ArticleThe journal of pain2008
Sympathetic vasoconstrictor antagonism and vasodilatation relieve mechanical allodynia in rats with chronic postischemia pain.
Article in The journal of pain, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- Effect of tadalafil on blood flow, pain, and function in chronic cold complex regional pain syndrome: a randomized controlled trial.BMC musculoskeletal disorders · 2008Trial
- Analgesic Effect of SKI306X on Chronic Postischemic Pain and Spinal Nerve Ligation-Induced Neuropathic Pain in Mice.Biomedicines · 2024Article
- Nrf2 Activation Mediates Antiallodynic Effect of Electroacupuncture on a Rat Model of Complex Regional Pain Syndrome Type-I through Reducing Local Oxidative Stress and Inflammation.Oxidative medicine and cellular longevity · 2022Article
- Immunoregulatory Effect of Preventive Supplementation of Omega-3 Fatty Acid in a Complex Regional Pain Syndrome Type I Model in Mice.Frontiers in integrative neuroscience · 2022Article
- The analgesic effect of propofol associated with the inhibition of hypoxia inducible factor and inflammasome in complex regional pain syndrome.Journal of biomedical science · 2019Article
- The Rodent Tibia Fracture Model: A Critical Review and Comparison With the Complex Regional Pain Syndrome Literature.The journal of pain · 2018Review
- Anti-allodynic Effect of Mangiferin in Rats With Chronic Post-ischemia Pain: A Model of Complex Regional Pain Syndrome Type I.Frontiers in pharmacology · 2018Article
- Sympathetic fibre sprouting in the skin contributes to pain-related behaviour in spared nerve injury and cuff models of neuropathic pain.Molecular pain · 2015Article
- Inhibition of endogenous NGF degradation induces mechanical allodynia and thermal hyperalgesia in rats.Molecular pain · 2013Article
- Janus molecule I: dichotomous effects of COMT in neuropathic vs nociceptive pain modalities.CNS & neurological disorders drug targets · 2012Review
- Complex regional pain syndrome: what's in a name?The journal of pain · 2011Article
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- Role of NFkappaB in an animal model of complex regional pain syndrome-type I (CRPS-I).The journal of pain · 2009Article
- Behavioral models of pain states evoked by physical injury to the peripheral nerve.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2009Review
- Regulation of peripheral blood flow in complex regional pain syndrome: clinical implication for symptomatic relief and pain management.BMC musculoskeletal disorders · 2009Review
- Objectifying CRPS-I.Pain · 2008Article
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Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledChronic pain that responds to antisympathetic treatments and alpha-adrenergic antagonists is clinically referred to as sympathetically maintained pain. Animal models of neuropathic pain have shown mixed results in terms of antinociceptive effectiveness of antisympathetic agents. The effectiveness of these agents have not been yet investigated in animal models of complex regional pain syndrome-type 1 (CRPS-I). In this study, we examined the effectiveness of antisympathetic agents and sympathetic vasoconstrictor antagonists, as well as agents that are vasodilators, in relieving mechanical allodynia in a recently developed animal model of CRPS-I (chronic postischemia pain or CPIP) produced by 3 hours of hind paw ischemia-reperfusion injury. Systemic guanethidine, phentolamine, clonidine, and prazosin are effective in reducing mechanical allodynia particularly at 2 days after reperfusion, and less so at 7 days after reperfusion. A nitric oxide donor vasodilator, SIN-1, also reduces mechanical allodynia more effectively at 2 days after reperfusion, but not at 7 days after reperfusion. These results suggest that the pain of CPIP, and possibly also CRPS-I, is relieved by reducing sympathetically mediated vasoconstriction, or enhancing vasodilatation. PERSPECTIVE: The results of this study indicate that sympathetic block, or administration of alpha(1)-adrenergic antagonists, clonidine, or a nitric oxide donor, relieve allodynia in an animal model of CRPS-I. Thus, the pain of CRPS-I may depend on enhanced vasoconstrictor responsiveness, which may be relieved by blocking sympathetic efferent-dependent vasoconstriction, or by enhancing nitric oxide-dependent vasodilatation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.