Dose Of Detomidine Research Articles

Detomidine reduces isoflurane anesthetic requirement (MAC) in horses

ObjectiveTo quantitate the dose- and time-related magnitude of the anesthetic sparing effect of, and selected physiological responses to detomidine during isoflurane anesthesia in horses. Study designRandomized cross-over study. AnimalsThree, healthy, young adult horses weighing 485 ± 14 kg. MethodsHorses were anesthetized on two occasions to determine the minimum alveolar concentration (MAC) of isoflurane in O2 and then to measure the anesthetic sparing effect (time-related MAC reduction) following IV detomidine (0.03 and 0.06 mg kg−1). Selected common measures of cardiopulmonary function, blood glucose and urinary output were also recorded. ResultsIsoflurane MAC was 1.44 ± 0.07% (mean ± SEM). This was reduced by 42.8 ± 5.4% and 44.8 ± 3.0% at 83 ± 23 and 125 ± 36 minutes, respectively, following 0.03 and 0.06 mg kg−1, detomidine. The MAC reduction was detomidine dose- and time-dependent. There was a tendency for mild cardiovascular and respiratory depression, especially following the higher detomidine dose. Detomidine increased both blood glucose and urine flow; the magnitude of these changes was time- and dose-dependent ConclusionsDetomidine reduces anesthetic requirement for isoflurane and increases blood glucose concentration and urine flow in horses. These changes were dose- and time-related. Clinical relevanceThe results imply potent anesthetic sparing actions by detomidine. The detomidine-related increased urine flow should be considered in designing anesthetic protocols for individual horses.

Investigation of romifidine and detomidine for the clinical sedation of horses

The effects of two intravenous doses of romifidine (80 and 120 μg/kg) and one dose of detomidine (20 μg/kg) were compared in a blinded study in 30 horses requiring to...

The sedative and analgesic effects of detomidine-butorphanol and detomidine alone in donkeys.

Butorphanol and detomidine constitute an effective combination for sedation and analgesia in horses. This trial was undertaken to assess the effectiveness of this combination in donkeys. The detomidine and butorphanol were given intravenously one after the other. A dose of 10 microg/kg of detomidine and 25 microg/kg of butorphanol was used. Sedation is easily extended by additional doses of butorphanol. The average dose of detomidine was 11.24 microg/kg and that of butorphanol was 28.0 microg/kg. Four donkeys in the detomidine group required additional sedation and analgesia. Detomidine alone did not totally eliminate coronary band pain. Heart rates dropped significantly in the first minute after the injection of the combination. One donkey developed an atrioventricular block, while another developed a sino-atrial block. Four donkeys developed a Cheyne-Stokes respiratory pattern. The combination of detomidine and butorphanol is an effective combination for sedation and analgesia of donkeys for standing procedures.

Antagonism of detomidine sedation with atipamezole in horses

SUMMARY The reversal of detomidine-induced sedation with iv atipamezole was studied in 6 horses. All horses were injected iv with 10 μg and 20 μg/kg bwt detomidine and 15 min later this was followed by 6-, 8- and 10-fold doses of iv atipamezole. Atipamezole caused a quick arousal in all horses with minor side effects. Bradycardia, rhythm disturbances and head ptosis caused by detomidine were not abolished completely at the end of the 15 min observation period, even with the highest atipamezole doses. All horses remained slightly sedated but without ataxia. There were no significant differences in head height, heart rate and sedation score between the different doses of atipamezole for either dose of detomidine. According to the degree of sedation, doses of 100 μg to 160 μg/kg bwt atipamezole are adequate to antagonise detomidine-induced sedation in the horse.

