Development of animal model for vasculatic neuropathy: Induction by ischemic-reperfusion in the rat femoral artery
Ischemic-reperfusion (I/R) is common in various pathological conditions like diabetic complication, complex regional pain syndrome type II (CRPS II), necrotizing vascular occlusive disease and trauma. We have developed an animal model of ischemic-reperfusion injury induced nociceptive sensory neurop...
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Veröffentlicht in: | Journal of neuroscience methods 2010-02, Vol.186 (2), p.215-221 |
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description | Ischemic-reperfusion (I/R) is common in various pathological conditions like diabetic complication, complex regional pain syndrome type II (CRPS II), necrotizing vascular occlusive disease and trauma. We have developed an animal model of ischemic-reperfusion injury induced nociceptive sensory neuropathy in rats. The model was validated after 2, 4 and 6
h of ischemia followed by prolonged reperfusion. The sensory behavioral assessment revealed thermal and mechanical hyperalgesia in paw and in tail which expressed the peripheral and central neuropathic pain respectively. We observed a decrease in the serum IL-10 and nerve conduction velocity and increase in the serum nitrate, malondialdehyde (MDA) and TNF-α levels in the 4 and 6
h I/R groups in biochemical and electrophysiological evaluations. Histopathological study had revealed the decrease in nerve fiber density in the moderate and severe I/R groups. We selected the moderate (4
h) ischemic-reperfusion injury as beneficial model because of the good correlation with clinical status for the development of neuropathy in human associated with severe pain disorders. This model can be used to explore pathophysiological mechanisms implied in the genesis of neuropathic pain and also to evaluate the new analgesic agents, peripheral neuro-vasoactive substances and neuroprotective drugs. |
doi_str_mv | 10.1016/j.jneumeth.2009.12.004 |
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h of ischemia followed by prolonged reperfusion. The sensory behavioral assessment revealed thermal and mechanical hyperalgesia in paw and in tail which expressed the peripheral and central neuropathic pain respectively. We observed a decrease in the serum IL-10 and nerve conduction velocity and increase in the serum nitrate, malondialdehyde (MDA) and TNF-α levels in the 4 and 6
h I/R groups in biochemical and electrophysiological evaluations. Histopathological study had revealed the decrease in nerve fiber density in the moderate and severe I/R groups. We selected the moderate (4
h) ischemic-reperfusion injury as beneficial model because of the good correlation with clinical status for the development of neuropathy in human associated with severe pain disorders. This model can be used to explore pathophysiological mechanisms implied in the genesis of neuropathic pain and also to evaluate the new analgesic agents, peripheral neuro-vasoactive substances and neuroprotective drugs.</description><identifier>ISSN: 0165-0270</identifier><identifier>EISSN: 1872-678X</identifier><identifier>DOI: 10.1016/j.jneumeth.2009.12.004</identifier><identifier>PMID: 20026113</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Disease Models, Animal ; Femoral Artery ; Foot ; Hot Temperature ; Hyperalgesia ; Interleukin-10 - blood ; Ischemia–reperfusion ; Malondialdehyde - blood ; Nerve conduction velocity ; Neural Conduction ; Neuropathy ; Nitrates - blood ; Pain Measurement ; Peripheral Nervous System Diseases - etiology ; Peripheral Nervous System Diseases - pathology ; Peripheral Nervous System Diseases - physiopathology ; Physical Stimulation ; Rats ; Rats, Wistar ; Reperfusion Injury - complications ; Reperfusion Injury - pathology ; Reperfusion Injury - physiopathology ; Sensation Disorders - etiology ; Sensation Disorders - pathology ; Sensation Disorders - physiopathology ; Tail ; Time Factors ; Tumor Necrosis Factor-alpha - blood</subject><ispartof>Journal of neuroscience methods, 2010-02, Vol.186 (2), p.215-221</ispartof><rights>2010 Elsevier B.V.