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Hyperglycemia protects the heart after myocardial infarction: aspects of programmed cell survival and cell death
Author(s) -
Malfitano Christiane,
Loureiro Tatiana Carolina Alba,
Rodrigues Bruno,
Sirvente Raquel,
Rabechi Nara B,
Lacchini Silvia,
Curi Rui,
Irigoyen Maria Claudia C
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.1036.11
Subject(s) - medicine , myocardial infarction , cardiology , ejection fraction , infarction , cardiac function curve , angiogenesis , fibrosis , diastole , isovolumetric contraction , endocrinology , heart failure , blood pressure
This study was designed to evaluate the role of diabetic hyperglycemia after myocardial infarction on cardiac function and on programmed cell survival and death in rats (Wistar) hearts divided into 4 groups: control (C), diabetic (D), myocardial infarction (MI) and diabetic myocardial infarction (DI). The size of MI, systolic and diastolic function by echocardiography, cytokines expression by ELISA (TNF‐α, IL‐1β, IL‐6 and IL‐10), gene expression by real time PCR (Bax, Fas, p53, Bcl‐2, HIF‐1a, VEGF and IL8r), caspase 3 activity by espectrofluorimetric assay, capillary density and fibrosis by histological analysis. The systolic function (ejection fraction and shortening) was improved by hyperglycemia in DI group although these changes were accompanied by maintenance of diastolic dysfunction (isovolumetric relaxation time and peak E deceleration time). Reduction of 36% in MI size, pro‐inflammatory cytokines reduction, apoptosis activation and increase in cell survival factors (HIF‐1a, VEGFa and IL8r) were observed after 15 days of myocardial infarction. Moreover the hyperglycemic status probably induced angiogenesis (increase of capillary density) before and after MI, accompanied by reduction in fibrosis. In conlusion, these results suggest greater plasticity and cellular resistance to ischemic injury induced by chronic diabetic hyperglycemia in heart rats. Financial support: CNPq and CAPES