Document Detail

Hyperglycaemia protects the heart after myocardial infarction: aspects of programmed cell survival and cell death.
MedLine Citation:
PMID:  20406798     Owner:  NLM     Status:  MEDLINE    
AIMS: Exposure to a high glucose medium or diabetes has been found to protect the heart against ischaemia. The activation of antiapoptotic and proliferative factors seems to be involved in this cardioprotection. This study was designed to evaluate the role of hyperglycaemia in cardiac function, programmed cell survival, and cell death in diabetic rats after myocardial infarction (MI).
METHODS AND RESULTS: Male Wistar rats were divided into four groups (n = 8): control (C), diabetic (D), myocardial infarcted (MI), and diabetic myocardial infarcted (DI). The following measures were assessed in the left ventricle: size of MI, systolic and diastolic function by echocardiography, cytokines by ELISA (TNF-alpha, IL-1beta, IL-6, and IL-10), gene expression by real-time PCR (Bax, Fas, p53, Bcl-2, HIF1-alpha, VEGF, and IL8r), caspase-3 activity by spectrofluorometric assay, glucose transporter type 1 and 4 (GLUT-1 and GLUT-4) protein expression by western blotting, and capillary density and fibrosis by histological analysis. Systolic function was improved by hyperglycaemia in the DI group, and this was accompanied by no improvement in diastolic dysfunction, a reduction of 36% in MI size, reduced proinflammatory cytokines, apoptosis activation, and an increase in cell survival factors (HIF1-alpha, VEGFa and IL8r) assessed 15 days post-MI. Moreover, hyperglycaemia resulted in angiogenesis (increased capillary density) before and after MI, accompanied by a reduction in fibrosis.
CONCLUSION: Together, these results suggest that greater plasticity and cellular resistance to ischaemic injury result from chronic diabetic hyperglycaemia in rat hearts.
Christiane Malfitano; Tatiana C Alba Loureiro; Bruno Rodrigues; Raquel Sirvente; Vera Maria Cury Salemi; Nara B Rabechi; Silvia Lacchini; Rui Curi; Maria Claudia C Irigoyen
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-04-20
Journal Detail:
Title:  European journal of heart failure     Volume:  12     ISSN:  1879-0844     ISO Abbreviation:  Eur. J. Heart Fail.     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-06-25     Completed Date:  2010-10-01     Revised Date:  2011-06-08    
Medline Journal Info:
Nlm Unique ID:  100887595     Medline TA:  Eur J Heart Fail     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  659-67     Citation Subset:  IM    
Hypertension Unit, Heart Institute InCor, University of São Paulo, Medical School, Av Eneas de Carvalho Aguiar 44, São Paulo, Brazil.
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MeSH Terms
Apoptosis / physiology
Caspase 3 / metabolism
Cell Survival / physiology
Cytokines / analysis
Diabetes Mellitus, Experimental / physiopathology*
Glucose Transport Proteins, Facilitative / metabolism
Heart / physiopathology*
Hyperglycemia / physiopathology*
Myocardial Infarction / physiopathology*
Myocytes, Cardiac / physiology*
Tumor Necrosis Factor-alpha / metabolism
Vascular Endothelial Growth Factor A / metabolism
Reg. No./Substance:
0/Cytokines; 0/Glucose Transport Proteins, Facilitative; 0/Tumor Necrosis Factor-alpha; 0/Vascular Endothelial Growth Factor A; EC 3.4.22.-/Caspase 3

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