</rights><rights>Copyright 2010 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c399t-8569106a61687f62c07a37fb40adaf2cfa481d01aea02e188649eaebf79bb1f33</citedby><cites>FETCH-LOGICAL-c399t-8569106a61687f62c07a37fb40adaf2cfa481d01aea02e188649eaebf79bb1f33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0165027009006475$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20026113$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Muthuraman, Arunachalam</creatorcontrib><creatorcontrib>Ramesh, Muthusamy</creatorcontrib><creatorcontrib>Sood, Shailja</creatorcontrib><title>Development of animal model for vasculatic neuropathy: Induction by ischemic-reperfusion in the rat femoral artery</title><title>Journal of neuroscience methods</title><addtitle>J Neurosci Methods</addtitle><description>Ischemic-reperfusion (I/R) is common in various pathological conditions like diabetic complication, complex regional pain syndrome type II (CRPS II), necrotizing vascular occlusive disease and trauma. We have developed an animal model of ischemic-reperfusion injury induced nociceptive sensory neuropathy in rats. The model was validated after 2, 4 and 6
h of ischemia followed by prolonged reperfusion. The sensory behavioral assessment revealed thermal and mechanical hyperalgesia in paw and in tail which expressed the peripheral and central neuropathic pain respectively. We observed a decrease in the serum IL-10 and nerve conduction velocity and increase in the serum nitrate, malondialdehyde (MDA) and TNF-α levels in the 4 and 6
h I/R groups in biochemical and electrophysiological evaluations. Histopathological study had revealed the decrease in nerve fiber density in the moderate and severe I/R groups. We selected the moderate (4
h) ischemic-reperfusion injury as beneficial model because of the good correlation with clinical status for the development of neuropathy in human associated with severe pain disorders. This model can be used to explore pathophysiological mechanisms implied in the genesis of neuropathic pain and also to evaluate the new analgesic agents, peripheral neuro-vasoactive substances and neuroprotective drugs.</description><subject>Animals</subject><subject>Disease Models, Animal</subject><subject>Femoral Artery</subject><subject>Foot</subject><subject>Hot Temperature</subject><subject>Hyperalgesia</subject><subject>Interleukin-10 - blood</subject><subject>Ischemia–reperfusion</subject><subject>Malondialdehyde - blood</subject><subject>Nerve conduction velocity</subject><subject>Neural Conduction</subject><subject>Neuropathy</subject><subject>Nitrates - blood</subject><subject>Pain Measurement</subject><subject>Peripheral Nervous System Diseases - etiology</subject><subject>Peripheral Nervous System Diseases - pathology</subject><subject>Peripheral Nervous System Diseases - physiopathology</subject><subject>Physical Stimulation</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reperfusion Injury - complications</subject><subject>Reperfusion Injury - pathology</subject><subject>Reperfusion Injury - physiopathology</subject><subject>Sensation Disorders - etiology</subject><subject>Sensation Disorders - pathology</subject><subject>Sensation Disorders - physiopathology</subject><subject>Tail</subject><subject>Time Factors</subject><subject>Tumor Necrosis Factor-alpha - blood</subject><issn>0165-0270</issn><issn>1872-678X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1r3DAQxUVpabZp_4WgW092NbKjj55a0q9AoJcWehOyPGK12JYryQv731fLJr3mNDD83rzhPUJugLXAQHw4tIcFtxnLvuWM6RZ4y1j_guxASd4Iqf68JLsK3jaMS3ZF3uR8YJXQTLwmV1XCBUC3I-kLHnGK64xLodFTu4TZTnSOI07Ux0SPNrttsiU4Wg1TXG3Znz7S-2XcXAlxocOJhuz2OAfXJFwx-S2f92GhZY802UI9zjHVqzYVTKe35JW3U8Z3j_Oa_P729dfdj-bh5_f7u88Pjeu0Lo26FRqYsAKEkl5wx6TtpB96ZkfrufO2VzAysGgZR1BK9BotDl7qYQDfddfk_eXumuLfDXMxc30Up8kuGLdslNS9VD2oZ0nZdUoLkLKS4kK6FHNO6M2aamDpZICZczHmYJ6KMediDHBTY6_Cm0eLbZhx_C97aqICny4A1kiOAZPJLuDicAwJXTFjDM95_AMJR6Tx</recordid><startdate>20100215</startdate><enddate>20100215</enddate><creator>Muthuraman, Arunachalam</creator><creator>Ramesh, Muthusamy</creator><creator>Sood, Shailja</creator><general>Elsevier B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7TK</scope></search><sort><creationdate>20100215</creationdate><title>Development of animal model for vasculatic neuropathy: Induction by ischemic-reperfusion in the rat femoral artery</title><author>Muthuraman, Arunachalam ; Ramesh, Muthusamy ; Sood, Shailja</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c399t-8569106a61687f62c07a37fb40adaf2cfa481d01aea02e188649eaebf79bb1f33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Animals</topic><topic>Disease