A411 Sedative and Hemodynamic Effects of Dexmedetomidine in Humans

Bloor, B. C.; Belleville, Jon P.; Maze, Mervyn

doi:10.1097/00000542-199009001-00409

Cited by 13 publications

(25 citation statements)

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“…The duration of action of atropine sulphate is only 60 to 90 min , so the decrease in heart rate recorded after 60 or 70 min may be because of potential effects of alpha-2 agonists and opioids to induce bradycardia (Ko et al 2000). Bradycardia occurring due to dexmedetomidine is thought to be of parasympathetic origin (Bloor et al 1992). The results of this study also conformed to the observations of Kuusela (2004) who reported decreased HR after dexmedetomidine administration in dogs.…”

Section: Resultssupporting

confidence: 86%

Evaluation of midazolam as intravenous induction agent for anaesthesia in dogs

Rafee

Kinjavdekar

Amarpal

et al. 2017

Indian J of Anim Sci

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A randomized, blinded, clinical study was conducted on 24 healthy mixed breed female dogs to evaluate midazolam as an induction agent for anaesthesia and its effect on vital parameters during elective ovariohysterectomy. Animals were administered atropine and divided randomly into groups D, DB and DP and premedicated with dexmedetomidine, dexmedetomidine and butorphanol, and dexmedetomidine and pentazocine, respectively. After 10 min of premedication, anaesthesia was induced with midazolam (0.8 mg/kg IV), in all the groups and maintained with 1% ketamine as and when needed. Time loss of pedal reflex was considered as the time of induction and it was recorded as 5.00±3.12, 4.75±2.92 and 4.75A±2.66 min in groups D, DB and DP, respectively. Laryngeal reflex was abolished completely, permitting intubation in all the groups. Recovery was smooth and uneventful and recovery time and duration of anaesthesia were comparable in all the groups. Heart rate showed an initial increase followed by a decrease, while respiratory rate decreased below the baseline in all the groups. SBP, DBP and MAP increased initially in all the groups and then decreased until 120 min interval. However, mean arterial pressure remained above the baseline throughout the observation period in all the groups. SpO2 decreased gradually from the baseline throughout the observation period. The results showed that midazolam at the rate of 0.8 mg/kg IV can be used safely as an induction agent in dogs premedicated with dexmedetomidine alone or with butorphanol or pentazocine while preserving the vital parameters.

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Section: Resultssupporting

confidence: 86%

Evaluation of midazolam as intravenous induction agent for anaesthesia in dogs

Rafee

Kinjavdekar

Amarpal

et al. 2017

Indian J of Anim Sci

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“…Although dexmedetomidine is potentially a hypertensive agent by its peripheral a 2 vasoconstricting effect on vascular smooth muscle, no differences were seen between the two groups. Previous studies in healthy volunteers suggest this to be a transient event with overall dominance of the central effects [6]. The incidence of nausea and vomiting requiring an antiemetic was higher in patients receiving dexmedetomidine; this was contrary to previous findings in women undergoing minor gynaecological surgery [11].…”

Section: ¹1mentioning

confidence: 58%

“…Activation of postsynaptic receptors by a 2 agonists in the CNS leads to inhibition of sympathetic activity, decreases in blood pressure and heart rate, and sedation, while binding of agonists to a 2 adrenoceptors in the spinal cord produces analgesia [3]. Peripheral a 2 receptors in blood vessels mediate vascular smooth muscle contraction and a rapid injection of a potent a 2 agonist can result in transient hypertension [6]. Dexmedetomidine is rapidly and extensively distributed to tissues with a distribution half-life of 5 min and elimination half-life of 2-3 h. It is extensively metabolised by phase one and phase two reactions in the liver and both urinary and faecal excretion are involved in elimination of dexmedetomidine and its metabolites (Personal communication.…”

Section: Discussionmentioning

confidence: 99%

Preliminary UK experience of dexmedetomidine, a novel agent for postoperative sedation in the intensive care unit

et al. 1999

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SummaryDexmedetomidine, a highly selective and potent a 2 -adrenergic agonist, has a potentially useful role as a sedative agent in patients requiring intensive care. As part of a larger European multicentre trial, a total of 119 postoperative cardiac and general surgical patients requiring ventilation and sedation in an intensive care unit were enrolled in four centres in the United Kingdom. One hundred and five patients were randomly allocated to receive either dexmedetomidine or placebo with rescue sedation and analgesia provided by midazolam and morphine, respectively. Compared with the control group, intubated patients receiving dexmedetomidine required 80% less midazolam [mean 4.9 (5.8) mg.kg ¹1.h ¹1 vs. 23.7 (27.5) mg.kg ¹1.h ¹1 , p < 0.0001], and 50% less morphine [11.2 (13.4) mg.kg. Cardiovascular effects and adverse events could be predicted from the known properties of alpha-2 agonists. In conclusion, dexmedetomidine is a useful agent for the provision of postoperative analgesia and sedation.

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“…Although α 2 -adrenergic receptor agonists are among the most potent sedatives we have available for small animals, 2 they have substantial cardiovascular adverse effects, namely a potent albeit transient vasoconstriction, reflex bradycardia, and decrease in cardiac output. 3,4 There has been controversy about the use of anticholinergics to either prevent 5-8 or treat 4,9 Evaluation of the sedative and cardiovascular effects of intramuscular administration of dexmedetomidine with and without concurrent atropine administration in dogs…”

mentioning

confidence: 99%