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Adenosine inhibition of neutrophil damage during reperfusion does not involve KATP-channel activation
1 Department of Cardiothoracic Surgery, Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, North Carolina 27157-1096; and 2 Department of Emergency Medicine, Jefferson Medical College, Philadelphia, Pennsylvania 19107 This study tests the hypothesis that cardioprotection exer...
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| Published in: | American journal of physiology. Heart and circulatory physiology 1997-10, Vol.273 (4), p.H1677 |
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| Format: | Article |
| Language: | English |
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| container_issue | 4 |
| container_start_page | H1677 |
| container_title | American journal of physiology. Heart and circulatory physiology |
| container_volume | 273 |
| creator | Zhao, Zhi-Qing Todd, James C Sato, Hiroki Ma, Xin-Liang Vinten-Johansen, J |
| description | 1 Department of Cardiothoracic
Surgery, Bowman Gray School of Medicine of Wake Forest University,
Winston-Salem, North Carolina 27157-1096; and
2 Department of Emergency
Medicine, Jefferson Medical College, Philadelphia, Pennsylvania 19107
This study tests the hypothesis that
cardioprotection exerted by adenosine
A 2 -receptor activation and
neutrophil-related events involves stimulation of ATP-sensitive
potassium (K ATP ) channels on
neutrophils during reperfusion. The adenosine
A 2 agonist CGS-21680 (CGS)
inhibited superoxide radical generation from isolated rabbit polymorphonuclear neutrophils (PMNs) in a dose-dependent manner from
17.7 ± 2.1 to 7.4 ± 1.3 nmol/5 × 10 6 PMNs
( P |
| format | article |
| fullrecord | <record><control><sourceid>highwire</sourceid><recordid>TN_cdi_highwire_physiology_ajpheart_273_4_H1677</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>ajpheart_273_4_H1677</sourcerecordid><originalsourceid>FETCH-highwire_physiology_ajpheart_273_4_H16773</originalsourceid><addsrcrecordid>eNqdzEFLwzAYxvEgjlmd3yFfoJjmtSnD0xDHwIuH3kNc3jYZMQlJWt23dwMRL152ei7P739FqqblvG5aWF-TioGAWjTQ3pDbnA-MsbYTsCTLNQjOgVUENxp9yNYjtd7Yd1ts8DQM1ONUUojGOqrVhxqR6ilZP9KEEdMw5fNPB8zUh3Kyc3Az0tdN_1bvjfIeHVX7Ymd1Dq7IYlAu4_3P3pGH7Uv_vKuNHc2nTSijOZ6KLoxHqQ7RoEpF8g7ko9w1ouvgEvH0v9hOzvX4VX7pHymjHuAbVupqCg</addsrcrecordid><sourcetype>Enrichment Source</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Adenosine inhibition of neutrophil damage during reperfusion does not involve KATP-channel activation</title><source>American Physiological Society Free</source><creator>Zhao, Zhi-Qing ; Todd, James C ; Sato, Hiroki ; Ma, Xin-Liang ; Vinten-Johansen, J</creator><creatorcontrib>Zhao, Zhi-Qing ; Todd, James C ; Sato, Hiroki ; Ma, Xin-Liang ; Vinten-Johansen, J</creatorcontrib><description>1 Department of Cardiothoracic
Surgery, Bowman Gray School of Medicine of Wake Forest University,
Winston-Salem, North Carolina 27157-1096; and
2 Department of Emergency
Medicine, Jefferson Medical College, Philadelphia, Pennsylvania 19107
This study tests the hypothesis that
cardioprotection exerted by adenosine
A 2 -receptor activation and
neutrophil-related events involves stimulation of ATP-sensitive
potassium (K ATP ) channels on
neutrophils during reperfusion. The adenosine
A 2 agonist CGS-21680 (CGS)
inhibited superoxide radical generation from isolated rabbit polymorphonuclear neutrophils (PMNs) in a dose-dependent manner from
17.7 ± 2.1 to 7.4 ± 1.3 nmol/5 × 10 6 PMNs
( P < 0.05). Pinacidil, a
K ATP -channel opener, partially inhibited superoxide radical production, which was completely reversed
by glibenclamide (Glib). Incremental doses of Glib in combination with
CGS (1 µM) did not alter CGS-induced inhibition of superoxide radical
generation. CGS significantly reduced PMN adherence to the endothelial
surface of aortic segments in a dose-dependent manner from 189 ± 8 to 50 ± 6 PMNs/mm 2
( P < 0.05), which was also not
altered by incremental doses of Glib. Infusion of CGS (0.025 mg/kg)
before reperfusion reduced infarct size from 29 ± 2% in
the Vehicle group to 15 ± 1% in rabbits undergoing 30 min of
ischemia and 120 min of reperfusion ( P < 0.05). Glib (0.3 mg/kg) did not change the infarct size (28 ± 2%) vs. the Vehicle group and did not attenuate infarct size reduction by CGS (16 ± 1%). Glib did not change blood glucose levels.