Models, Animal</topic><topic>Femoral Artery</topic><topic>Foot</topic><topic>Hot Temperature</topic><topic>Hyperalgesia</topic><topic>Interleukin-10 - blood</topic><topic>Ischemia–reperfusion</topic><topic>Malondialdehyde - blood</topic><topic>Nerve conduction velocity</topic><topic>Neural Conduction</topic><topic>Neuropathy</topic><topic>Nitrates - blood</topic><topic>Pain Measurement</topic><topic>Peripheral Nervous System Diseases - etiology</topic><topic>Peripheral Nervous System Diseases - pathology</topic><topic>Peripheral Nervous System Diseases - physiopathology</topic><topic>Physical Stimulation</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reperfusion Injury - complications</topic><topic>Reperfusion Injury - pathology</topic><topic>Reperfusion Injury - physiopathology</topic><topic>Sensation Disorders - etiology</topic><topic>Sensation Disorders - pathology</topic><topic>Sensation Disorders - physiopathology</topic><topic>Tail</topic><topic>Time Factors</topic><topic>Tumor Necrosis Factor-alpha - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Muthuraman, Arunachalam</creatorcontrib><creatorcontrib>Ramesh, Muthusamy</creatorcontrib><creatorcontrib>Sood, Shailja</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><jtitle>Journal of neuroscience methods</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Muthuraman, Arunachalam</au><au>Ramesh, Muthusamy</au><au>Sood, Shailja</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Development of animal model for vasculatic neuropathy: Induction by ischemic-reperfusion in the rat femoral artery</atitle><jtitle>Journal of neuroscience methods</jtitle><addtitle>J Neurosci Methods</addtitle><date>2010-02-15</date><risdate>2010</risdate><volume>186</volume><issue>2</issue><spage>215</spage><epage>221</epage><pages>215-221</pages><issn>0165-0270</issn><eissn>1872-678X</eissn><abstract>Ischemic-reperfusion (I/R) is common in various pathological conditions like diabetic complication, complex regional pain syndrome type II (CRPS II), necrotizing vascular occlusive disease and trauma. We have developed an animal model of ischemic-reperfusion injury induced nociceptive sensory neuropathy in rats. The model was validated after 2, 4 and 6
h of ischemia followed by prolonged reperfusion. The sensory behavioral assessment revealed thermal and mechanical hyperalgesia in paw and in tail which expressed the peripheral and central neuropathic pain respectively. We observed a decrease in the serum IL-10 and nerve conduction velocity and increase in the serum nitrate, malondialdehyde (MDA) and TNF-α levels in the 4 and 6
h I/R groups in biochemical and electrophysiological evaluations. Histopathological study had revealed the decrease in nerve fiber density in the moderate and severe I/R groups. We selected the moderate (4
h) ischemic-reperfusion injury as beneficial model because of the good correlation with clinical status for the development of neuropathy in human associated with severe pain disorders. This model can be used to explore pathophysiological mechanisms implied in the genesis of neuropathic pain and also to evaluate the new analgesic agents, peripheral neuro-vasoactive substances and neuroprotective drugs.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>20026113</pmid><doi>10.1016/j.jneumeth.2009.12.004</doi><tpages>7</tpages></addata></record> |
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subjects | Animals Disease Models, Animal Femoral Artery Foot Hot Temperature Hyperalgesia Interleukin-10 - blood Ischemia–reperfusion Malondialdehyde - blood Nerve conduction velocity Neural Conduction Neuropathy Nitrates - blood Pain Measurement Peripheral Nervous System Diseases - etiology Peripheral Nervous System Diseases - pathology Peripheral Nervous System Diseases - physiopathology Physical Stimulation Rats Rats, Wistar Reperfusion Injury - complications Reperfusion Injury - pathology Reperfusion Injury - physiopathology Sensation Disorders - etiology Sensation Disorders - pathology Sensation Disorders - physiopathology Tail Time Factors Tumor Necrosis Factor-alpha - blood |
title | Development of animal model for vasculatic neuropathy: Induction by ischemic-reperfusion in the rat femoral artery |
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