Thoracic spinal neuron responses to repeated myocardial ischemia and epicardial bradykinin
Bradykinin has been strongly implicated as a mediator of cardiac nociception. During coronary artery occlusion, the content of bradykinin in coronary sinus blood increases. In non-cardiac tissues nociception to bradykinin exhibits tachyphylaxis, however, this phenomenon has not been rigorously studi...
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| Veröffentlicht in: | Brain research 1998-04, Vol.790 (1), p.293-303 |
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| creator | Gutterman, David D. Pardubsky, P.D. Pettersen, M. Marcus, M.L. Gebhart, G.F. |
| description | Bradykinin has been strongly implicated as a mediator of cardiac nociception. During coronary artery occlusion, the content of bradykinin in coronary sinus blood increases. In non-cardiac tissues nociception to bradykinin exhibits tachyphylaxis, however, this phenomenon has not been rigorously studied in the heart. This raises the question that repeated coronary occlusions may also result in tachyphylaxis, thereby reducing cardiac sensation on subsequent ischemic stimulation. We therefore examined the hypothesis that repetitive episodes of myocardial ischemia and of epicardial application of bradykinin demonstrate tachyphylaxis. Mongrel cats were anesthetized with
α-chloralose and heart rate, arterial pressure, and thoracic spinal neuron firing rate were recorded during 60 s of anterior descending coronary occlusion or local epicardial application of bradykinin (10
μM). Neurons were identified by cutaneous receptive fields in the left shoulder area. Sixty-one of 93 neurons tested responded with an increase in firing rate to coronary artery occlusion only (
n=24), bradykinin only (
n=19) or to both (
n=18). On repetitive coronary occlusion, 14 of 25 neurons demonstrated tachyphylaxis compared to 12 of 15 tested with bradykinin (
p |
| doi_str_mv | 10.1016/S0006-8993(98)00081-X |
| format | Article |
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α-chloralose and heart rate, arterial pressure, and thoracic spinal neuron firing rate were recorded during 60 s of anterior descending coronary occlusion or local epicardial application of bradykinin (10
μM). Neurons were identified by cutaneous receptive fields in the left shoulder area. Sixty-one of 93 neurons tested responded with an increase in firing rate to coronary artery occlusion only (
n=24), bradykinin only (
n=19) or to both (
n=18). On repetitive coronary occlusion, 14 of 25 neurons demonstrated tachyphylaxis compared to 12 of 15 tested with bradykinin (
p<0.05). Similar responses were observed in thoracic spinal neurons that projected to the brain. In neurons demonstrating tachyphylaxis, dorsal cervical cold block partially restored the neuronal activation to coronary occlusion but not to bradykinin. We conclude, based on neuronal responses to repetitive stimuli, that afferent spinal responses to coronary occlusion and bradykinin are different. These data suggest that bradykinin is not the sole mediator of myocardial ischemic pain. The tachyphylaxis to repeated coronary artery occlusions may contribute to the clinical phenomenon of silent myocardial ischemia.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/S0006-8993(98)00081-X</identifier><identifier>PMID: 9593951</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>London: Elsevier B.V</publisher><subject>Afferent ; Animals ; Autonomic ; Autonomic Nervous System - physiology ; Biological and medical sciences ; Bradykinin - pharmacology ; Cardiac pain ; Cardiology. Vascular system ; Cats ; Cold Temperature ; Coronary heart disease ; Coronary Vessels - physiology ; Electrophysiology ; Heart ; Heart Rate - drug effects ; Ischemia ; Ligation ; Medical sciences ; Myocardial Ischemia - physiopathology ; Neural Inhibition - physiology ; Neurons, Afferent - drug effects ; Neurons, Afferent - physiology ; Pain - physiopathology ; Pericardium - drug effects ; Pericardium - innervation ; Reaction Time - physiology ; Reflex ; Reflex - physiology ; Reperfusion ; Spinal Cord - cytology ; Spinal Cord - drug effects ; Tachyphylaxis - physiology</subject><ispartof>Brain research, 1998-04, Vol.790 (1), p.293-303</ispartof><rights>1998 Elsevier Science B.V.</rights><rights>1998 INIST-CNRS</rights><rights>Copyright 1998 Elsevier Science B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c420t-a684f87940d26d066e04ab401bb3355410a2b40309a3b8aa9fb1302efbaf4c1d3</citedby><cites>FETCH-LOGICAL-c420t-a684f87940d26d066e04ab401bb3355410a2b40309a3b8aa9fb1302efbaf4c1d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0006-8993(98)00081-X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2256017$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9593951$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gutterman, David D.