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Cholestatic liver disease modulates susceptibility to ischemia/reperfusion-induced arrhythmia, but not necrosis and hemodynamic instability: The role of endogenous opioid peptides
Acute cholestasis is associated with cardiovascular complications, which mainly manifest during stressful conditions. The goal of this study is to evaluate susceptibility of 7-day bile duct-ligated rats to ischemia/reperfusion-induced injury. Sham-operated and cholestatic rats, treated with daily no...
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| Published in: | Journal of hepatology 2005-09, Vol.43 (3), p.491-498 |
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| cites | cdi_FETCH-LOGICAL-c384t-3ed651385d5dd21536ee9db3c0fb7bf07a92b3da2d9ea8a820132bb5cce4a3bb3 |
| container_end_page | 498 |
| container_issue | 3 |
| container_start_page | 491 |
| container_title | Journal of hepatology |
| container_volume | 43 |
| creator | Hajrasouliha, Amir Reza Tavakoli, Sina Jabehdar-Maralani, Pejman Ebrahimi, Farzad Shafaroodi, Hamed Mirkhani, Seyyed Hamid Amanpour, Saied Dehpour, Ahmad Reza |
| description | Acute cholestasis is associated with cardiovascular complications, which mainly manifest during stressful conditions. The goal of this study is to evaluate susceptibility of 7-day bile duct-ligated rats to ischemia/reperfusion-induced injury.
Sham-operated and cholestatic rats, treated with daily normal saline, L-NAME (a non-selective NO synthase inhibitor) naltrexone, or both L-NAME and naltrexone were subjected to 30
min of ischemia followed by 2
h of reperfusion.
Cholestatic rats demonstrated significant bradycardia, hypotension (
P |
| doi_str_mv | 10.1016/j.jhep.2005.02.043 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_68455140</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0168827805002825</els_id><sourcerecordid>68455140</sourcerecordid><originalsourceid>FETCH-LOGICAL-c384t-3ed651385d5dd21536ee9db3c0fb7bf07a92b3da2d9ea8a820132bb5cce4a3bb3</originalsourceid><addsrcrecordid>eNp9kcuO1DAQRSMEYnoGfoAF8gZWk4wfSTpBs0EtXtJIbIa15UeFVCuxg-2M1N_FD-KoW5odC6sWPnXrVt2ieMdoxShr747VcYSl4pQ2FeUVrcWLYsdaSkva1uxlsctQV3Z8310V1zEeKaWC9vXr4ipDXPCG7Yq_h9FPEJNKaMiETxCIxQgqApm9XSeVIJK4RgNLQo0TphNJnmA0I8yo7gIsEIY1onclOrsasESFMJ7SmL9viV4TcT4_MMFHjEQ5S3Krtyen5jwTXR5-Fv5EHkcgIfshfiDgrP8Nzq-R-AU9WrJsHizEN8WrQU0R3l7qTfHr65fHw_fy4ee3H4fPD6URXZ1KAbZtmOga21jLWSNagN5qYeig93qge9VzLazitgfVqY5TJrjWjTFQK6G1uCk-nnWX4P-s-UhyznvDNCkH2ZZsu7ppWE0zyM_gtmMMMMgl4KzCSTIqt6jkUW5RyS0qSbnMUeWm9xf1Vc9gn1su2WTgwwVQ0ahpCMoZjM_cnrKeizZz92cO8i2eEIKMBsHlJDCASdJ6_J-Pfyy-uK0</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>68455140</pqid></control><display><type>article</type><title>Cholestatic liver disease modulates susceptibility to ischemia/reperfusion-induced arrhythmia, but not necrosis and hemodynamic instability: The role of endogenous opioid peptides</title><source>Elsevier</source><creator>Hajrasouliha, Amir Reza ; Tavakoli, Sina ; Jabehdar-Maralani, Pejman ; Ebrahimi, Farzad ; Shafaroodi, Hamed ; Mirkhani, Seyyed Hamid ; Amanpour, Saied ; Dehpour, Ahmad Reza</creator><creatorcontrib>Hajrasouliha, Amir Reza ; Tavakoli, Sina ; Jabehdar-Maralani, Pejman ; Ebrahimi, Farzad ; Shafaroodi, Hamed ; Mirkhani, Seyyed Hamid ; Amanpour, Saied ; Dehpour, Ahmad Reza</creatorcontrib><description><![CDATA[Acute cholestasis is associated with cardiovascular complications, which mainly manifest during stressful conditions. The goal of this study is to evaluate susceptibility of 7-day bile duct-ligated rats to ischemia/reperfusion-induced injury.
Sham-operated and cholestatic rats, treated with daily normal saline, L-NAME (a non-selective NO synthase inhibitor) naltrexone, or both L-NAME and naltrexone were subjected to 30
min of ischemia followed by 2
h of reperfusion.
