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Intravenous Sedation with Low-Dose Dexmedetomidine: Its Potential for Use in Dentistry
Sachie OgawaDDS,
Hiroaki SeinoDDS,
Hiroshi ItoDDS,
Shinya YamazakiDDS, PhD,
Steven GanzbergDMD, MS, and
Hiroyoshi KawaaiDDS, PhD
Article Category: Research Article
Volume/Issue: Volume 55: Issue 3
Online Publication Date: Jan 01, 2008
DOI: 10.2344/0003-3006-55.3.82
Page Range: 82 – 88

Dexmedetomidine (Dex) is a sedative and analgesic agent that acts through an α 2 -agonist effect. 1 In Japan and the United States, it is licensed as a sedative agent for intensive care unit (ICU) sedation after surgery. The effects of α 2 -agonists have been associated with reduced anesthetic requirements and attenuated blood pressure and heart rate in response to stressful events. 2 – 5 The α 2 -receptors within the spinal cord modulate pain pathways, thereby providing some degree of analgesia. 6 – 8 In addition, Dex induces a sedative

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Alpha-2 Adrenergic Receptor Agonists: A Review of Current Clinical Applications
Joseph A. Giovannitti JrDMD,
Sean M. ThomsDMD, MS, and
James J. CrawfordDMD
Article Category: Other
Volume/Issue: Volume 62: Issue 1
Online Publication Date: Jan 01, 2015
DOI: 10.2344/0003-3006-62.1.31
Page Range: 31 – 38

neurotransmitter release from the presynaptic neuron. 3 The α-receptor antagonists prazosin and yohimbine were used to further subclassify these receptors as α-1 and α-2. 4 Later, many α-2 adrenergic agonists were developed for use in the clinical setting, including their use as anesthesia adjuncts. The use of α-2 agonists as adjuncts gained popularity when early reports by Brodsky and Bravo 5 found that withholding a single dose of clonidine prior to anesthesia caused a patient to experience an acute hypertensive crisis. It was discovered that α-2 agonists produce effects

Figure 1; Time course of the investigation. Subjects were sedated with dexmedetomidine (Dex) at a loading dose of 6 mcg/kg/h for 5 minutes and a continuous infusion dose of 0.2 mcg/kg/h for 25 minutes. The recovery process was observed for 60 minutes after cessation of the Dex infusion. (Control value was not measured in Ramsay score.)
Sachie Ogawa,
Hiroaki Seino,
Hiroshi Ito,
Shinya Yamazaki,
Steven Ganzberg, and
Hiroyoshi Kawaai
Figure 1
Figure 1

Time course of the investigation. Subjects were sedated with dexmedetomidine (Dex) at a loading dose of 6 mcg/kg/h for 5 minutes and a continuous infusion dose of 0.2 mcg/kg/h for 25 minutes. The recovery process was observed for 60 minutes after cessation of the Dex infusion. (Control value was not measured in Ramsay score.)

Figure 2; Changes in tidal volume (TV), respiratory rate (RR), and minute volume (MV). TV decreased significantly from 5 minutes to 30 minutes after the start of dexmedetomidine (Dex) infusion. However, RR and MV did not show significant changes. TV decreased significantly from an average of 580 mL (control value) to approximately 430 to 470 mL (P < .05).
Sachie Ogawa,
Hiroaki Seino,
Hiroshi Ito,
Shinya Yamazaki,
Steven Ganzberg, and
Hiroyoshi Kawaai
Figure 2
Figure 2

Changes in tidal volume (TV), respiratory rate (RR), and minute volume (MV). TV decreased significantly from 5 minutes to 30 minutes after the start of dexmedetomidine (Dex) infusion. However, RR and MV did not show significant changes. TV decreased significantly from an average of 580 mL (control value) to approximately 430 to 470 mL (P < .05).

Figure 3; Changes in end-tidal carbon dioxide (ETCO2) and oxygen saturation (SpO2). Respiratory rate (RR) and SpO2 did not show significant changes. Sedation with dexmedetomidine (Dex) had no effect on ETCO2 and SpO2.
Sachie Ogawa,
Hiroaki Seino,
Hiroshi Ito,
Shinya Yamazaki,
Steven Ganzberg, and
Hiroyoshi Kawaai
Figure 3
Figure 3

Changes in end-tidal carbon dioxide (ETCO2) and oxygen saturation (SpO2). Respiratory rate (RR) and SpO2 did not show significant changes. Sedation with dexmedetomidine (Dex) had no effect on ETCO2 and SpO2.

