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Anesthetic Considerations for Patients on Antidepressant Therapy—Part I
Mana Saraghi DMD,
 Leonard R. Golden MD, and
 Elliot V. Hersh DMD, MS, PhD
Article Category: Other
Volume/Issue: Volume 64: Issue 4
Online Publication Date: Jan 01, 2017
DOI: 10.2344/anpr-64-04-14
Page Range: 253 – 261

the provider to understand the pharmacology of antidepressant medications and herbal supplements with alleged antidepressant/antianxiety properties, their adverse effects, and potential perioperative drug-drug interactions, effects on bleeding, and interactions with various adrenergic agonists used in local anesthetics and anesthesiology practice. In part I of this series, antidepressant pharmacology and interactions with adrenergic agonists will be discussed. In part II, other anesthetic drug interactions and serotonin syndrome will be discussed

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Alpha-2 Adrenergic Receptor Agonists: A Review of Current Clinical Applications
Joseph A. Giovannitti Jr DMD,
 Sean M. Thoms DMD, MS, and
 James J. Crawford DMD
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

In early scientific theory of adrenergic mechanisms, it was believed that adrenergic receptors were classified into 2 groups: those whose actions resulted in either excitation or inhibition of effector cells. 2 This theory was the accepted concept until Ahlquist 2 demonstrated that there were 2 subtypes of receptors in the class, which he termed α and β ( Table 1 ). Each had both excitatory and inhibitory effects based upon where that receptor was located. 2 Further study led researchers to discover that one of the α receptors inhibited

A Combination of Dexmedetomidine and Lidocaine Is a Cardiovascularly Safe Dental Local Anesthetic for Hypertensive Rats Treated With a Nonselective β-Adrenergic Antagonist
Yukako Tsutsui DDS, PhD and
 Katsuhisa Sunada DDS, 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

Dentists use vasoconstrictors such as epinephrine to prolong the duration of dental local anesthesia. However, vasoconstrictors occasionally produce adverse cardiovascular side effects such as hypertension and bradycardia, especially when administered to hypertensive patients. For those patients already taking nonselective β-adrenergic antagonists who were administered epinephrine, a large increase in blood pressure (BP) has previously been reported. 1 , 2 This occurs because nonselective β-adrenergic antagonists causes epinephrine, which

Involvement of α- and β-Adrenergic Receptors in Skeletal Muscle Blood Flow Changes During Hyper-/Hypocapnia in Anesthetized Rabbits
Kyotaro Koshika DDS, PhD,
 Rumi Kaneko DDS,
 Mai Shionoya DDS,
 Kotaro Shimizu DDS,
 Yuka Sendai DDS,
 Nobutaka Matsuura DDS,
 Yui Akiike DDS, PhD, and
 Tatsuya Ichinohe DDS, PhD
Article Category: Research Article
Volume/Issue: Volume 70: Issue 2
Online Publication Date: Jun 28, 2023
DOI: 10.2344/anpr-70-02-02
Page Range: 58 – 64

Meanwhile, although the densities of vascular α1- and β-adrenergic receptors are similar in slow- and fast-twitch muscles, resistance arterioles are far more numerous in slow-twitch muscles. 8 , 9 Accordingly, it has been speculated that the differences in vascular regulation in fast- and slow-twitch muscles are attributable to the differences in vascular innervation or SNS activity and in the densities or functional reserves of vascular α-adrenergic receptors. 10 If changes in skeletal muscle blood flow induced by variations in ETCO 2 arise primarily from

Figure 4.; Mechanism of vasopressinergic vs adrenergic vasoconstriction. Vasopressin (V1) receptor activation by vasopressin produces short-term vasoconstriction that increases vascular resistance and mean arterial pressure (MAP).14 V1 receptor agonists are effective in patients with severe hypotension and renin-angiotensin-aldosterone system (RAAS) blockade when conventional adrenergic treatment fails.15
Caitlin M. Waters,
 Kristen Pelczar,
 Edward C. Adlesic,
 Paul J. Schwartz, and
 Joseph A. Giovannitti Jr
Figure 4.
Figure 4.

Mechanism of vasopressinergic vs adrenergic vasoconstriction. Vasopressin (V1) receptor activation by vasopressin produces short-term vasoconstriction that increases vascular resistance and mean arterial pressure (MAP). 14 V1 receptor agonists are effective in patients with severe hypotension and renin-angiotensin-aldosterone system (RAAS) blockade when conventional adrenergic treatment fails. 15

; Figure 3. The adrenergic synapse. The nerve impulse releases norepinephrine (NE), which binds to specific adrenergic receptors on the cell membranes of target tissue. (α1, β1, β2). The neuronal endings contain α2 prejunctional receptors. When activated by NE, further release of the neurotransmitter is inhibited. Adrenergic ligands also arrive at the synapse via the circulatory system. These include epinephrine (E) and norepinephrine (NE) secreted by the adrenal medulla or adrenergic drugs (D). The termination of norepinephrine (NE) is due primarily to reuptake into the nerve ending. Epinephrine (E) from the adrenal medulla and adrenergic drugs (D) are metabolized by monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT) in local tissues or the liver following absorption. (See text for further explanation.)
Daniel E. Becker

Figure 3. The adrenergic synapse. The nerve impulse releases norepinephrine (NE), which binds to specific adrenergic receptors on the cell membranes of target tissue. (α1, β1, β2). The neuronal endings contain α2 prejunctional receptors. When activated by NE, further release of the neurotransmitter is inhibited. Adrenergic ligands also arrive at the synapse via the circulatory system. These include epinephrine (E) and norepinephrine (NE) secreted by the adrenal medulla or adrenergic drugs (D). The termination of norepinephrine (NE) is due primarily to reuptake into the nerve ending. Epinephrine (E) from the adrenal medulla and adrenergic drugs (D) are metabolized by monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT) in local tissues or the liver following absorption. (See text for further explanation.)

Figure 1.  ; Antidepressant medications within the 4 therapeutic drug classes.
Mana Saraghi,
 Leonard R. Golden, and
 Elliot V. Hersh
<bold>Figure 1. </bold>
Figure 1. 

Antidepressant medications within the 4 therapeutic drug classes.

Figure 2.  ; Vasoconstrictor interaction with tricyclic antidepressants and serotonin-norepinephrine reuptake inhibitors.
Mana Saraghi,
 Leonard R. Golden, and
 Elliot V. Hersh
<bold>Figure 2. </bold>
Figure 2. 

Vasoconstrictor interaction with tricyclic antidepressants and serotonin-norepinephrine reuptake inhibitors.

Figure 3.  ; (A) Naïve nerve terminal. (B) Nerve terminal plus a monoamine oxidase inhibitor. (C) Nerve terminal with epinephrine. (D) Nerve terminal with ephedrine.
Mana Saraghi,
 Leonard R. Golden, and
 Elliot V. Hersh
<bold>Figure 3. </bold>
Figure 3. 

(A) Naïve nerve terminal. (B) Nerve terminal plus a monoamine oxidase inhibitor. (C) Nerve terminal with epinephrine. (D) Nerve terminal with ephedrine.

Figure 4.  ; Lack of vasoconstrictor interaction with selective serotonin reuptake inhibitors.
Mana Saraghi,
 Leonard R. Golden, and
 Elliot V. Hersh
<bold>Figure 4. </bold>
Figure 4. 

Lack of vasoconstrictor interaction with selective serotonin reuptake inhibitors.