Cholestatic rats demonstrated significant bradycardia, hypotension (
P<0.01), and QT prolongation (
P<0.001). The incidence of premature ventricular contractions (
P<0.01), incidence and duration of ventricular tachycardia (
P<0.05), but not ventricular fibrillation, were significantly lower in cholestatic rats. There was no significant difference in hemodynamic instability and infarct size between the groups. L-NAME corrected QT prolongation in cholestatic rats (
P<0.05), with no effect on heart rate, blood pressure and arrhythmia. Naltrexone restored normal heart rate (
P<0.05), blood pressure (
P<0.05) and susceptibility to arrhythmia (
P<0.05) in cholestatic animals, with no significant effect on QT interval. L-NAME and naltrexone co-administration corrected bradycardia (
P<0.05), hypotension (
P<0.05), QT prolongation (
P<0.05) and abolished resistance of cholestatic rats against arrhythmia (
P<0.05).
This study suggests that short-term cholestasis is associated with resistance against ischemia/reperfusion-induced arrhythmia, which depends on availability of endogenous opioids.]]></description><identifier>ISSN: 0168-8278</identifier><identifier>EISSN: 1600-0641</identifier><identifier>DOI: 10.1016/j.jhep.2005.02.043</identifier><identifier>PMID: 16023251</identifier><identifier>CODEN: JOHEEC</identifier><language>eng</language><publisher>Oxford: Elsevier B.V</publisher><subject>Animals ; Arrhythmia ; Arrhythmias, Cardiac - etiology ; Arrhythmias, Cardiac - physiopathology ; Bile duct-ligation ; Biological and medical sciences ; Blood Pressure ; Cardiac dysrhythmias ; Cardiology. Vascular system ; Cholestasis ; Cholestasis, Intrahepatic - pathology ; Cholestasis, Intrahepatic - physiopathology ; Electrocardiography ; Endogenous opioid peptides ; Gastroenterology. Liver. Pancreas. Abdomen ; Heart ; Heart Rate ; Hemodynamics ; Ischemia/reperfusion ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Medical sciences ; Myocardial Infarction - pathology ; Myocardial Infarction - physiopathology ; Naltrexone - pharmacology ; Necrosis ; NG-Nitroarginine Methyl Ester - pharmacology ; Nitric oxide (NO) ; Other diseases. Semiology ; Rat ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury - physiopathology</subject><ispartof>Journal of hepatology, 2005-09, Vol.43 (3), p.491-498</ispartof><rights>2005 European Association for the Study of the Liver</rights><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c384t-3ed651385d5dd21536ee9db3c0fb7bf07a92b3da2d9ea8a820132bb5cce4a3bb3</citedby><cites>FETCH-LOGICAL-c384t-3ed651385d5dd21536ee9db3c0fb7bf07a92b3da2d9ea8a820132bb5cce4a3bb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17019236$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16023251$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hajrasouliha, Amir Reza</creatorcontrib><creatorcontrib>Tavakoli, Sina</creatorcontrib><creatorcontrib>Jabehdar-Maralani, Pejman</creatorcontrib><creatorcontrib>Ebrahimi, Farzad</creatorcontrib><creatorcontrib>Shafaroodi, Hamed</creatorcontrib><creatorcontrib>Mirkhani, Seyyed Hamid</creatorcontrib><creatorcontrib>Amanpour, Saied</creatorcontrib><creatorcontrib>Dehpour, Ahmad Reza</creatorcontrib><title>Cholestatic liver disease modulates susceptibility to ischemia/reperfusion-induced arrhythmia, but not necrosis and hemodynamic instability: The role of endogenous opioid peptides</title><title>Journal of hepatology</title><addtitle>J Hepatol</addtitle><description><![CDATA[Acute cholestasis is associated with cardiovascular complications, which mainly manifest during stressful conditions. The goal of this study is to evaluate susceptibility of 7-day bile duct-ligated rats to ischemia/reperfusion-induced injury.
Sham-operated and cholestatic rats, treated with daily normal saline, L-NAME (a non-selective NO synthase inhibitor) naltrexone, or both L-NAME and naltrexone were subjected to 30
min of ischemia followed by 2
h of reperfusion.
Cholestatic rats demonstrated significant bradycardia, hypotension (
P<0.01), and QT prolongation (
P<0.001). The incidence of premature ventricular contractions (
P<0.01), incidence and duration of ventricular tachycardia (
P<0.05), but not ventricular fibrillation, were significantly lower in cholestatic rats. There was no significant difference in hemodynamic instability and infarct size between the groups. L-NAME corrected QT prolongation in cholestatic rats (
P<0.05), with no effect on heart rate, blood pressure and arrhythmia. Naltrexone restored normal heart rate (
P<0.05), blood pressure (
P<0.05) and susceptibility to arrhythmia (
P<0.05) in cholestatic animals, with no significant effect on QT interval. L-NAME and naltrexone co-administration corrected bradycardia (
P<0.05), hypotension (
P<0.05), QT prolongation (
P<0.05) and abolished resistance of cholestatic rats against arrhythmia (
P<0.05).
