Document Type

Article

Publication Date

6-18-2013

Comments

This article has been peer reviewed. It was published in: Cardiovascular diabetology

Volume 12, Issue 1, June 2013, Pages 91.

The published version is available at DOI: 10.1186/1475-2840-12-91. Copyright © BioMed Central

Abstract

BACKGROUND: Diabetic patients, through incompletely understood mechanisms, endure exacerbated ischemic heart injury compared to non-diabetic patients. Intermedin (IMD) is a novel calcitonin gene-related peptide (CGRP) superfamily member with established cardiovascular protective effects. However, whether IMD protects against diabetic myocardial ischemia/reperfusion (MI/R) injury is unknown. METHODS: Diabetes was induced by streptozotocin in Sprague--Dawley rats. Animals were subjected to MI via left circumflex artery ligation for 30 minutes followed by 2 hours R. IMD was administered formally 10 minutes before R. Outcome measures included left ventricular function, oxidative stress, cellular death, infarct size, and inflammation. RESULTS: IMD levels were significantly decreased in diabetic rats compared to control animals. After MI/R, diabetic rats manifested elevated intermedin levels, both in plasma (64.95 +/- 4.84 pmol/L, p < 0.05) and myocardial tissue (9.8 +/- 0.60 pmol/L, p < 0.01) compared to pre-MI control values (43.62 +/- 3.47 pmol/L and 4.4 +/- 0.41). IMD administration to diabetic rats subjected to MI/R decreased oxidative stress product generation, apoptosis, infarct size, and inflammatory cytokine release (p < 0.05 or p < 0.01). CONCLUSIONS: By reducing oxidative stress, inflammation, and apoptosis, IMD may represent a promising novel therapeutic target mitigating diabetic ischemic heart injury.

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