2006
DOI: 10.1097/00000542-200611000-00010
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Effects of Low and High Plasma Concentrations of Dexmedetomidine on Myocardial Perfusion and Cardiac Function in Healthy Male Subjects

Abstract: In healthy subjects, plasma concentrations of dexmedetomidine that significantly exceed the recommended therapeutic level do not seriously attenuate myocardial perfusion below the level that is observed with usual therapeutic concentrations and do not induce evident myocardial ischemia.

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Cited by 114 publications
(104 citation statements)
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“…The specific stimulation of alpha2-adrenergic receptors (subtypes 2A, 2B and 2C) in the nervous system determines the analgosedative effects observed during Dex administration [4,5]. Dex also shows a biphasic blood pressure response, with an initial increase attributable to vasoconstriction after activation of alpha2/beta-adrenergic receptors in the vascular smooth muscle, followed by a decrease in blood pressure, after activation of alpha2A-adrenergic receptors in the central nervous system [6][7][8]. Furthermore, stimulation of postsynaptic alpha2-adrenergic receptors on endothelial cells produces vasodilatation [9].…”
Section: Introductionmentioning
confidence: 99%
See 1 more Smart Citation
“…The specific stimulation of alpha2-adrenergic receptors (subtypes 2A, 2B and 2C) in the nervous system determines the analgosedative effects observed during Dex administration [4,5]. Dex also shows a biphasic blood pressure response, with an initial increase attributable to vasoconstriction after activation of alpha2/beta-adrenergic receptors in the vascular smooth muscle, followed by a decrease in blood pressure, after activation of alpha2A-adrenergic receptors in the central nervous system [6][7][8]. Furthermore, stimulation of postsynaptic alpha2-adrenergic receptors on endothelial cells produces vasodilatation [9].…”
Section: Introductionmentioning
confidence: 99%
“…Furthermore, stimulation of postsynaptic alpha2-adrenergic receptors on endothelial cells produces vasodilatation [9]. The drug also reduces the release of stress hormones and catecholamines [8]. The modulation of the sympathetic nervous system theoretically maintains the balance in the input/demand relationship of myocardial oxygen.…”
Section: Introductionmentioning
confidence: 99%
“…The effect of dexmedetomidine in I/R models depends on several factors, such as the route of administration (intravenous (39), intraperitoneal (12,19), dosage, type of ischemic tissue or organ, duration and temperature of ischemia, timing of administration (before (12,19,22) or after (18) ischemia) and the species itself.…”
Section: Discussionmentioning
confidence: 99%
“…Since then, a growing number of research articles have emerged and reported other possible indications, such as regional and general anesthesia (15,16). Dexmedetomidine was reported to be effective in protection against focal ischemia in rabbits, in cardiac I/R injury in rats in kidney I/R injury in rats, and in incom-plete forebrain ischemia in rats (12,(17)(18)(19). Despite its increased clinical use, especially, in critically ill patients, the effect of dexmedetomidine on liver I/R injury has not been investigated yet (20).…”
mentioning
confidence: 99%
“…Because mechanism of dexmedetomidine is not mediated by the γ -aminobutyric acid system, dexmedetomidine is unique in that it does not cause respiratory depression [9]. In on vascular smooth muscle cells [10]. Furthermore, the overall effect of dexmedetomidine on MAP and HR is biphasic and dose-dependent [11], characterized by an initial short-term increase in BP followed by a longer lasting reduction in BP and HR.…”
mentioning
confidence: 99%