Hyperglycaemia protects the heart after myocardial infarction: aspects of programmed cell survival and cell death

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, progr...

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Published in:European journal of heart failure 2010-07, Vol.12 (7), p.659-667
Main Authors: Malfitano, Christiane, Alba Loureiro, Tatiana C., Rodrigues, Bruno, Sirvente, Raquel, Salemi, Vera Maria Cury, Rabechi, Nara B., Lacchini, Silvia, Curi, Rui, Irigoyen, Maria Claudia C.
Format: Article
Language:English
Subjects:
Angiogenesis
Animals
Apoptosis
Apoptosis - physiology
Caspase 3 - metabolism
Cell Survival - physiology
Cytokines - analysis
Diabetes Mellitus, Experimental - physiopathology
Diabetic hyperglycaemia
Fibrosis
Glucose Transport Proteins, Facilitative - metabolism
Heart - physiopathology
Hyperglycemia - physiopathology
Inflammation
Male
Myocardial infarction
Myocardial Infarction - physiopathology
Myocytes, Cardiac - physiology
Rats
Tumor Necrosis Factor-alpha - metabolism
Vascular Endothelial Growth Factor A - metabolism
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Summary: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‐α, IL‐1β, IL‐6, and IL‐10), gene expression by real‐time PCR (Bax, Fas, p53, Bcl‐2, HIF1‐α, 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‐α, 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.
ISSN:1388-9842
1879-0844
DOI:10.1093/eurjhf/hfq053