Chemical preconditioning with 3-nitropropionic acid in hearts: role of mitochondrial K(ATP) channel
We investigated the cardioprotective effect of 3-nitropropionic acid (3-NPA), an inhibitior of mitochondrial succinate dehydrogenase, and we wanted to show whether this protection is mediated by of opening mitochondrial ATP-sensitive potassium (K(ATP)) channels. Adult rabbits were treated with eithe...
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Veröffentlicht in: | American journal of physiology. Heart and circulatory physiology 2001-05, Vol.280 (5), p.H2406-H2411 |
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creator | Ockaili, R A Bhargava, P Kukreja, R C |
description | We investigated the cardioprotective effect of 3-nitropropionic acid (3-NPA), an inhibitior of mitochondrial succinate dehydrogenase, and we wanted to show whether this protection is mediated by of opening mitochondrial ATP-sensitive potassium (K(ATP)) channels. Adult rabbits were treated with either 3-NPA (3 mg/kg iv) or saline (n = 6 rabbits/group). After 30 min (for early phase) or 24 h (for late phase) of the treatment, the animals were subjected to 30 min of ischemia and 3 h of reperfusion (ischemia-reperfusion). 5-Hydroxydecanoate (5-HD, 5 mg/kg iv),the mitochondrial K(ATP) channel blocker, was administered 10 min before ischemia-reperfusion in the saline- and 3-NPA-treated rabbits. 3-NPA caused a decrease in the infarct size from 27.8 +/- 4.2% in the saline group to 16.5 +/- 1.0% in the 3-NPA-treated rabbits during early phase and from 30.4 +/- 4.2% in the saline group to 17.6 +/- 1.05 in the 3-NPA group during delayed phase (P < 0.05, % of risk area). The anti-infarct effect of 3-NPA was blocked by 5-HD as shown by an increase in infarct size to 33 +/- 2.7% (early phase) and 31 +/- 2.4% (delayed phase) (P < 0.05 vs. 3-NPA groups). 5-HD had no proischemic effect in control animals. Also, 3-NPA had no effect on systemic hemodynamics. We conclude that 3-NPA induces long-lasting anti-ischemic effects via opening of mitochondrial K(ATP) channels. |
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Adult rabbits were treated with either 3-NPA (3 mg/kg iv) or saline (n = 6 rabbits/group). After 30 min (for early phase) or 24 h (for late phase) of the treatment, the animals were subjected to 30 min of ischemia and 3 h of reperfusion (ischemia-reperfusion). 5-Hydroxydecanoate (5-HD, 5 mg/kg iv),the mitochondrial K(ATP) channel blocker, was administered 10 min before ischemia-reperfusion in the saline- and 3-NPA-treated rabbits. 3-NPA caused a decrease in the infarct size from 27.8 +/- 4.2% in the saline group to 16.5 +/- 1.0% in the 3-NPA-treated rabbits during early phase and from 30.4 +/- 4.2% in the saline group to 17.6 +/- 1.05 in the 3-NPA group during delayed phase (P < 0.05, % of risk area). The anti-infarct effect of 3-NPA was blocked by 5-HD as shown by an increase in infarct size to 33 +/- 2.7% (early phase) and 31 +/- 2.4% (delayed phase) (P < 0.05 vs. 3-NPA groups). 5-HD had no proischemic effect in control animals. Also, 3-NPA had no effect on systemic hemodynamics. We conclude that 3-NPA induces long-lasting anti-ischemic effects via opening of mitochondrial K(ATP) channels.</description><identifier>ISSN: 0363-6135</identifier><identifier>PMID: 11299248</identifier><language>eng</language><publisher>United States</publisher><subject>Adenosine Triphosphate - metabolism ; Animals ; Anti-Arrhythmia Agents - pharmacology ; Antihypertensive Agents - pharmacology ; Blood Pressure ; Decanoic Acids - pharmacology ; Heart Rate ; Hydroxy Acids - pharmacology ; Ischemic Preconditioning, Myocardial ; Male ; Mitochondria - metabolism ; Myocardial Infarction - metabolism ; Myocardial Infarction - mortality ; Myocardium - metabolism ; Nitro Compounds ; Oxidative Phosphorylation ; Potassium Channel Blockers ; Potassium Channels - metabolism ; Propionates - pharmacology ; Rabbits ; Succinate Dehydrogenase - metabolism</subject><ispartof>American journal of physiology. Heart and circulatory physiology, 2001-05, Vol.280 (5), p.H2406-H2411</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11299248$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ockaili, R A</creatorcontrib><creatorcontrib>Bhargava, P</creatorcontrib><creatorcontrib>Kukreja, R C</creatorcontrib><title>Chemical preconditioning with 3-nitropropionic acid in hearts: role of mitochondrial K(ATP) channel</title><title>American journal of physiology. Heart and circulatory physiology</title><addtitle>Am J Physiol Heart Circ Physiol</addtitle><description>We investigated the cardioprotective effect of 3-nitropropionic acid (3-NPA), an inhibitior of mitochondrial succinate dehydrogenase, and we wanted to show whether this protection is mediated by of opening mitochondrial ATP-sensitive potassium (K(ATP)) channels. Adult rabbits were treated with either 3-NPA (3 mg/kg iv) or saline (n = 6 rabbits/group). After 30 min (for early phase) or 24 h (for late phase) of the treatment, the animals were subjected to 30 min of ischemia and 3 h of reperfusion (ischemia-reperfusion). 5-Hydroxydecanoate (5-HD, 5 mg/kg iv),the mitochondrial K(ATP) channel blocker, was administered 10 min before ischemia-reperfusion in the saline- and 3-NPA-treated rabbits. 3-NPA caused a decrease in the infarct size from 27.8 +/- 4.2% in the saline group to 16.5 +/- 1.0% in the 3-NPA-treated rabbits during early phase and from 30.4 +/- 4.2% in the saline group to 17.6 +/- 1.05 in the 3-NPA group during delayed phase (P < 0.05, % of risk area). The anti-infarct effect of 3-NPA was blocked by 5-HD as shown by an increase in infarct size to 33 +/- 2.7% (early phase) and 31 +/- 2.4% (delayed phase) (P < 0.05 vs. 3-NPA groups). 5-HD had no proischemic effect in control animals. Also, 3-NPA had no effect on systemic hemodynamics. We conclude that 3-NPA induces long-lasting anti-ischemic effects via opening of mitochondrial K(ATP) channels.</description><subject>Adenosine Triphosphate - metabolism</subject><subject>Animals</subject><subject>Anti-Arrhythmia Agents - pharmacology</subject><subject>Antihypertensive Agents - pharmacology</subject><subject>Blood Pressure</subject><subject>Decanoic Acids - pharmacology</subject><subject>Heart Rate</subject><subject>Hydroxy Acids - pharmacology</subject><subject>Ischemic Preconditioning, Myocardial</subject><subject>Male</subject><subject>Mitochondria - metabolism</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardial Infarction - mortality</subject><subject>Myocardium - metabolism</subject><subject>Nitro Compounds</subject><subject>Oxidative Phosphorylation</subject><subject>Potassium Channel Blockers</subject><subject>Potassium Channels - metabolism</subject><subject>Propionates - pharmacology</subject><subject>Rabbits</subject><subject>Succinate Dehydrogenase - metabolism</subject><issn>0363-6135</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1UM1KxDAYzEFx19VXkJxED4WkaZPG27L4hwt66L2kX77aSJvUpIv49lZcYWBgmBmGOSFrJqTIJBflipyn9MEYK5UUZ2TFea51XlRrArseRwdmoFNECN662QXv_Dv9cnNPRebdHMO04FcGasBZ6jzt0cQ53dEYBqSho6ObA_RLPrql6-VmW7_dUuiN9zhckNPODAkvj7wh9cN9vXvK9q-Pz7vtPpvKosq04qxkxthOioq3kFdMtS3jyoICNCAL3ZadAK0RwdpKIoocmMyBowYuxIZc_9Uuaz8PmOZmdAlwGIzHcEiNUqwsilwvxquj8dCOaJsputHE7-b_FfEDMzZeQg</recordid><startdate>200105</startdate><enddate>200105</enddate><creator>Ockaili, R A</creator><creator>Bhargava, P</creator><creator>Kukreja, R C</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>200105</creationdate><title>Chemical preconditioning with 3-nitropropionic acid in hearts: role of mitochondrial K(ATP) channel</title><author>Ockaili, R A ; Bhargava, P ; Kukreja, R C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p548-971050aadf6381bc2807bb017dc7ceac649b5f3c99eecdd86ee32c062c1e9c133</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Adenosine