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Benzodiazepine Allergy With Anesthesia Administration: A Review of Current Literature

Elliot HaybargerDMD,

Andrew S. YoungDDS, and

Joseph A. Giovannitti JrDMD

Article Category: Research Article

Volume/Issue: Volume 63: Issue 3

Online Publication Date: Jan 01, 2016

DOI: 10.2344/16-00019.1

Page Range: 160 – 167

Serious complications during surgery have been shown to occur rather infrequently (0.4% of 83,844 cases), but anesthesia-related complications contribute to more than one third of these events. 1 Allergic reactions to medications are among the major factors affecting morbidity and mortality peri- and postoperatively. 1 , 2 The relative allergenicity of benzodiazepines, arguably the most commonly used anxiolytic premedication and a cornerstone in moderate to deep sedation, is explored in an attempt to quantify its allergic history

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Figure 2.; Dose-response curve for benzodiazepines.

Mark Donaldson,

Gino Gizzarelli, and

Brian Chanpong

Figure 2.

Dose-response curve for benzodiazepines.

A Comparison of Fospropofol to Midazolam for Moderate Sedation During Outpatient Dental Procedures

Philip YenDDS, MS,

Simon PriorBDS, MS, PhD,

Cara RileyDMD, MS,

William JohnstonMS, PhD,

Megann SmileyDMD, MS, and

Sarat ThikkurissyDDS, MS

Article Category: Other

Volume/Issue: Volume 60: Issue 4

Online Publication Date: Jan 01, 2013

DOI: 10.2344/0003-3006-60.4.162

Page Range: 162 – 177

agent, midazolam, as an intravenous (IV) moderate sedation medication. Midazolam provides anxiolysis, sedation, anterograde amnesia, and skeletal muscle relaxation with a wide therapeutic index, and can be administered by a variety of routes. A key feature that confers a greater degree of safety is the availability of an antagonist drug in the form of flumazenil, which can help reverse the effects of benzodiazepine overdose. The major drawbacks with midazolam are its slow onset, inadequate alleviation of procedure-related discomfort, increased depth of

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Figure 3.; Biotransformation of various benzodiazepines. Parent drugs and their active metabolites vary in their elimination half-lives: L, >24 hours; I, 6–24 hours; and S, <6 hours (derived from Mihic and Harris7).

Daniel E. Becker

Figure 3.

Biotransformation of various benzodiazepines. Parent drugs and their active metabolites vary in their elimination half-lives: L, >24 hours; I, 6–24 hours; and S, <6 hours (derived from Mihic and Harris7).

Figure 1. ; Schematic of GABAA receptor depicting competitive antagonism between flumazenil and midazolam at the benzodiazepine (BZD) binding site. Flumazenil acts as a negative allosteric modulator of GABA by facilitating closure of the chloride ion (Cl−) channel and preventing the influx of Cl− ions.

Michelle Wong

Figure 1.

Schematic of GABA_A receptor depicting competitive antagonism between flumazenil and midazolam at the benzodiazepine (BZD) binding site. Flumazenil acts as a negative allosteric modulator of GABA by facilitating closure of the chloride ion (Cl⁻) channel and preventing the influx of Cl⁻ ions.

Figure 2.; The GABAA receptor complex. The GABAA receptor complex consists of several protein subunits, with each comprised further of subunit families. These subunits provide myriad sites or receptors at which drugs may bind. While GABA and its precise receptor is the normal “commander” of the chloride channel, benzodiazepines can potentiate its influence. Additional drugs such as propofol and barbiturates not only potentiate the influence of GABA but are able to open the channel directly.

Daniel E. Becker

Figure 2.

The GABA_A receptor complex. The GABA_A receptor complex consists of several protein subunits, with each comprised further of subunit families. These subunits provide myriad sites or receptors at which drugs may bind. While GABA and its precise receptor is the normal “commander” of the chloride channel, benzodiazepines can potentiate its influence. Additional drugs such as propofol and barbiturates not only potentiate the influence of GABA but are able to open the channel directly.

Figure 3.; Mechanism of N2O-induced anxiolysis. N2O is thought to cause activation of the benzodiazepine (BZ) binding site as its effects are blocked by flumazenil. This action facilitates γ-aminobutyric acid (GABA) activation of its binding site, resulting in chloride ion influx. The increased chloride ion concentration in the neuron might cause activation of calmodulin (CaM), which then activates the enzyme nitric oxide synthase (NOS). NOS converts the amino acid L-arginine (L-Arg) to L-citrulline (L-Cit) and NO, which stimulates the enzyme soluble guanylyl cyclase producing the second messenger cyclic guanosine monophosphate (cyclic GMP). The cyclic GMP, in turn, stimulates a cyclic GMP-dependent protein kinase (PKG) that leads to the anxiolytic drug effect.

Dimitris E. Emmanouil and

Raymond M. Quock

Figure 3.

Mechanism of N₂O-induced anxiolysis. N₂O is thought to cause activation of the benzodiazepine (BZ) binding site as its effects are blocked by flumazenil. This action facilitates γ-aminobutyric acid (GABA) activation of its binding site, resulting in chloride ion influx. The increased chloride ion concentration in the neuron might cause activation of calmodulin (CaM), which then activates the enzyme nitric oxide synthase (NOS). NOS converts the amino acid L-arginine (L-Arg) to L-citrulline (L-Cit) and NO, which stimulates the enzyme soluble guanylyl cyclase producing the second messenger cyclic guanosine monophosphate (cyclic GMP). The cyclic GMP, in turn, stimulates a cyclic GMP-dependent protein kinase (PKG) that leads to the anxiolytic drug effect.