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Remifentanil protects myocardium through activation of anti-apoptotic pathways of survival in ischemia-reperfused rat heart
H. S. Kim, J. E. Cho, S. W. Hong, S. O. Kim, J. K. Shim, Y. L. Kwak
Language English Country Czech Republic
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- MeSH
- Adjuvants, Anesthesia MeSH
- Apoptosis drug effects MeSH
- Time Factors MeSH
- Cytochromes c metabolism MeSH
- Financing, Organized MeSH
- Phosphorylation MeSH
- Hemodynamics drug effects MeSH
- Homeostasis MeSH
- Myocardial Infarction MeSH
- Rats MeSH
- RNA, Messenger metabolism MeSH
- Mitogen-Activated Protein Kinase 1 metabolism MeSH
- Mitogen-Activated Protein Kinase 3 metabolism MeSH
- Disease Models, Animal MeSH
- Myocardium metabolism pathology MeSH
- Piperidines administration & dosage pharmacology MeSH
- Reverse Transcriptase Polymerase Chain Reaction MeSH
- Rats, Sprague-Dawley MeSH
- bcl-2-Associated X Protein metabolism MeSH
- Proto-Oncogene Proteins c-bcl-2 metabolism MeSH
- Gene Expression Regulation drug effects MeSH
- Myocardial Reperfusion MeSH
- Sarcoplasmic Reticulum metabolism MeSH
- Calcium metabolism MeSH
- Cell Survival drug effects MeSH
- Blotting, Western MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
Remifentanil is a commonly used opioid in anesthesia with cardioprotective effect in ischemia-reperfused (I/R) heart. We evaluated the influence of remifentanil on myocardial infarct size and expressions of proteins involved in apoptosis in I/R rat heart following various time protocols of remifentanil administration. Artificially ventilated anesthetized Sprague-Dawley rats were subjected to a 30 min of left anterior descending coronary artery occlusion followed by 2 h of reperfusion. Rats were randomly assigned to one of five groups; Sham, I/R only, remifentanil preconditioning, postconditioning and continuous infusion group. Myocardial infarct size, the phosphorylation of ERK1/2, Bcl2, Bax and cytochrome c and the expression of genes influencing Ca2+ homeostasis were assessed. In remifentanil-administered rat hearts, regardless of the timing and duration of administration, infarct size was consistently reduced compared to I/R only rats. Remifentanil improved expression of ERK 1/2 and anti-apoptotic protein Bcl2, and expression of sarcoplasmic reticulum genes which were significantly reduced in the I/R rats only. Remifentanil reduced expression of pro-apoptotic protein, Bax and cytochrome c. These suggested that remifentanil produced cardioprotective effect by preserving the expression of proteins involved in anti-apoptotic pathways, and the expression of sarcoplasmic reticulum genes in I/R rat heart, regardless of the timing of administration.
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Lit.: 28
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- $a Remifentanil is a commonly used opioid in anesthesia with cardioprotective effect in ischemia-reperfused (I/R) heart. We evaluated the influence of remifentanil on myocardial infarct size and expressions of proteins involved in apoptosis in I/R rat heart following various time protocols of remifentanil administration. Artificially ventilated anesthetized Sprague-Dawley rats were subjected to a 30 min of left anterior descending coronary artery occlusion followed by 2 h of reperfusion. Rats were randomly assigned to one of five groups; Sham, I/R only, remifentanil preconditioning, postconditioning and continuous infusion group. Myocardial infarct size, the phosphorylation of ERK1/2, Bcl2, Bax and cytochrome c and the expression of genes influencing Ca2+ homeostasis were assessed. In remifentanil-administered rat hearts, regardless of the timing and duration of administration, infarct size was consistently reduced compared to I/R only rats. Remifentanil improved expression of ERK 1/2 and anti-apoptotic protein Bcl2, and expression of sarcoplasmic reticulum genes which were significantly reduced in the I/R rats only. Remifentanil reduced expression of pro-apoptotic protein, Bax and cytochrome c. These suggested that remifentanil produced cardioprotective effect by preserving the expression of proteins involved in anti-apoptotic pathways, and the expression of sarcoplasmic reticulum genes in I/R rat heart, regardless of the timing of administration.
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