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5‐Aminoimidazole‐4‐carboxamide‐1‐β‐ d ‐ribofuranoside Increases Myocardial Glucose Uptake during Reperfusion and Induces Late Pre‐conditioning: Potential Role of AMP‐Activated Protein Kinase
Author(s) -
Kristiansen Steen B.,
Solskov Lasse,
Jessen Niels,
Løfgren Bo,
Schmitz Ole,
NielsenKudsk Jens Erik,
Nielsen Torsten T.,
Bøtker Hans Erik,
Lund Sten
Publication year - 2009
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/j.1742-7843.2009.00402.x
Subject(s) - ampk , medicine , endocrinology , amp activated protein kinase , protein kinase a , chemistry , kinase , biochemistry
Late pre‐conditioning protects against myocardial ischaemic‐reperfusion injury. AMP‐activated protein kinase (AMPK) is activated by exercise and 5‐aminoimidazole‐4‐carboxamide‐1‐β‐ d ‐ribofuranoside (AICAR). Early pre‐conditioning involves AMPK activation and increased myocardial glucose uptake. The aim of the present study was to determine whether AICAR activates myocardial AMPK and induces late pre‐conditioning and whether myocardial glucose uptake during reperfusion was modulated. Twenty‐four hours after AICAR treatment or exercise, Wistar rats were subjected to ischaemia and reperfusion in a Langendorff model and compared to control rats. AMPK activity increased immediately 2.5‐fold in AICAR‐treated animals (P < 0.01) and twofold in exercised animals (P < 0.05). AICAR and exercise reduced infarct size by 60% and 50% (both P < 0.01), respectively, and increased myocardial glucose uptake during reperfusion (AICAR; 45%, P < 0.05, exercise; 40%, P < 0.05). In conclusion, AICAR induces late pre‐conditioning and increases myocardial glucose uptake during reperfusion in rat hearts. AICAR and exercise activate AMPK, suggesting a role of AMPK in the signalling mechanisms behind late pre‐conditioning.