Cholestatic liver disease modulates susceptibility to ischemia/reperfusion- induced arrhythmia, but not necrosis and hemodynamic instability: The role of endogenous opioid peptides

Amir R. Hajrasouliha, Sina Tavakoli, Pejman Jabehdar-Maralani, Farzad Ebrahimi, Hamed Shafaroodi, Seyyed Hamid Mirkhani, Saied Amanpour, Ahmad Reza Dehpour

Research output: Contribution to journalArticle

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Abstract

Background/Aims: 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. Methods: 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. Results: 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). Conclusions: This study suggests that short-term cholestasis is associated with resistance against ischemia/reperfusion-induced arrhythmia, which depends on availability of endogenous opioids.

Original languageEnglish (US)
Pages (from-to)491-498
Number of pages8
JournalJournal of Hepatology
Volume43
Issue number3
DOIs
StatePublished - Sep 1 2005
Externally publishedYes

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Opioid Peptides
Disease Susceptibility
Reperfusion
Liver Diseases
Cardiac Arrhythmias
Naltrexone
Necrosis
Ischemia
Hemodynamics
NG-Nitroarginine Methyl Ester
Cholestasis
Bradycardia
Hypotension
Heart Rate
Blood Pressure
Ventricular Premature Complexes
Incidence
Ventricular Fibrillation
Ventricular Tachycardia
Bile Ducts

Keywords

  • Arrhythmia
  • Bile duct-ligation
  • Cholestasis
  • Endogenous opioid peptides
  • Ischemia/reperfusion
  • Necrosis
  • Nitric oxide (NO)
  • Rat

ASJC Scopus subject areas

  • Hepatology

Cite this

Cholestatic liver disease modulates susceptibility to ischemia/reperfusion- induced arrhythmia, but not necrosis and hemodynamic instability : The role of endogenous opioid peptides. / Hajrasouliha, Amir R.; Tavakoli, Sina; Jabehdar-Maralani, Pejman; Ebrahimi, Farzad; Shafaroodi, Hamed; Mirkhani, Seyyed Hamid; Amanpour, Saied; Dehpour, Ahmad Reza.

In: Journal of Hepatology, Vol. 43, No. 3, 01.09.2005, p. 491-498.

Research output: Contribution to journalArticle

Hajrasouliha, Amir R. ; Tavakoli, Sina ; Jabehdar-Maralani, Pejman ; Ebrahimi, Farzad ; Shafaroodi, Hamed ; Mirkhani, Seyyed Hamid ; Amanpour, Saied ; Dehpour, Ahmad Reza. / Cholestatic liver disease modulates susceptibility to ischemia/reperfusion- induced arrhythmia, but not necrosis and hemodynamic instability : The role of endogenous opioid peptides. In: Journal of Hepatology. 2005 ; Vol. 43, No. 3. pp. 491-498.
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T1 - Cholestatic liver disease modulates susceptibility to ischemia/reperfusion- induced arrhythmia, but not necrosis and hemodynamic instability

T2 - The role of endogenous opioid peptides

AU - Hajrasouliha, Amir R.

AU - Tavakoli, Sina

AU - Jabehdar-Maralani, Pejman

AU - Ebrahimi, Farzad

AU - Shafaroodi, Hamed

AU - Mirkhani, Seyyed Hamid

AU - Amanpour, Saied

AU - Dehpour, Ahmad Reza

PY - 2005/9/1

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N2 - Background/Aims: 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. Methods: 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. Results: 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). Conclusions: This study suggests that short-term cholestasis is associated with resistance against ischemia/reperfusion-induced arrhythmia, which depends on availability of endogenous opioids.

AB - Background/Aims: 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. Methods: 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. Results: 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). Conclusions: This study suggests that short-term cholestasis is associated with resistance against ischemia/reperfusion-induced arrhythmia, which depends on availability of endogenous opioids.

KW - Arrhythmia

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KW - Cholestasis

KW - Endogenous opioid peptides

KW - Ischemia/reperfusion

KW - Necrosis

KW - Nitric oxide (NO)

KW - Rat

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