Effect of xylazine, detomidine, and a combination of xylazine and butorphanol on equine duodenal motility

Abstract Objective To evaluate the effect on equine duodenal motility of some analgesic agents commonly used to treat colic. Animals 4 healthy adult healthy horses—2 mares and 2 geldings—which were carrying an indwelling gastric cannula made of silastic rubber. One horse also carried 2 long-term indwelling bipolar electrodes that had been sutured onto the duodenum and jejunum. Procedure To ensure an empty stomach, solid food was withheld from horses for around 20 hours prior to an experiment. Using videoendoscopic guidance, an 8-F catheter with 3 small, discrete pressure sensors was passed through the gastric cannula and directed into the proximal portion of the duodenum. Deflection of the recording pen, to which the catheter was attached, indicated a motile event in that section. Drugs (treatment) were given into the jugular vein in a randomized block design, 1 treatment/experiment, after a 1-hour baseline recording. Treatments were: 2 ml of 0.9% NaCl, xylazine (XYL, 0.5 mg/kg of body weight), detomidine (DET, 0.0125 mg/kg), or a xylazine/butorphanol combination (XYB, 0.5/0.05 mg/kg). Each horse received each treatment twice. All positive pressure peaks > 5 mm of Hg recorded from the most proximal sensor on the catheter were counted in 15-minute blocks. Each mean 15-minute posttreatment value was compared with the baseline value for that specific treatment. Results There was no significant difference between baseline values. All treatments significantly (P < 0.05) reduced frequency of pressure peaks below their respective pretreatment values, but to variable degrees and durations. Comparatively, XYL had the least effect, with mild, though significant, reduction for only the first 30 posttreatment minutes; DET and XYB caused a significant marked reduction for 1 hour after treatment. Conclusions The profound suppressive effect of a routine dose of detomidine or xylazine/butorphanol combination on equine duodenal motility must be considered when using these agents for management of colic, especially when encouragement of intestinal motility is desirable. (Am J Vet Res 1998;59:619–623)

Evaluation of propofol for general anesthesia in premedicated horses

Abstract Objective To evaluate selected hemodynamic, respiratory, and behavioral responses to propofol in horses premedicated with xylazine or detomidine. Design Xylazine (0.5 and 1.0 mg/kg of body weight) was administered IV on different days to each of 6 horses prior to IV administration of propofol (2 mg/ kg). In a second group of 6 horses, detomidine (15 and 30 µg/kg) was similarly studied. Animals 2 groups of 6 mature healthy horses. Procedure Rectal temperature, heart and respiratory rates, arterial blood gas tensions, and direct arterial blood pressures were recorded before and at fixed intervals after drug administration. Induction and recovery events were quantitatively and qualitatively assessed. Cardiopulmonary and behavioral data to follow were statistically analyzed (P< 0.05). Results Heart rate decreased in dose-dependent manner from a mean (± SD) of 39.5 ± 5.1 beats/min after xylazine and detomidine. Second-degree atrioventricular dissociation was commonly seen at the higher drug doses. After propofol administration, heart rate either transiently increased or was less depressed early in recumbency, compared with predrug values. Direct arterial blood pressures varied inconsistently from predrug values. Mean arterial carbon dioxide tension tended to increase after drug administration (significance variable) from predrug values of 42 to 46 mm of Hg in both drug groups. After xylazine or detomidine administration, arterial oxygen tension decreased significantly from predrug values of 97 to 103 mm of Hg. The magnitude and duration of decrease was dose-dependent and greatest during recumbency. Behavioral responses to anesthetic induction were variable, but horses were uniformly calm and coordinated during recovery. Recumbency time increased in reponse to the higher dose of either premedicant drug. Mean (± SD) times to standing were 25.02 ± 4.42 and 35.57 ± 6.83 minutes for the low and high doses of xylazine, respectively and 41.04 ± 11.21 and 52.64 ± 14.67 minutes for the low and high doses of detomidine, respectively. Conclusion Neither xylazine nor detomidine prevented excitation associated with propofol injection in horses. Clinical Relevance Xylazine- or detomidine-propofol combinations likely will not replace common anesthetic induction techniques for horses. However, recovery characteristics associated with propofol encourage further study in horses. (Am J Vet Res 1996;57:512–516)

The Effect of Detomidine Hydrochloride on the Electrical Activity of Uterus in Pregnant Mares

The effect of detomidine on the electrical activity of the uterus was studied during the last trimester of pregnancy in 6 mares. The effect was observed in 3-5 min after the i.m. injection and it lasted for 50-70 min. 20 and 40 micrograms/kg b.w. doses of detomidine decreased the myometrial electrical activity, whereas 60 micrograms/kg dose did not have any effect on the activity. The results suggested that 20, 40 and 60 micrograms/kg b.w. doses of detomidine can be administered to mares during the last trimester of pregnancy without the risk of abortion induced by increased uterine electrical activity.

