Droperidol, a Selective Antagonist of Postsynaptic α-Adrenoceptors in the Canine Saphenous Vein

Hyatt, Mark C.; Muldoon, Sheila M.; Rorie, Duane K.

doi:10.1097/00000542-198010000-00003

Cited by 15 publications

(4 citation statements)

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“…Droperidol is known primarily as an antagonist at D2 dopamine receptors, but it has also been shown to inhibit α1 adrenergic receptors. 47,48 Therefore our results with droperidol are consistent with the notion that dopaminergic and noradrenergic neurotransmission play important roles in methylphenidate-induced emergence. Further studies will be necessary to elucidate which arousal pathways are responsible for the specific actions of methylphenidate, although it is likely that the simultaneous activation of multiple monoaminergic arousal pathways contributes to its efficacy.…”

Section: Discussionsupporting

confidence: 88%

Methylphenidate Actively Induces Emergence from General Anesthesia

et al. 2011

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Background Although accumulating evidence suggests that arousal pathways in the brain play important roles in emergence from general anesthesia, the roles of monoaminergic arousal circuits are unclear. In this study we tested the hypothesis that methylphenidate (an inhibitor of dopamine and norepinephrine transporters) induces emergence from isoflurane anesthesia. Methods Using adult rats we tested the effect of methylphenidate IV on time to emergence from isoflurane anesthesia. We then performed experiments to test separately for methylphenidate-induced changes in arousal and changes in minute ventilation. A dose-response study was performed to test for methylphenidate–induced restoration of righting during continuous isoflurane anesthesia. Surface electroencephalogram recordings were performed to observe neurophysiological changes. Plethysmography recordings and arterial blood gas analysis were performed to assess methylphenidate-induced changes in respiratory function. Droperidol IV was administered to test for inhibition of methylphenidate's actions. Results Methylphenidate decreased median time to emergence from 280 to 91 s. The median difference in time to emergence without compared to with methylphenidate was 200 [155, 331] s (median, [95% confidence interval]). During continuous inhalation of isoflurane, methylphenidate induced return of righting in a dose-dependent manner, induced a shift in electroencephalogram power from delta to theta, and induced an increase in minute ventilation. Administration of droperidol (0.5 mg/kg IV) prior to methylphenidate (5 mg/kg IV) largely inhibited methylphenidate-induced emergence behavior, electroencephalogram changes, and changes in minute ventilation. Conclusions Methylphenidate actively induces emergence from isoflurane anesthesia by increasing arousal and respiratory drive, possibly through activation of dopaminergic and adrenergic arousal circuits. Our findings suggest that methylphenidate may be clinically useful as an agent to reverse general anesthetic-induced unconsciousness and respiratory depression at the end of surgery.

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Section: Discussionsupporting

confidence: 88%

Methylphenidate Actively Induces Emergence from General Anesthesia

et al. 2011

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“…The increase in SVR may also he related to the increase of antidiuretic hormone or activation of the renin angioterisin system (14)(15)(16)(17). It has been reported that droperidol acts in oi/ro as an alpha-adrenoreceptor blocking agent on the vasculature (18)(19)(20). Thus the vasodilating efl'ect of droperidol should be related to the preiri-jection level of SVR, which in turn is dependent on the activity in the sympathetic nervous system.…”

Section: Discussionmentioning

confidence: 99%

Effects of droperidol on peripheral vasculature: use of cardiopulmonary bypass as a study model

Videcoq

Marty

et al. 1987

Acta Anaesthesiol Scand

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The effects of droperidol on the systemic vascular resistance (SVR) and the venous capacitance were studied during cardiopulmonary bypass (CPB) in 24 patients. CPB was performed with either pulsatile or non-pulsatile flow. During non-pulsatile flow, droperidol (0.15 mg X kg-1 and 0.30 mg X kg-1) decreased SVR and increased venous capacitance. These values were significantly different after the 2nd and the 7th min, respectively. During pulsatile flow, the initial SVR was lower. The decremental effect of 0.30 mg X kg-1 droperidol on SVR was proportional to the preinjection level of SVR (r = 0.64). The increase in venous capacitance related to droperidol was independent of the dose and of the type of flow in all patients. It can be concluded that the vasodilating action of droperidol during CPB on the arterial bed is transient, independent of dose, and related to the preinjection level of SVR. The effect of droperidol on venous capacitance is not as rapid but has a longer duration.

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“…Droperidol has been suggested as an agent which does not cause cardiovascular instability, 15 but some authors found that it causes hypertensive crises, 16 and it has been shown to potentiate noradrenaline release from synaptic terminals. 17 Because most of these tumours are intraabdominal, muscle paralysis is required. A1curonium IS suitable for intubation.…”

Section: Discussionmentioning

confidence: 99%

Phaeochromocytoma in a Child

1985

Anaesth Intensive Care

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Phaeochromocytoma has been reported to occur in 0.32070 of hypertensive patients with less than 5% of cases occurring in children. A five-year-old Indian boy weighing 12 kg was admitted with a blood pressure of 240/150 mmHg, and a heart which was clinically enlarged. There were no other signs of hypertension. A chest X-ray showed cardiomegaly, the ECG demonstrating left ventricular hypertrophy. Treatment was started with hydrallazine 2.5 mg q.d.s. and propranolol 20 mg t.d.s., changing to labetolol 50 mg b.d. These doses were increased to hydrallazine 7.5 mg t.d.s., and labetololl00 mg b.d. However, paroxysms of hypertension still occurred, which were treated with injections of diazoxide 60 mg. The urinary catecholamine metabolite levels were found to be elevated and a provisional diagnosis of phaeochromocytoma was made. Phenoxybenzamine 2.5 mg b.d. was added to his medication, and increased over a week to 25 mg b.d., while the other anti-hypertensive drugs were reduced. Because of persistent tachycardia he was given propranolol 20 mg b.d., increasing to 40 mg b.d. His blood pressure was now controlled and the paroxysms of hypertension reduced. His haemoglobin was 13 gldl and potassium 3.0-3.5 mEql1 throughout this period. His first anaesthetic was for an aortic angiogram. No premedication was given. Anaesthesia was induced with sodium thiopentone 50 mg and alcuronium 3 mg. He was ventilated by hand using a mask and 33%

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Droperidol, a Selective Antagonist of Postsynaptic α-Adrenoceptors in the Canine Saphenous Vein

Cited by 15 publications

References 0 publications

Methylphenidate Actively Induces Emergence from General Anesthesia

Methylphenidate Actively Induces Emergence from General Anesthesia

Effects of droperidol on peripheral vasculature: use of cardiopulmonary bypass as a study model

Phaeochromocytoma in a Child

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