This study suggests that short-term cholestasis is associated with resistance against ischemia/reperfusion-induced arrhythmia, which depends on availability of endogenous opioids.]]></description><subject>Animals</subject><subject>Arrhythmia</subject><subject>Arrhythmias, Cardiac - etiology</subject><subject>Arrhythmias, Cardiac - physiopathology</subject><subject>Bile duct-ligation</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure</subject><subject>Cardiac dysrhythmias</subject><subject>Cardiology. Vascular system</subject><subject>Cholestasis</subject><subject>Cholestasis, Intrahepatic - pathology</subject><subject>Cholestasis, Intrahepatic - physiopathology</subject><subject>Electrocardiography</subject><subject>Endogenous opioid peptides</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Heart</subject><subject>Heart Rate</subject><subject>Hemodynamics</subject><subject>Ischemia/reperfusion</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Naltrexone - pharmacology</subject><subject>Necrosis</subject><subject>NG-Nitroarginine Methyl Ester - pharmacology</subject><subject>Nitric oxide (NO)</subject><subject>Other diseases. Semiology</subject><subject>Rat</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reperfusion Injury - physiopathology</subject><issn>0168-8278</issn><issn>1600-0641</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><recordid>eNp9kcuO1DAQRSMEYnoGfoAF8gZWk4wfSTpBs0EtXtJIbIa15UeFVCuxg-2M1N_FD-KoW5odC6sWPnXrVt2ieMdoxShr747VcYSl4pQ2FeUVrcWLYsdaSkva1uxlsctQV3Z8310V1zEeKaWC9vXr4ipDXPCG7Yq_h9FPEJNKaMiETxCIxQgqApm9XSeVIJK4RgNLQo0TphNJnmA0I8yo7gIsEIY1onclOrsasESFMJ7SmL9viV4TcT4_MMFHjEQ5S3Krtyen5jwTXR5-Fv5EHkcgIfshfiDgrP8Nzq-R-AU9WrJsHizEN8WrQU0R3l7qTfHr65fHw_fy4ee3H4fPD6URXZ1KAbZtmOga21jLWSNagN5qYeig93qge9VzLazitgfVqY5TJrjWjTFQK6G1uCk-nnWX4P-s-UhyznvDNCkH2ZZsu7ppWE0zyM_gtmMMMMgl4KzCSTIqt6jkUW5RyS0qSbnMUeWm9xf1Vc9gn1su2WTgwwVQ0ahpCMoZjM_cnrKeizZz92cO8i2eEIKMBsHlJDCASdJ6_J-Pfyy-uK0</recordid><startdate>20050901</startdate><enddate>20050901</enddate><creator>Hajrasouliha, Amir Reza</creator><creator>Tavakoli, Sina</creator><creator>Jabehdar-Maralani, Pejman</creator><creator>Ebrahimi, Farzad</creator><creator>Shafaroodi, Hamed</creator><creator>Mirkhani, Seyyed Hamid</creator><creator>Amanpour, Saied</creator><creator>Dehpour, Ahmad Reza</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>7X8</scope></search><sort><creationdate>20050901</creationdate><title>Cholestatic liver disease modulates susceptibility to ischemia/reperfusion-induced arrhythmia, but not necrosis and hemodynamic instability: The role of endogenous opioid peptides</title><author>Hajrasouliha, Amir Reza ; Tavakoli, Sina ; Jabehdar-Maralani, Pejman ; Ebrahimi, Farzad ; Shafaroodi, Hamed ; Mirkhani, Seyyed Hamid ; Amanpour, Saied ; Dehpour, Ahmad Reza</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c384t-3ed651385d5dd21536ee9db3c0fb7bf07a92b3da2d9ea8a820132bb5cce4a3bb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Arrhythmia</topic><topic>Arrhythmias, Cardiac - etiology</topic><topic>Arrhythmias, Cardiac - physiopathology</topic><topic>Bile duct-ligation</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure</topic><topic>Cardiac dysrhythmias</topic><topic>Cardiology. Vascular system</topic><topic>Cholestasis</topic><topic>Cholestasis, Intrahepatic - pathology</topic><topic>Cholestasis, Intrahepatic - physiopathology</topic><topic>Electrocardiography</topic><topic>Endogenous opioid peptides</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Heart</topic><topic>Heart Rate</topic><topic>Hemodynamics</topic><topic>Ischemia/reperfusion</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Naltrexone - pharmacology</topic><topic>Necrosis</topic><topic>NG-Nitroarginine Methyl Ester - pharmacology</topic><topic>Nitric oxide (NO)</topic><topic>Other diseases. Semiology</topic><topic>Rat</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reperfusion Injury - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hajrasouliha, Amir