Interaction between Intrathecal Neostigmine and Epidural Clonidine in Human Volunteers

Hood, David D.; Mallak, Kathryn A.; Eisenach, James C.; Tong, Chuanyao

doi:10.1097/00000542-199608000-00013

Cited by 135 publications

(50 citation statements)

References 19 publications

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“…2 Spinal neostigmine is advantageous over other currently used spinal drugs as it causes no hypotension (excitation of sympathetic outflow), no sedation, no respiratory depression or neurological dysfunction. 2,3 In our study the mean lowest heart rate during spinal anaesthesia in all the three groups were comparable and statistically insignificant. On comparing the haemodynamic parameters, we found that the mean systolic blood pressure before spinal anaesthesia and the lowest mean systolic blood pressure and lowest mean diastolic blood pressure did not differ significantly between the three groups.…”

Section: Discussionsupporting

confidence: 49%

“…2 Spinal neostigmine is advantageous over other currently used spinal drugs as it causes no hypotension (excitation of sympathetic outflow), no sedation, no respiratory depression or neurological dysfunction. 2,3 Bupivacaine was the first local anaesthetic that produced adequate pain relief, without a major effect on motor fibres. 4 Neostigmine has been shown to counteract haemodynamic effects of clonidine and bupivacaine.…”

mentioning

confidence: 99%

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Evaluation of intrathecal neostigmine in different doses added to bupivacaine for postoperative analgesia

Bhat¹,

Ommid

Gupta

et al. 2011

Sri Lankan J Anaesthesiol

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Section: Discussionsupporting

confidence: 49%

“…2 Spinal neostigmine is advantageous over other currently used spinal drugs as it causes no hypotension (excitation of sympathetic outflow), no sedation, no respiratory depression or neurological dysfunction. 2,3 Bupivacaine was the first local anaesthetic that produced adequate pain relief, without a major effect on motor fibres. 4 Neostigmine has been shown to counteract haemodynamic effects of clonidine and bupivacaine.…”

mentioning

confidence: 99%

Evaluation of intrathecal neostigmine in different doses added to bupivacaine for postoperative analgesia

Bhat¹,

Ommid

Gupta

et al. 2011

Sri Lankan J Anaesthesiol

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show abstract

“…For these reasons, investigations of low-dose combination therapies with different mechanisms of drug action to induce effective analgesic action should be valuable to reduce adverse effects. Combined administrations of clonidine and morphine (33), clonidine and neostigmine (34), as well as morphine and neostigmine (35), into the intrathecal or epidural space have produced effective analgesia with fewer adverse events. The promising results of our present experiments suggest that i.t.…”

Section: Effects Of K + Channels On Bethanechol-induced Antinociceptionmentioning

confidence: 99%

Involvement of Potassium Channels in Spinal Antinociceptions Induced by Fentanyl, Clonidine and Bethanechol in Rats

Yamazumi

Okuda

Koga

2001

Japanese Journal of Pharmacology

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ABSTRACT-In the central nervous systems, intracellular and extracellular movement of potassium ions plays an important role in regulating neuronal excitability and the release of neurotransmitters. The purpose of our study was to determine whether nicorandil (adenosine triphosphate-sensitive K + channel opener) exerts antinociceptive effects by itself or in combination with fentanyl, clonidine and bethanechol and whether glibenclamide (adenosine triphosphate-sensitive K + channel blocker) and charybdotoxin (Ca 2+ -activated K + channel blocker) may antagonize the antinociceptive action of fentanyl, clonidine and bethanechol. Antinociceptive effects were assessed using the tail-flick test in rats. Nicorandil (100 mg) and antinociceptively ineffective doses of fentanyl (1 m g), clonidine (2.5 m g) or bethanechol (10 m g) were coadministered intrathecally (i.t.). Glibenclamide (100 mg) or charybdotoxin (2.5 ng) were administered i.t. at 5 min before each effective dose of fentanyl (2.5 mg), clonidine (10 mg) or bethanechol (40 mg). The present findings demonstrated that i.t. administration of nicorandil alone exerted no influence on the tail-flick latency. However, concomitant administrations of antinociceptively inactive doses of fentanyl, clonidine or bethanechol with nicorandil elicited significant suppression of the thermonociceptive response. Also, each antinociception induced by fentanyl, clonidine or bethanechol was partially antagonized by both glibenclamide and charybdotoxin. These findings showed that activation of the K + channel might enhance the antinociceptive effects of fentanyl, clonidine and bethanechol.

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“…[4][5][6] A recent study demonstrated that the oral administration of donepezil, an approved cholinesterase inhibitor for the symptomatic treatment of Alzheimer dementia, produced an antihypersensitivity effect in rats after nerve injury but not in normal animals; this involved a spinal mechanism. 7 Although the detailed mechanism is not fully understood, manipulations that increase acetylcholine (ACh) release in the spinal cord produce analgesia via both muscarinic and nicotinic receptors.…”

mentioning

confidence: 99%

Relief of Hypersensitivity after Nerve Injury from Systemic Donepezil Involves Spinal Cholinergic and γ-Aminobutyric Acid Mechanisms

Kimura¹,

Hayashida²,

Eisenach

et al. 2013

Anesthesiology

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Background: Evoking spinal release of acetylcholine (ACh) produces antinociception in normal animals and reduces hypersensitivity after nerve injury, and some studies suggest that ACh-mediated analgesia relies on γ-aminobutyric acid (GABA)-ergic signaling in the spinal cord. In this study, the authors tested the spinal mechanisms underlying the antihypersensitivity effects of donepezil, a central nervous system-penetrating cholinesterase inhibitor, in a rat model of neuropathic pain. Methods: Male Sprague-Dawley rats were anesthetized, and L5 spinal nerve ligation was performed unilaterally. Withdrawal threshold to a paw pressure test was measured before and after intraperitoneal administration of donepezil, with or without intrathecal antagonists for cholinergic and GABAergic receptors. Microdialysis studies in the ipsilateral dorsal horn of the lumbar spinal cord were also performed to measure extracellular ACh and GABA. Results: Donepezil increased the withdrawal threshold in spinal nerve ligation rats but not in normal rats. The antihypersensitivity effect of donepezil (1 mg/kg) in spinal nerve ligation rats was reduced by intrathecal pretreatment with atropine (30 μg), a muscarinic receptor antagonist; mecamylamine (100 μg), a nicotinic receptor antagonist; bicuculline (0.03 μg), a γ-aminobutyric acid receptor type

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Interaction between Intrathecal Neostigmine and Epidural Clonidine in Human Volunteers

Abstract: These results support enhancement of alpha 2-adrenergic analgesia by intrathecal neostigmine, but do not demonstrate synergy, as observed in animals. Lack of enhancement of side effects suggests this combination may be clinically useful.

Cited by 135 publications

References 19 publications

Evaluation of intrathecal neostigmine in different doses added to bupivacaine for postoperative analgesia

Evaluation of intrathecal neostigmine in different doses added to bupivacaine for postoperative analgesia

Involvement of Potassium Channels in Spinal Antinociceptions Induced by Fentanyl, Clonidine and Bethanechol in Rats

Relief of Hypersensitivity after Nerve Injury from Systemic Donepezil Involves Spinal Cholinergic and γ-Aminobutyric Acid Mechanisms

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