</creatorcontrib><creatorcontrib>Pardubsky, P.D.</creatorcontrib><creatorcontrib>Pettersen, M.</creatorcontrib><creatorcontrib>Marcus, M.L.</creatorcontrib><creatorcontrib>Gebhart, G.F.</creatorcontrib><title>Thoracic spinal neuron responses to repeated myocardial ischemia and epicardial bradykinin</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>Bradykinin has been strongly implicated as a mediator of cardiac nociception. During coronary artery occlusion, the content of bradykinin in coronary sinus blood increases. In non-cardiac tissues nociception to bradykinin exhibits tachyphylaxis, however, this phenomenon has not been rigorously studied in the heart. This raises the question that repeated coronary occlusions may also result in tachyphylaxis, thereby reducing cardiac sensation on subsequent ischemic stimulation. We therefore examined the hypothesis that repetitive episodes of myocardial ischemia and of epicardial application of bradykinin demonstrate tachyphylaxis. Mongrel cats were anesthetized with
α-chloralose and heart rate, arterial pressure, and thoracic spinal neuron firing rate were recorded during 60 s of anterior descending coronary occlusion or local epicardial application of bradykinin (10
μM). Neurons were identified by cutaneous receptive fields in the left shoulder area. Sixty-one of 93 neurons tested responded with an increase in firing rate to coronary artery occlusion only (
n=24), bradykinin only (
n=19) or to both (
n=18). On repetitive coronary occlusion, 14 of 25 neurons demonstrated tachyphylaxis compared to 12 of 15 tested with bradykinin (
p<0.05). Similar responses were observed in thoracic spinal neurons that projected to the brain. In neurons demonstrating tachyphylaxis, dorsal cervical cold block partially restored the neuronal activation to coronary occlusion but not to bradykinin. We conclude, based on neuronal responses to repetitive stimuli, that afferent spinal responses to coronary occlusion and bradykinin are different. These data suggest that bradykinin is not the sole mediator of myocardial ischemic pain. The tachyphylaxis to repeated coronary artery occlusions may contribute to the clinical phenomenon of silent myocardial ischemia.</description><subject>Afferent</subject><subject>Animals</subject><subject>Autonomic</subject><subject>Autonomic Nervous System - physiology</subject><subject>Biological and medical sciences</subject><subject>Bradykinin - pharmacology</subject><subject>Cardiac pain</subject><subject>Cardiology. Vascular system</subject><subject>Cats</subject><subject>Cold Temperature</subject><subject>Coronary heart disease</subject><subject>Coronary Vessels - physiology</subject><subject>Electrophysiology</subject><subject>Heart</subject><subject>Heart Rate - drug effects</subject><subject>Ischemia</subject><subject>Ligation</subject><subject>Medical sciences</subject><subject>Myocardial Ischemia - physiopathology</subject><subject>Neural Inhibition - physiology</subject><subject>Neurons, Afferent - drug effects</subject><subject>Neurons, Afferent - physiology</subject><subject>Pain - physiopathology</subject><subject>Pericardium - drug effects</subject><subject>Pericardium - innervation</subject><subject>Reaction Time - physiology</subject><subject>Reflex</subject><subject>Reflex - physiology</subject><subject>Reperfusion</subject><subject>Spinal Cord - cytology</subject><subject>Spinal Cord - drug effects</subject><subject>Tachyphylaxis - physiology</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1r3DAQhkVpSbdpf0LAh1Lag9ORZcvSqZTQj0Agh6QQehFjaUzU2pIreQv776tkt3vNaXhnnpGGh7EzDuccuPx4AwCyVlqL91p9KEHx-u4Z23DVN7VsWnjONkfkJXuV868ShdBwwk50p4Xu-Ib9vL2PCa23VV58wKkKtE0xVInyEkOmXK2xhIVwJVfNu2gxOV84n-09zR4rDK6ixf_vDwnd7rcPPrxmL0acMr051FP24-uX24vv9dX1t8uLz1e1bRtYa5SqHVWvW3CNdCAlQYtDC3wYhOi6lgM2JQrQKAaFqMeBC2hoHHBsLXfilL3bv7uk-GdLeTVzOY6mCQPFbTa9Vr2UQj0JcikEyEYXsNuDNsWcE41mSX7GtDMczIN88yjfPJg1WplH-eau7J0dPtgOM7nj1sF2mb89zDFbnMaEwfp8xJqmk8D7gn3aY1Ss_fWUTLaegiXnE9nVuOifOOQfZrKhsw</recordid><startdate>19980420</startdate><enddate>19980420</enddate><creator>Gutterman, David D.</creator><creator>Pardubsky, P.D.</creator><creator>Pettersen, M.</creator><creator>Marcus, M.L.</creator><creator>Gebhart, G.F.