Intravenous lidocaine infusion — a new treatment of chronic painful diabetic neuropathy?

Kastrup, Jens; Petersen, Palle; Dejgård, A; Angelo, Helle R.; Hilsted, J.

doi:10.1016/0304-3959(87)91061-x

Cited by 282 publications

(107 citation statements)

References 16 publications

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“…Tactile allodynia develops within 7 ± 10 days of the onset of hyperglycaemia, persists for many weeks and is prevented by insulin therapy. Low doses of systemically administered lignocaine alleviated tactile allodynia in diabetic rats and have also been shown to be e ective in treating some cases of painful diabetic neuropathy (Kastrup et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

Spinal pharmacology of tactile allodynia in diabetic rats

Calcutt¹,

Chaplan²

1997

British J Pharmacology

137

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1 Rats develop tactile allodynia to stimulation of the plantar surface of the hindpaw with von Frey ®laments within days of the onset of streptozotocin-induced diabetes. This is prevented by insulin and alleviated by systemic lignocaine, but the aetiology is unknown. 2 Using indwelling lumbar intrathecal catheters to deliver pharmacological agents, we have investigated whether tactile allodynia in streptozotocin-diabetic rats is dependent on mechanisms associated with spinal sensitization, by assessing the e cacy of agents that inhibit speci®c components of spinal nociceptive processing. 3 Dose-dependent inhibition of tactile allodynia in diabetic rats was noted with the N-type calcium channel antagonist SNX 239, the a 2 -adrenoceptor agonist dexmedetomidine, the m-opioid receptor agonist morphine, the N-methyl-D-aspartate (NMDA) receptor antagonist AP5 and the non-NMDA receptor antagonist NBQX.4 No e ect on tactile allodynia was noted after intrathecal administration of the nitric oxide synthase inhibitor N G -nitro-L-arginine methyl ester (L-NAME), the cyclo-oxygenase inhibitor ketorolac, the Ltype calcium channel inhibitor diltiazem or any vehicle. 5 These data suggest that the tactile allodynia of diabetic rats involves spinal glutamatergic pathways but is not associated with spinal release of nitric oxide or prostaglandins.

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Section: Introductionmentioning

confidence: 99%

Spinal pharmacology of tactile allodynia in diabetic rats

Calcutt¹,

Chaplan²

1997

British J Pharmacology

137

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“…These include neoplastic pain (Cavallini & Beltrami, 1968), post-operative pain (McLachlin, 1945; Keats et al, 1951;De Clive-Lowe, 1958;Bartlett & Hutaserani, 1961;Nalda Felipe et al, 1977;De Gaudio et al, 1978;Marchisio, 1980), post-traumatic pain (Schnapp, 1981), neuralgic pain (Boas et al, 1982;Lindblom & Lindstrdm, 1984), muscular pain (Usubiaga et al, 1967;Haldia et al, 1973), adiposa dolorosa (Iwane et al, 1976;Lindstr6m & Lindblom, 1987;Kastrup et al, 'Author for correspondence.…”

Section: Introductionmentioning

confidence: 99%

Antinociception induced by systemic administration of local anaesthetics depends on a central cholinergic mechanism

Bartolini

Galli

Ghelardini

et al. 1987

British J Pharmacology

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The antinociceptive effects of systemically‐administered procaine, lignocaine and bupivacaine were examined in mice and rats by using the hot‐plate, writhing and tail flick tests. In both species all three local anaesthetics produced significant antinociception which was prevented by atropine (5 mg kg−1, i.p.) and by hemicholinium‐3 (1 μg per mouse, i.c.v.), but not by naloxone (3 mg kg−1, i.p.), α‐methyl‐p‐tyrosine (100 mg kg−1, s.c.), reserpine (2 mg kg−1, i.p.) or atropine methylbromide (5.5 mg kg−1, i.p.). Atropine (5 mg kg−1, i.p.) which totally antagonized oxotremorine (40 μg kg−1, s.c.) antinociception did not modify morphine (5 mg kg−1, s.c.) or baclofen (4 mg kg−1, s.c.) antinociception. On the other hand, hemicholinium, which antagonized local anaesthetic antinociception, did not prevent oxotremorine, morphine or baclofen antinociception. Intracerebroventricular injection in mice of procaine (200 μg), lignocaine (150 μg) and bupivacaine (25 μg), doses which were largely ineffective by parenteral routes, induced an antinociception whose intensity equalled that obtainable subcutaneously. Moreover, the i.c.v. injection of antinociceptive doses did not impair performance on the rota‐rod test. Concentrations below 10−10 m of procaine, lignocaine and bupivacaine did not evoke any response on the isolated longitudinal muscle strip of guinea‐pig ileum, or modify acetylcholine (ACh)‐induced contractions. On the other hand, they always increased electrically‐evoked twitches. The same concentrations of local anaesthetics which induced antinociception did not inhibit acetylcholinesterase (AChE) in vitro. On the basis of the above findings and the existing literature, a facilitation of cholinergic transmission by the local anaesthetics is postulated; this could be due to blockade of presynaptic muscarinic receptors.

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“…Although the analgesic effects of systemic lidocaine have been proven for chronic pain, particularly for neuropathic pain states [27][28][29] , conflicting results have been achieved for acute pain, such as postoperative pain 12,25,30 .…”

Section: Discussionmentioning

confidence: 99%

Analgesic comparison of systemic lidocaine, morphine or lidocaine plus morphine infusion in dogs undergoing fracture repair

et al. 2014

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Intellectual and scientific content of the study, statistical analysis, critical revision. ABSTRACT PURPOSE:To compare the postoperative analgesic effects of lidocaine, morphine and lidocaine plus morphine administered by constant rate infusion (CRI) and analyzing their effects on opioid requirements after orthopedic surgery in dogs. METHODS:Twenty-four dogs underwent fracture repairs were premedicated with IM acepromazine (0.05 mg/kg) combined with morphine (0.3mg/kg). Anesthesia was induced with IV propofol (4 to 5 mg/ kg) and maintained with isoflurane. The dogs were randomly assigned to 3 groups and administered a CRI IV of lidocaine (T-L), morphine (T-M) or lidocaine plus morphine (T-LM) at the same doses. Postoperative analgesia was assessed for 24 hours using a Visual Analog Scale (VAS) and the Glasgow Composite Pain Scale (GCPS). Rescue analgesia was performed if the evaluation score exceeded 50% of the VAS and/or 33% of the GCPS. RESULTS:The pain score and postoperative opioid requirements did not differ among the treatments. Rescue analgesia was administered to 1/8 dogs in the T-M and T-LM, and to 3/8 dogs in the T-L. CONCLUSION:Lidocaine, morphine or lidocaine/morphine CRI may be efficacious techniques for pain management in the first 24 hours post-surgery. However, the two drugs administered together did not reduce the postoperative opioid requirement in dogs undergoing fracture repair.

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Intravenous lidocaine infusion — a new treatment of chronic painful diabetic neuropathy?

Cited by 282 publications

References 16 publications

Spinal pharmacology of tactile allodynia in diabetic rats

Spinal pharmacology of tactile allodynia in diabetic rats

Antinociception induced by systemic administration of local anaesthetics depends on a central cholinergic mechanism

Analgesic comparison of systemic lidocaine, morphine or lidocaine plus morphine infusion in dogs undergoing fracture repair

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