Cardiac myeloperoxidase activity was decreased in the ischemic
tissue of the CGS group (0.15 ± 0.03 U/100 mg tissue) compared with
the Vehicle group (0.37 ± 0.05 U/100 mg tissue;
P < 0.05). We conclude that
adenosine A 2 activation before
reperfusion partially reduces infarct size by inhibiting neutrophil
activity and that this effect does not involve
K ATP -channel stimulation.
adenosine 5'-triphosphate-sensitive potassium channel; infarct size; neutrophil; reperfusion injury</description><identifier>ISSN: 0363-6135</identifier><identifier>EISSN: 1522-1539</identifier><identifier>PMID: 9362230</identifier><language>eng</language><ispartof>American journal of physiology. Heart and circulatory physiology, 1997-10, Vol.273 (4), p.H1677</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids></links><search><creatorcontrib>Zhao, Zhi-Qing</creatorcontrib><creatorcontrib>Todd, James C</creatorcontrib><creatorcontrib>Sato, Hiroki</creatorcontrib><creatorcontrib>Ma, Xin-Liang</creatorcontrib><creatorcontrib>Vinten-Johansen, J</creatorcontrib><title>Adenosine inhibition of neutrophil damage during reperfusion does not involve KATP-channel activation</title><title>American journal of physiology. Heart and circulatory physiology</title><description>1 Department of Cardiothoracic
Surgery, Bowman Gray School of Medicine of Wake Forest University,
Winston-Salem, North Carolina 27157-1096; and
2 Department of Emergency
Medicine, Jefferson Medical College, Philadelphia, Pennsylvania 19107
This study tests the hypothesis that
cardioprotection exerted by adenosine
A 2 -receptor activation and
neutrophil-related events involves stimulation of ATP-sensitive
potassium (K ATP ) channels on
neutrophils during reperfusion. The adenosine
A 2 agonist CGS-21680 (CGS)
inhibited superoxide radical generation from isolated rabbit polymorphonuclear neutrophils (PMNs) in a dose-dependent manner from
17.7 ± 2.1 to 7.4 ± 1.3 nmol/5 × 10 6 PMNs
( P < 0.05). Pinacidil, a
K ATP -channel opener, partially inhibited superoxide radical production, which was completely reversed
by glibenclamide (Glib). Incremental doses of Glib in combination with
CGS (1 µM) did not alter CGS-induced inhibition of superoxide radical
generation. CGS significantly reduced PMN adherence to the endothelial
surface of aortic segments in a dose-dependent manner from 189 ± 8 to 50 ± 6 PMNs/mm 2
( P < 0.05), which was also not
altered by incremental doses of Glib. Infusion of CGS (0.025 mg/kg)
before reperfusion reduced infarct size from 29 ± 2% in
the Vehicle group to 15 ± 1% in rabbits undergoing 30 min of
ischemia and 120 min of reperfusion ( P < 0.05). Glib (0.3 mg/kg) did not change the infarct size (28 ± 2%) vs. the Vehicle group and did not attenuate infarct size reduction by CGS (16 ± 1%). Glib did not change blood glucose levels.
Cardiac myeloperoxidase activity was decreased in the ischemic
tissue of the CGS group (0.15 ± 0.03 U/100 mg tissue) compared with
the Vehicle group (0.37 ± 0.05 U/100 mg tissue;
P < 0.05). We conclude that
adenosine A 2 activation before
reperfusion partially reduces infarct size by inhibiting neutrophil
activity and that this effect does not involve
K ATP -channel stimulation.
