α<sub>2</sub>-Adrenergic agonists as analgesic agents

Boyd, Robert E.

doi:10.1517/13543776.10.11.1741

Cited by 4 publications

(2 citation statements)

References 16 publications

(5 reference statements)

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“…In addition to modulating vasoconstriction and iris diameter, α 2 -ARs are involved in platelet aggregation (via the α 2a -ARs), neurotransmitter release, and antinociception. 15 In the urinary bladder, α 2 -ARs are found primarily in the urethral submucosa and bladder mucosa (not the muscle), suggesting a role in the regulation of blood flow and urethral lubrication, but not on smooth muscle. 16 However, α 2 -ARs function as autoreceptors to decrease norepinephrine outflow and could alter contractility through this mechanism.…”

Section: Discussionmentioning

confidence: 96%

In vivo evaluation of α2-adrenoceptors in cats with idiopathic cystitis

Westropp¹,

Kass²,

Buffington³

2007

ajvr

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Section: Discussionmentioning

confidence: 96%

In vivo evaluation of α2-adrenoceptors in cats with idiopathic cystitis

Westropp¹,

Kass²,

Buffington³

2007

ajvr

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“…However, a2 receptors have also been found postsynaptically, making this way of classification confusing and less popular (Boyd 2000).…”

Section: Dexmedetomidinementioning

confidence: 99%

Use of intravenous lidocaine to treat dexmedetomidine-induced bradycardia in sedated and anesthetized dogs

Tisotti

Valverde

Hopkins

et al. 2021

Veterinary Anaesthesia and Analgesia

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This thesis evaluated the use of intravenous lidocaine to treat the bradycardia associated with the administration of the sedative dexmedetomidine in canine anesthetic protocols. Research Beagle dogs were assigned to three different groups in a randomized crossover design that involved the administration of intravenous dexmedetomidine in different modalities of the anesthetic protocol. In two groups, dexmedetomidine was administered to dogs while awake and in the third group while anesthetized with isoflurane.After receiving dexmedetomidine, dogs were given intravenous lidocaine as a bolus 30 minutes later, followed by a second bolus and a constant rate infusion 20 minutes after the first bolus, in one of the awake groups and the anesthetized group. The other awake group received the lidocaine bolus and constant rate infusion 5 minutes after the dexmedetomidine.Intravenous lidocaine increased heart rate in awake and anesthetized dogs pretreated with intravenous dexmedetomidine. Additional benefits from lidocaine administration included an increase in cardiac index and a decrease in systemic vascular resistance.iii DEDICATIONIn Memoriam of my grandparents Ieda Hainzenreder and João de Mesquita.Foremost, I would like to thank my supervisor, Dr. Alexander Valverde, for opening the doors for me, for being resolute, tireless and for his guidance during my program. I would also like to thank all the anesthesia faculties I had the opportunity to work with and absorb some of their knowledge, but specially to Drs. Andrea Sanchez, Carolyn Kerr and Melissa Sinclair for the personal and professional support along these three years.

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Descending control of pain

Millan

2002

Progress in Neurobiology

2,624

2,043

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Upon receipt in the dorsal horn (DH) of the spinal cord, nociceptive (pain-signalling) information from the viscera, skin and other organs is subject to extensive processing by a diversity of mechanisms, certain of which enhance, and certain of which inhibit, its transfer to higher centres. In this regard, a network of descending pathways projecting from cerebral structures to the DH plays a complex and crucial role. Specific centrifugal pathways either suppress (descending inhibition) or potentiate (descending facilitation) passage of nociceptive messages to the brain. Engagement of descending inhibition by the opioid analgesic, morphine, fulfils an important role in its pain-relieving properties, while induction of analgesia by the adrenergic agonist, clonidine, reflects actions at alpha(2)-adrenoceptors (alpha(2)-ARs) in the DH normally recruited by descending pathways. However, opioids and adrenergic agents exploit but a tiny fraction of the vast panoply of mechanisms now known to be involved in the induction and/or expression of descending controls. For example, no drug interfering with descending facilitation is currently available for clinical use. The present review focuses on: (1) the organisation of descending pathways and their pathophysiological significance; (2) the role of individual transmitters and specific receptor types in the modulation and expression of mechanisms of descending inhibition and facilitation and (3) the advantages and limitations of established and innovative analgesic strategies which act by manipulation of descending controls. Knowledge of descending pathways has increased exponentially in recent years, so this is an opportune moment to survey their operation and therapeutic relevance to the improved management of pain.

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α₂-Adrenergic agonists as analgesic agents

Cited by 4 publications

References 16 publications

In vivo evaluation of α2-adrenoceptors in cats with idiopathic cystitis

In vivo evaluation of α2-adrenoceptors in cats with idiopathic cystitis

Use of intravenous lidocaine to treat dexmedetomidine-induced bradycardia in sedated and anesthetized dogs

Descending control of pain

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α2-Adrenergic agonists as analgesic agents

Cited by 4 publications

References 16 publications

In vivo evaluation of α2-adrenoceptors in cats with idiopathic cystitis

In vivo evaluation of α2-adrenoceptors in cats with idiopathic cystitis

Use of intravenous lidocaine to treat dexmedetomidine-induced bradycardia in sedated and anesthetized dogs

Descending control of pain

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Product

Resources

About

α₂-Adrenergic agonists as analgesic agents