Triphosphate - metabolism</topic><topic>Animals</topic><topic>Anti-Arrhythmia Agents - pharmacology</topic><topic>Antihypertensive Agents - pharmacology</topic><topic>Blood Pressure</topic><topic>Decanoic Acids - pharmacology</topic><topic>Heart Rate</topic><topic>Hydroxy Acids - pharmacology</topic><topic>Ischemic Preconditioning, Myocardial</topic><topic>Male</topic><topic>Mitochondria - metabolism</topic><topic>Myocardial Infarction - metabolism</topic><topic>Myocardial Infarction - mortality</topic><topic>Myocardium - metabolism</topic><topic>Nitro Compounds</topic><topic>Oxidative Phosphorylation</topic><topic>Potassium Channel Blockers</topic><topic>Potassium Channels - metabolism</topic><topic>Propionates - pharmacology</topic><topic>Rabbits</topic><topic>Succinate Dehydrogenase - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ockaili, R A</creatorcontrib><creatorcontrib>Bhargava, P</creatorcontrib><creatorcontrib>Kukreja, R C</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ockaili, R A</au><au>Bhargava, P</au><au>Kukreja, R C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chemical preconditioning with 3-nitropropionic acid in hearts: role of mitochondrial K(ATP) channel</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><addtitle>Am J Physiol Heart Circ Physiol</addtitle><date>2001-05</date><risdate>2001</risdate><volume>280</volume><issue>5</issue><spage>H2406</spage><epage>H2411</epage><pages>H2406-H2411</pages><issn>0363-6135</issn><abstract>We investigated the cardioprotective effect of 3-nitropropionic acid (3-NPA), an inhibitior of mitochondrial succinate dehydrogenase, and we wanted to show whether this protection is mediated by of opening mitochondrial ATP-sensitive potassium (K(ATP)) channels. Adult rabbits were treated with either 3-NPA (3 mg/kg iv) or saline (n = 6 rabbits/group). After 30 min (for early phase) or 24 h (for late phase) of the treatment, the animals were subjected to 30 min of ischemia and 3 h of reperfusion (ischemia-reperfusion). 5-Hydroxydecanoate (5-HD, 5 mg/kg iv),the mitochondrial K(ATP) channel blocker, was administered 10 min before ischemia-reperfusion in the saline- and 3-NPA-treated rabbits. 3-NPA caused a decrease in the infarct size from 27.8 +/- 4.2% in the saline group to 16.5 +/- 1.0% in the 3-NPA-treated rabbits during early phase and from 30.4 +/- 4.2% in the saline group to 17.6 +/- 1.05 in the 3-NPA group during delayed phase (P < 0.05, % of risk area). The anti-infarct effect of 3-NPA was blocked by 5-HD as shown by an increase in infarct size to 33 +/- 2.7% (early phase) and 31 +/- 2.4% (delayed phase) (P < 0.05 vs. 3-NPA groups). 5-HD had no proischemic effect in control animals. Also, 3-NPA had no effect on systemic hemodynamics. We conclude that 3-NPA induces long-lasting anti-ischemic effects via opening of mitochondrial K(ATP) channels.</abstract><cop>United States</cop><pmid>11299248</pmid></addata></record> |
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source | MEDLINE; American Physiological Society Paid; EZB-FREE-00999 freely available EZB journals |
subjects | Adenosine Triphosphate - metabolism Animals Anti-Arrhythmia Agents - pharmacology Antihypertensive Agents - pharmacology Blood Pressure Decanoic Acids - pharmacology Heart Rate Hydroxy Acids - pharmacology Ischemic Preconditioning, Myocardial Male Mitochondria - metabolism Myocardial Infarction - metabolism Myocardial Infarction - mortality Myocardium - metabolism Nitro Compounds Oxidative Phosphorylation Potassium Channel Blockers Potassium Channels - metabolism Propionates - pharmacology Rabbits Succinate Dehydrogenase - metabolism |
title | Chemical preconditioning with 3-nitropropionic acid in hearts: role of mitochondrial K(ATP) channel |
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