Figure 4; Changes in mean arterial pressure (MAP) and heart rate (HR). The transient increase in MAP was observed at 5 minutes after the start of dexmedetomidine (Dex) infusion (not significant); MAP decreased significantly from an average of 86 mm Hg (control value) to approximately 70 to 77 mm Hg over 80 minutes since 10 minutes after the start of Dex infusion (P < .05). HR decreased significantly since 5 minutes after the start of Dex infusion, and HR decreased significantly from an average of 65 beats per minute (bpm) (control value) to approximately 53 to 57 bpm (P < .05).
Sachie Ogawa,
Hiroaki Seino,
Hiroshi Ito,
Shinya Yamazaki,
Steven Ganzberg, and
Hiroyoshi Kawaai
Figure 4
Figure 4

Changes in mean arterial pressure (MAP) and heart rate (HR). The transient increase in MAP was observed at 5 minutes after the start of dexmedetomidine (Dex) infusion (not significant); MAP decreased significantly from an average of 86 mm Hg (control value) to approximately 70 to 77 mm Hg over 80 minutes since 10 minutes after the start of Dex infusion (P < .05). HR decreased significantly since 5 minutes after the start of Dex infusion, and HR decreased significantly from an average of 65 beats per minute (bpm) (control value) to approximately 53 to 57 bpm (P < .05).

Figure 5; Changes in bispectral index (BIS) and Ramsay score (RS). BIS decreased significantly from 10 minutes after the start of dexmedetomidine (Dex) infusion to 30 minutes after the end of Dex infusion (P < .05). RS showed the optimal sedation level from 10 minutes to 30 minutes after the start of Dex infusion.
Sachie Ogawa,
Hiroaki Seino,
Hiroshi Ito,
Shinya Yamazaki,
Steven Ganzberg, and
Hiroyoshi Kawaai
Figure 5
Figure 5

Changes in bispectral index (BIS) and Ramsay score (RS). BIS decreased significantly from 10 minutes after the start of dexmedetomidine (Dex) infusion to 30 minutes after the end of Dex infusion (P < .05). RS showed the optimal sedation level from 10 minutes to 30 minutes after the start of Dex infusion.

Figure 6; Changes in Trieger dot test plus error ratio test (TDT p.e.r.) and 1-leg standing with eyes closed test (O-L test). TDT p.e.r. increased significantly at 5 and 10 minutes from the end of dexmedetomidine (Dex) infusion (P < .05). All subjects passed the O-L test at 60 minutes after cessation of Dex infusion.
Sachie Ogawa,
Hiroaki Seino,
Hiroshi Ito,
Shinya Yamazaki,
Steven Ganzberg, and
Hiroyoshi Kawaai
Figure 6
Figure 6

Changes in Trieger dot test plus error ratio test (TDT p.e.r.) and 1-leg standing with eyes closed test (O-L test). TDT p.e.r. increased significantly at 5 and 10 minutes from the end of dexmedetomidine (Dex) infusion (P < .05). All subjects passed the O-L test at 60 minutes after cessation of Dex infusion.

Figure 7; Amnesia. Amnesia was recognized with a 27-gauge needle prick test performed in 69% of subjects at 21 minutes after the start of dexmedetomidine (Dex) infusion.
Sachie Ogawa,
Hiroaki Seino,
Hiroshi Ito,
Shinya Yamazaki,
Steven Ganzberg, and
Hiroyoshi Kawaai
Figure 7
Figure 7

Amnesia. Amnesia was recognized with a 27-gauge needle prick test performed in 69% of subjects at 21 minutes after the start of dexmedetomidine (Dex) infusion.

A Combination of Dexmedetomidine and Lidocaine Is a Cardiovascularly Safe Dental Local Anesthetic for Hypertensive Rats Treated With a Nonselective β-Adrenergic Antagonist
Yukako TsutsuiDDS, PhD and
Katsuhisa SunadaDDS, PhD
Article Category: Research Article
Volume/Issue: Volume 64: Issue 4
Online Publication Date: Jan 01, 2017
DOI: 10.2344/anpr-64-04-09
Page Range: 221 – 225

-adrenergic antagonists. 1 , 2 Therefore, safer and more effective dental local anesthetics are needed for hypertensive patients who are taking nonselective β-adrenergic antagonists. Recent reports suggest that dexmedetomidine (DEX), an α 2 -adrenergic agonist, enhances the effect and prolongs the effective duration of local anesthesia. 3 − 6 Further, as with all α 2 -adrenergic agonists, hypotension and bradycardia are the predominant side effects of DEX that are caused by its central sympatholytic effects. 7 − 10 Therefore, we hypothesized that a combination of DEX and