adenosine 5'-triphosphate-sensitive potassium channel; infarct size; neutrophil; reperfusion injury</description><issn>0363-6135</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid/><recordid>eNqdzEFLwzAYxvEgjlmd3yFfoJjmtSnD0xDHwIuH3kNc3jYZMQlJWt23dwMRL152ei7P739FqqblvG5aWF-TioGAWjTQ3pDbnA-MsbYTsCTLNQjOgVUENxp9yNYjtd7Yd1ts8DQM1ONUUojGOqrVhxqR6ilZP9KEEdMw5fNPB8zUh3Kyc3Az0tdN_1bvjfIeHVX7Ymd1Dq7IYlAu4_3P3pGH7Uv_vKuNHc2nTSijOZ6KLoxHqQ7RoEpF8g7ko9w1ouvgEvH0v9hOzvX4VX7pHymjHuAbVupqCg</recordid><startdate>19971001</startdate><enddate>19971001</enddate><creator>Zhao, Zhi-Qing</creator><creator>Todd, James C</creator><creator>Sato, Hiroki</creator><creator>Ma, Xin-Liang</creator><creator>Vinten-Johansen, J</creator><scope/></search><sort><creationdate>19971001</creationdate><title>Adenosine inhibition of neutrophil damage during reperfusion does not involve KATP-channel activation</title><author>Zhao, Zhi-Qing ; Todd, James C ; Sato, Hiroki ; Ma, Xin-Liang ; Vinten-Johansen, J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-highwire_physiology_ajpheart_273_4_H16773</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhao, Zhi-Qing</creatorcontrib><creatorcontrib>Todd, James C</creatorcontrib><creatorcontrib>Sato, Hiroki</creatorcontrib><creatorcontrib>Ma, Xin-Liang</creatorcontrib><creatorcontrib>Vinten-Johansen, J</creatorcontrib><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhao, Zhi-Qing</au><au>Todd, James C</au><au>Sato, Hiroki</au><au>Ma, Xin-Liang</au><au>Vinten-Johansen, J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Adenosine inhibition of neutrophil damage during reperfusion does not involve KATP-channel activation</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><date>1997-10-01</date><risdate>1997</risdate><volume>273</volume><issue>4</issue><spage>H1677</spage><pages>H1677-</pages><issn>0363-6135</issn><eissn>1522-1539</eissn><abstract>1 Department of Cardiothoracic
Surgery, Bowman Gray School of Medicine of Wake Forest University,
Winston-Salem, North Carolina 27157-1096; and
2 Department of Emergency
Medicine, Jefferson Medical College, Philadelphia, Pennsylvania 19107
This study tests the hypothesis that
cardioprotection exerted by adenosine
A 2 -receptor activation and
neutrophil-related events involves stimulation of ATP-sensitive
potassium (K ATP ) channels on
neutrophils during reperfusion. The adenosine
A 2 agonist CGS-21680 (CGS)
inhibited superoxide radical generation from isolated rabbit polymorphonuclear neutrophils (PMNs) in a dose-dependent manner from
17.7 ± 2.1 to 7.4 ± 1.3 nmol/5 × 10 6 PMNs
( P < 0.05). Pinacidil, a
K ATP -channel opener, partially inhibited superoxide radical production, which was completely reversed
by glibenclamide (Glib). Incremental doses of Glib in combination with
CGS (1 µM) did not alter CGS-induced inhibition of superoxide radical
generation. CGS significantly reduced PMN adherence to the endothelial
surface of aortic segments in a dose-dependent manner from 189 ± 8 to 50 ± 6 PMNs/mm 2
( P < 0.05), which was also not
altered by incremental doses of Glib. Infusion of CGS (0.025 mg/kg)
before reperfusion reduced infarct size from 29 ± 2% in
the Vehicle group to 15 ± 1% in rabbits undergoing 30 min of
ischemia and 120 min of reperfusion ( P < 0.05). Glib (0.3 mg/kg) did not change the infarct size (28 ± 2%) vs. the Vehicle group and did not attenuate infarct size reduction by CGS (16 ± 1%). Glib did not change blood glucose levels.
Cardiac myeloperoxidase activity was decreased in the ischemic
tissue of the CGS group (0.15 ± 0.03 U/100 mg tissue) compared with
the Vehicle group (0.37 ± 0.05 U/100 mg tissue;
P < 0.05). We conclude that
adenosine A 2 activation before
reperfusion partially reduces infarct size by inhibiting neutrophil
activity and that this effect does not involve
K ATP -channel stimulation.
adenosine 5'-triphosphate-sensitive potassium channel; infarct size; neutrophil; reperfusion injury</abstract><pmid>9362230</pmid></addata></record> |
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| identifier | ISSN: 0363-6135 |
| ispartof | American journal of physiology. Heart and circulatory physiology, 1997-10, Vol.273 (4), p.H1677 |
| issn | 0363-6135 1522-1539 |
| language | eng |
| recordid | cdi_highwire_physiology_ajpheart_273_4_H1677 |
| source | American Physiological Society Free |
| title | Adenosine inhibition of neutrophil damage during reperfusion does not involve KATP-channel activation |
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