Reza</creatorcontrib><creatorcontrib>Tavakoli, Sina</creatorcontrib><creatorcontrib>Jabehdar-Maralani, Pejman</creatorcontrib><creatorcontrib>Ebrahimi, Farzad</creatorcontrib><creatorcontrib>Shafaroodi, Hamed</creatorcontrib><creatorcontrib>Mirkhani, Seyyed Hamid</creatorcontrib><creatorcontrib>Amanpour, Saied</creatorcontrib><creatorcontrib>Dehpour, Ahmad Reza</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>MEDLINE - Academic</collection><jtitle>Journal of hepatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hajrasouliha, Amir Reza</au><au>Tavakoli, Sina</au><au>Jabehdar-Maralani, Pejman</au><au>Ebrahimi, Farzad</au><au>Shafaroodi, Hamed</au><au>Mirkhani, Seyyed Hamid</au><au>Amanpour, Saied</au><au>Dehpour, Ahmad Reza</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cholestatic liver disease modulates susceptibility to ischemia/reperfusion-induced arrhythmia, but not necrosis and hemodynamic instability: The role of endogenous opioid peptides</atitle><jtitle>Journal of hepatology</jtitle><addtitle>J Hepatol</addtitle><date>2005-09-01</date><risdate>2005</risdate><volume>43</volume><issue>3</issue><spage>491</spage><epage>498</epage><pages>491-498</pages><issn>0168-8278</issn><eissn>1600-0641</eissn><coden>JOHEEC</coden><abstract><![CDATA[Acute cholestasis is associated with cardiovascular complications, which mainly manifest during stressful conditions. The goal of this study is to evaluate susceptibility of 7-day bile duct-ligated rats to ischemia/reperfusion-induced injury.
Sham-operated and cholestatic rats, treated with daily normal saline, L-NAME (a non-selective NO synthase inhibitor) naltrexone, or both L-NAME and naltrexone were subjected to 30
min of ischemia followed by 2
h of reperfusion.
Cholestatic rats demonstrated significant bradycardia, hypotension (
P<0.01), and QT prolongation (
P<0.001). The incidence of premature ventricular contractions (
P<0.01), incidence and duration of ventricular tachycardia (
P<0.05), but not ventricular fibrillation, were significantly lower in cholestatic rats. There was no significant difference in hemodynamic instability and infarct size between the groups. L-NAME corrected QT prolongation in cholestatic rats (
P<0.05), with no effect on heart rate, blood pressure and arrhythmia. Naltrexone restored normal heart rate (
P<0.05), blood pressure (
P<0.05) and susceptibility to arrhythmia (
P<0.05) in cholestatic animals, with no significant effect on QT interval. L-NAME and naltrexone co-administration corrected bradycardia (
P<0.05), hypotension (
P<0.05), QT prolongation (
P<0.05) and abolished resistance of cholestatic rats against arrhythmia (
P<0.05).
This study suggests that short-term cholestasis is associated with resistance against ischemia/reperfusion-induced arrhythmia, which depends on availability of endogenous opioids.]]></abstract><cop>Oxford</cop><pub>Elsevier B.V</pub><pmid>16023251</pmid><doi>10.1016/j.jhep.2005.02.043</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0168-8278 |
| ispartof | Journal of hepatology, 2005-09, Vol.43 (3), p.491-498 |
| issn | 0168-8278 1600-0641 |
| language | eng |
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| source | Elsevier |
| subjects | Animals Arrhythmia Arrhythmias, Cardiac - etiology Arrhythmias, Cardiac - physiopathology Bile duct-ligation Biological and medical sciences Blood Pressure Cardiac dysrhythmias Cardiology. Vascular system Cholestasis Cholestasis, Intrahepatic - pathology Cholestasis, Intrahepatic - physiopathology Electrocardiography Endogenous opioid peptides Gastroenterology. Liver. Pancreas. Abdomen Heart Heart Rate Hemodynamics Ischemia/reperfusion Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences Myocardial Infarction - pathology Myocardial Infarction - physiopathology Naltrexone - pharmacology Necrosis NG-Nitroarginine Methyl Ester - pharmacology Nitric oxide (NO) Other diseases. Semiology Rat Rats Rats, Sprague-Dawley Reperfusion Injury - physiopathology |
| title | Cholestatic liver disease modulates susceptibility to ischemia/reperfusion-induced arrhythmia, but not necrosis and hemodynamic instability: The role of endogenous opioid peptides |
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