1 708

Cited 44 times in

Diabetes mellitus mitigates cardioprotective effects of remifentanil preconditioning in ischemia-reperfused rat heart in association with anti-apoptotic pathways of survival.

 Hyun Soo Kim  ;  Jang Eun Cho  ;  Ki Chul Hwang  ;  Yeon Hee Shim  ;  Jung Hwa Lee  ;  Young Lan Kwak 
 EUROPEAN JOURNAL OF PHARMACOLOGY, Vol.628(1-3) : 132-139, 2010 
Journal Title
Issue Date
Animals ; Apoptosis/drug effects* ; Cardiotonic Agents/pharmacology* ; Cell Survival/drug effects ; Diabetes Mellitus*/metabolism ; Diabetes Mellitus*/pathology ; Diabetes Mellitus*/physiopathology ; Gene Expression Regulation/drug effects ; Heart/drug effects* ; Heart/physiopathology ; Hemodynamics/drug effects ; Ischemic Preconditioning, Myocardial* ; Male ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/metabolism ; Myocardial Infarction/pathology ; Myocardium/metabolism ; Myocardium/pathology ; Phosphorylation/drug effects ; Piperidines/pharmacology* ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury/prevention & control* ; Sarcoplasmic Reticulum/drug effects ; Sarcoplasmic Reticulum/metabolism
Diabetes mellitus ; Remifentanil ; Ischemia–reperfusion
Diabetes mellitus has been known to mitigate ischemic or pharmacologic preconditioning in ischemia-reperfusion injuries. Remifentanil is a widely used opioid in cardiac anesthesia that possesses a cardioprotective effect against ischemia-reperfusion. We evaluated whether diabetes affected remifentanil preconditioning induced cardioprotection in ischemia-reperfusion rat hearts in view of anti-apoptotic pathways of survival and Ca(2+) homeostasis. Streptozotocin-induced, diabetic rats and age-matched wild-type Sprague-Dawley rats were subjected to a left anterior descending coronary artery occlusion for 30min followed by 1h of reperfusion. Each diabetic and wild-type rat was randomly assigned to the sham, ischemia-reperfusion only, or remifentanil preconditioning group. Myocardial infarct size, activities of ERK1/2, Bcl2, Bax and cytochrome c, and gene expression influencing Ca(2+) homeostasis were assessed. Remifentanil preconditioning significantly reduced myocardial infarct size compared to ischemia-reperfusion only in wild-type rats but not in diabetic rats. Remifentanil preconditioning increased expression of ERK1/2 and anti-apoptotic protein Bcl-2 and decreased expression of pro-apoptotic proteins, Bax and cytochrome c, compared to ischemia-reperfusion only in wild-type rats. In diabetic rat hearts, however, remifentanil preconditioning failed to recover the phosphorylation state of ERK1/2 and to repress apoptotic signaling. In addition, diabetes minimized remifentanil induced modulation of abnormal changes in sarcoplasmic reticulum genes and proteins in ischemia-reperfusion rat hearts. In conclusion, diabetes mitigated remifentanil induced cardioprotection against ischemia-reperfusion, which might be associated with reduced recovery of the activities of proteins involved in anti-apoptotic pathways including ERK1/2 and the abnormal expression of sarcoplasmic reticulum genes as a result of ischemia-reperfusion in rat hearts.
Full Text
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Anesthesiology and Pain Medicine (마취통증의학교실) > 1. Journal Papers
Yonsei Authors
Kwak, Young Lan(곽영란) ORCID logo https://orcid.org/0000-0002-2984-9927
Shim, Yon Hee(심연희) ORCID logo https://orcid.org/0000-0003-1921-3391
Lee, Jong Wha(이종화)
Cho, Jang Eun(조장은)
Hwang, Ki Chul(황기철)
사서에게 알리기


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.