block. However, a medetomidine dose-dependent increase in mean and diastolic blood pressures was observed, regardless of whether dogs received saline solution or atropine. Preemptive atropine administration effectively prevented bradycardia and seconddegree heart block but induced pulsus alternans and hypertension. The protective effects of atropine against bradycardia lasted 50 minutes. Blood gas values were within reference limits during all treatments and were not significantly different from baseline values. Higher doses of medetomidine resulted in a longer duration of lateral recumbency.
Conclusions and Clinical Relevance—Preemptive administration of atropine in dogs sedated with medetomidine effectively prevents bradycardia for 50 minutes but induces hypertension and pulsus alternans. ( J Am Vet Med Assoc 2001;218:52–58)
Objective—
To determine the median effective dose (ED50) of propofol required for induction of anesthesia in goats and the frequency of myoclonic activity and apnea associated with propofol administration.
Design—
Clinical trial.
Animals—
28 healthy mature goats.
Procedure—
ED50 was determined by use of the up-and-down method. The first goat was given 4 mg of propofol/kg (1.8 mg/lb) of body weight, IV. Dose was increased by 25% for the next goat if endotracheal intubation was not possible and decreased by 20% if it was. For each subsequent goat, dose was determined on the basis of response of the previous goat. The ED50 was calculated by use of probit analysis. Induction time, frequency and duration of apnea, frequency of myoclonus, and other adverse effects were recorded.
Results—
ED50 was determined to be 5.1 mg/kg (2.3 mg/lb). Mean (± SD) induction time was 23.2 ± 4.7 seconds. Apnea was observed in 27 of 28 goats; mean (± SD) duration of apnea was 72.9 ± 38.3 seconds. Dose did not correlate with duration of apnea. Myoclonic activity was observed in 16 of 28 goats; frequency of myoclonus was not associated with dose. Cyanosis, regurgitation, and signs of pain during injection were not observed.
Clinical Implications—
Administration of propofol at 5.1 mg/kg (2.3 mg/lb), IV, should permit endotracheal intubation in half of unpremedicated, healthy, mature goats. Myoclonus and apnea were associated with propofol administration. (J Am Vet Med Assoc 1997;211:86–88)
Objective—
To evaluate anesthetic and cardiorespiratory effects of an intramuscular injection of a tiletamine-zolazepam-medetomidine combination in cheetahs.
Design—
Prospective study.
Animals—
17 adult captive cheetahs.
Procedure—
The anesthetic combination was administered intramuscularly via a dart. Induction quality, duration of lateral recumbency, duration of recovery, and quality of anesthetic reversal with atipamezole were assessed. Cardiorespiratory variables (arterial blood gas partial pressures, arterial blood pressure, heart and respiratory rates, end-tidal CO2, oxygen saturation, and rectal temperature) were measured during anesthesia.
Results—
Sedation and lateral recumbency developed within 1.9 ± 1.0 (mean ± SD) and 4.3 ± 2.0 minutes of drug administration, respectively. Clinically acceptable cardiorespiratory and blood gas values were recorded for at least 87 minutes after drug administration in all but 1 cheetah. Hypoxemia and arrhythmias developed in 1 cheetah breathing room air but resolved after treatment with oxygen. Hypertension developed in all cheetahs. Significant differences in heart and respiratory rates, mean arterial blood pressure, arterial pH, partial pressure of oxygen, and hemoglobin saturation were found between cheetahs that did and did not receive oxygen supplementation. After administration of atipamezole, sternal recumbency and mobility returned within 6.9 ± 5.8 and 47.5 ± 102.2 minutes, respectively. Postreversal sedation, which lasted approximately 4 hours, developed in 4 cheetahs.
Clinical Implications—
Tiletamine-zolazepam-medetomidine delivered via a dart provided an alternative method for induction and maintenance of anesthesia in cheetahs. Atipamezole at the dose used was effective for reversal of this combination in the initial phase of anesthesia. (J Am Vet Med Assoc 1998:213:1022-1026)
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.
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.
Abstract
Objective—To compare the effect of oral administration of tramadol alone and with IV administration of butorphanol or hydromorphone on the minimum alveolar concentration (MAC) of sevoflurane in cats.
Design—Crossover study.
Animals—8 healthy 3-year-old cats.
Procedures—Cats were anesthetized with sevoflurane in 100% oxygen. A standard tail clamp method was used to determine the MAC of sevoflurane following administration of tramadol (8.6 to 11.6 mg/kg [3.6 to 5.3 mg/lb], PO, 5 minutes before induction of anesthesia), butorphanol (0.4 mg/kg [0.18 mg/lb], IV, 30 minutes after induction), hydromorphone (0.1 mg/kg [0.04 mg/lb], IV, 30 minutes after induction), saline (0.9% NaCl) solution (0.05 mL/kg [0.023 mL/lb], IV, 30 minutes after induction), or tramadol with butorphanol or with hydromorphone (same doses and routes of administration). Naloxone (0.02 mg/kg [0.009 mg/lb], IV) was used to reverse the effects of treatments, and MACs were redetermined.
Results—Mean ± SEM MACs for sevoflurane after administration of tramadol (1.48 ± 0.20%), butorphanol (1.20 ± 0.16%), hydromorphone (1.76 ± 0.15%), tramadol and butorphanol (1.48 ± 0.20%), and tramadol and hydromorphone (1.85 ± 0.20%) were significantly less than those after administration of saline solution (2.45 ± 0.22%). Naloxone reversed the reductions in MACs.
Conclusions and Clinical Relevance—Administration of tramadol, butorphanol, or hydromorphone reduced the MAC of sevoflurane in cats, compared with that in cats treated with saline solution. The reductions detected were likely mediated by effects of the drugs on opioid receptors. An additional reduction in MAC was not detected when tramadol was administered with butorphanol or hydromorphone.