Dose-related effects of detomidine on autonomic responses in the horse.

1. Detomidine is a novel veterinary sedative analgesic which is thought to act by stimulation of alpha 2 adrenoreceptors. The present study was undertaken to determine the direction, time course, and dose-response relationship of detomidine on specific autonomic responses in the unanaesthetized horse. 2. Detomidine was administered intravenously to eight adult thoroughbred racehorses at doses of 0.010-0.040 mg kg-1, according to a double-blind Latin square crossover design. Cardiac and respiratory rates, pupil diameter and rectal temperature were monitored for 180 min postinjection. 3. Detomidine produced prolonged dose-related bradycardia and bradypnoea. This was accompanied by a briefer period of dose-related mydriasis. Response duration, rather than peak was consistently increased as a function of dose. 4. Rectal temperature was not altered in a dose-dependent fashion. Low doses of detomidine produced late onset hypothermia, while high doses produced early and late onset hyperthermia. 5. These data indicate the uniqueness in autonomic response by the horse to alpha 2 adrenoreceptor stimulation.

Cardiovascular action of detomidine, a sedative and analgesic imidazole derivative with α-agonistic properties

The cardiovascular effects of detomidine, a new veterinary sedative and analgesic imidazole derivative were studied in rats and cats using as reference compound xylazine, a widely employed veterinary antinociceptive and sedative drug with α-agonistic potency. Detomidine (1–30 μg/kg i.v.) and xylazine (10–1000 μg/kg i.v.) had both dose-dependent hypotensive and bradycardiac effects in anaesthetized rats. After i.v. administration of 3–100 μg/kg detomidine and 0.1–3 mg/kg xylazine to conscious rats, detomidine was more active in reducing the heart rate than in lowering the blood pressure. In anaesthetized cats, detomidine (1–30 μg/kg i.v.) was hypotensive and bradycardiac in a dose-dependent manner. A low dose of detomidine into the vertebral artery was more effective than i.v. application in reducing blood pressure. Idazoxan (0.3 mg/kg i.v. and 0.03 mg/kg into the vertebral artery) antagonized the hypotensive and bradycardiac effects of detomidine injected into the femoral vein or vertebral artery, respectively. In pithed rats, detomidine and xylazine stimulated presynaptic and postsynaptic α 2-adrenoceptors, and to a lesser extent postsynaptic α 1-adrenoceptors. The results indicate that detomidine is an agonist of central and peripheral α 2-adrenoceptors which exerts its hypotensive and bradycardiac effects via activation of the central α 2-adrenoceptors.

Comparison of the effects of detomidine and xylazine on some α2-adrenoceptor-mediated responses in the central and peripheral nervous systems

The effects of detomidine, a novel veterinary sedative analgesic, on some ga 2-adrenoceptor-mediated responses in the central and peripheral nervous systems were studied. In pithed rats, detomidine was a very potent agonist at both pre- and postsynaptic α 2-adrenoceptors. Doses of 1.9 μg/kg and 6.5 μg/kg inhibited electrically induced tachycardia by 50% and increased mean blood pressure by 50 mmHg, respectively. In comparison, xylazine, though similar in specificity, was 40 times less potent than detomidine in this preparation. In unanaesthetized rats, detomidine both caused sedation and induced complex changes in body temperature. Low doses caused decreases in rectal temperature but these were reversed at the dose was increased. The decrease in rectal temperature could be blocked by yohimbine. Prazosin somewhat inhibited but did not eliminate the hyperthimia seen with the very high doses of detomidine. Xylazine caused much more severe falls in rectal temperature which could not be completely antagonized by α 2-adrenoceptor blockade. Both detomidine and xylazine caused dose-dependent mydriasis in anaesthetized rats, detomidine being about 10 times more potent than xylazine. The mydriatic effects of detomidine could be prevented by α 2- but not by α 1-adrenoceptor blockade. It is concluded that detomidine is a potent and rather specific α 2-adrenoceptor agonist in the central and peripheral nervous systems. In comparison with xylazine, detomidine has higher potency and greater specificity, especially at central α 2-adrenoceptors.