</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><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>7TK</scope><scope>7X8</scope></search><sort><creationdate>19980420</creationdate><title>Thoracic spinal neuron responses to repeated myocardial ischemia and epicardial bradykinin</title><author>Gutterman, David D. ; Pardubsky, P.D. ; Pettersen, M. ; Marcus, M.L. ; Gebhart, G.F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c420t-a684f87940d26d066e04ab401bb3355410a2b40309a3b8aa9fb1302efbaf4c1d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Afferent</topic><topic>Animals</topic><topic>Autonomic</topic><topic>Autonomic Nervous System - physiology</topic><topic>Biological and medical sciences</topic><topic>Bradykinin - pharmacology</topic><topic>Cardiac pain</topic><topic>Cardiology. Vascular system</topic><topic>Cats</topic><topic>Cold Temperature</topic><topic>Coronary heart disease</topic><topic>Coronary Vessels - physiology</topic><topic>Electrophysiology</topic><topic>Heart</topic><topic>Heart Rate - drug effects</topic><topic>Ischemia</topic><topic>Ligation</topic><topic>Medical sciences</topic><topic>Myocardial Ischemia - physiopathology</topic><topic>Neural Inhibition - physiology</topic><topic>Neurons, Afferent - drug effects</topic><topic>Neurons, Afferent - physiology</topic><topic>Pain - physiopathology</topic><topic>Pericardium - drug effects</topic><topic>Pericardium - innervation</topic><topic>Reaction Time - physiology</topic><topic>Reflex</topic><topic>Reflex - physiology</topic><topic>Reperfusion</topic><topic>Spinal Cord - cytology</topic><topic>Spinal Cord - drug effects</topic><topic>Tachyphylaxis - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gutterman, David D.</creatorcontrib><creatorcontrib>Pardubsky, P.D.</creatorcontrib><creatorcontrib>Pettersen, M.</creatorcontrib><creatorcontrib>Marcus, M.L.</creatorcontrib><creatorcontrib>Gebhart, G.F.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gutterman, David D.</au><au>Pardubsky, P.D.</au><au>Pettersen, M.</au><au>Marcus, M.L.</au><au>Gebhart, G.F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Thoracic spinal neuron responses to repeated myocardial ischemia and epicardial bradykinin</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>1998-04-20</date><risdate>1998</risdate><volume>790</volume><issue>1</issue><spage>293</spage><epage>303</epage><pages>293-303</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract>Bradykinin has been strongly implicated as a mediator of cardiac nociception. During coronary artery occlusion, the content of bradykinin in coronary sinus blood increases. In non-cardiac tissues nociception to bradykinin exhibits tachyphylaxis, however, this phenomenon has not been rigorously studied in the heart. This raises the question that repeated coronary occlusions may also result in tachyphylaxis, thereby reducing cardiac sensation on subsequent ischemic stimulation. We therefore examined the hypothesis that repetitive episodes of myocardial ischemia and of epicardial application of bradykinin demonstrate tachyphylaxis. Mongrel cats were anesthetized with
α-chloralose and heart rate, arterial pressure, and thoracic spinal neuron firing rate were recorded during 60 s of anterior descending coronary occlusion or local epicardial application of bradykinin (10
μM). Neurons were identified by cutaneous receptive fields in the left shoulder area. Sixty-one of 93 neurons tested responded with an increase in firing rate to coronary artery occlusion only (
n=24), bradykinin only (
n=19) or to both (
n=18). On repetitive coronary occlusion, 14 of 25 neurons demonstrated tachyphylaxis compared to 12 of 15 tested with bradykinin (
p<0.05). Similar responses were observed in thoracic spinal neurons that projected to the brain. In neurons demonstrating tachyphylaxis, dorsal cervical cold block partially restored the neuronal activation to coronary occlusion but not to bradykinin. We conclude, based on neuronal responses to repetitive stimuli, that afferent spinal responses to coronary occlusion and bradykinin are different. These data suggest that bradykinin is not the sole mediator of myocardial ischemic pain. The tachyphylaxis to repeated coronary artery occlusions may contribute to the clinical phenomenon of silent myocardial ischemia.</abstract><cop>London</cop><cop>Amsterdam</cop><cop>New York, NY</cop><pub>Elsevier B.V</pub><pmid>9593951</pmid><doi>10.1016/S0006-8993(98)00081-X</doi><tpages>11</tpages></addata></record> |
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| subjects | Afferent Animals Autonomic Autonomic Nervous System - physiology Biological and medical sciences Bradykinin - pharmacology Cardiac pain Cardiology. Vascular system Cats Cold Temperature Coronary heart disease Coronary Vessels - physiology Electrophysiology Heart Heart Rate - drug effects Ischemia Ligation Medical sciences Myocardial Ischemia - physiopathology Neural Inhibition - physiology Neurons, Afferent - drug effects Neurons, Afferent - physiology Pain - physiopathology Pericardium - drug effects Pericardium - innervation Reaction Time - physiology Reflex Reflex - physiology Reperfusion Spinal Cord - cytology Spinal Cord - drug effects Tachyphylaxis - physiology |
| title | Thoracic spinal neuron responses to repeated myocardial ischemia and epicardial bradykinin |
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