Comparison of two sulfonylureas with high and low myocardial KATP channel affinity on myocardial infarct size and metabolism in a rat model of type 2 diabetes

Kristiansen, Steen Buus; Løfgren, Bo; Nielsen, Jesper; Støttrup, Nicolaj Brejnholt; Buhl, Esben S.; Nielsen‐Kudsk, Jens Erik; Nielsen, Torsten Toftegaard; Rungby, Jørgen; Flyvbjerg, Allan; Bøtker, Hans Erik

doi:10.1007/s00125-010-1970-y

Cited by 23 publications

(21 citation statements)

References 36 publications

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“…[153] GK rat: Refs. [153, 154] No change in infarct size STZ (±alloxan)-induced DM (dog, rabbit, rat, mouse): Refs. [147, 149, 150, 155–165] GK rat: Refs.…”

Section: Myocardial Tolerance Against Ischemia/reperfusion-induced Nementioning

confidence: 99%

Diabetic cardiomyopathy: pathophysiology and clinical features

et al. 2012

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Since diabetic cardiomyopathy was first reported four decades ago, substantial information on its pathogenesis and clinical features has accumulated. In the heart, diabetes enhances fatty acid metabolism, suppresses glucose oxidation, and modifies intracellular signaling, leading to impairments in multiple steps of excitation–contraction coupling, inefficient energy production, and increased susceptibility to ischemia/reperfusion injury. Loss of normal microvessels and remodeling of the extracellular matrix are also involved in contractile dysfunction of diabetic hearts. Use of sensitive echocardiographic techniques (tissue Doppler imaging and strain rate imaging) and magnetic resonance spectroscopy enables detection of diabetic cardiomyopathy at an early stage, and a combination of the modalities allows differentiation of this type of cardiomyopathy from other organic heart diseases. Circumstantial evidence to date indicates that diabetic cardiomyopathy is a common but frequently unrecognized pathological process in asymptomatic diabetic patients. However, a strategy for prevention or treatment of diabetic cardiomyopathy to improve its prognosis has not yet been established. Here, we review both basic and clinical studies on diabetic cardiomyopathy and summarize problems remaining to be solved for improving management of this type of cardiomyopathy.

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“…[153] GK rat: Refs. [153, 154] No change in infarct size STZ (±alloxan)-induced DM (dog, rabbit, rat, mouse): Refs. [147, 149, 150, 155–165] GK rat: Refs.…”

Section: Myocardial Tolerance Against Ischemia/reperfusion-induced Nementioning

confidence: 99%

Diabetic cardiomyopathy: pathophysiology and clinical features

et al. 2012

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“…With a few exceptions [30,31], DM models with obesity and hyperinsulinemia showed increased myocardial susceptibility to ischemia/reperfusion-induced necrosis [32-41]. In contrast, high glucose level induced simply by glucose or dextrose infusion did not affect infarct size in the majority of studies, including two recent studies [42,43] (Table 2).…”

Section: Changes In Myocardial Susceptibility To Infarction By Dmmentioning

confidence: 99%

“…However, since they used a PC protocol with multiple cycles of ischemia/reperfusion only, the change in the threshold for inducing PC protection might have been missed in their study. In fact, impairment of PC by DM has been observed in multiple species (rats, rabbits and dogs) and different models of DM (STZ-induced type 1 DM and genetic models of type 2 DM) [30,37,50-54]. Mimetics of ischemic PC and PostC (diazoxide, erythropoietin, [D-Ala 2 , D-Leu 5 -enkephalin acetate [DADLE] and isoflurane) were also ineffective for limitation of infarct size in DM hearts [33,34,37,55-59], confirming that DM impairs intracellular signaling mechanisms relevant to myocardial protection.…”

Section: Defects In Intracellular Protective Signaling In Dm Heartsmentioning

confidence: 99%

Effects of diabetes on myocardial infarct size and cardioprotection by preconditioning and postconditioning

Miki

Itoh

Sunaga

et al. 2012

Cardiovasc Diabetol

127

137

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In spite of the current optimal therapy, the mortality of patients with ischemic heart disease (IHD) remains high, particularly in cases with diabetes mellitus (DM) as a co-morbidity. Myocardial infarct size is a major determinant of prognosis in IHD patients, and development of a novel strategy to limit infarction is of great clinical importance. Ischemic preconditioning (PC), postconditioning (PostC) and their mimetic agents have been shown to reduce infarct size in experiments using healthy animals. However, a variety of pharmacological agents have failed to demonstrate infarct size limitation in clinical trials. One of the possible reasons for the discrepancy between the results of animal experiments and clinical trials is that co-morbidities, including DM, modified myocardial responses to ischemia/reperfusion and to cardioprotective agents. Here we summarize observations of the effects of DM on myocardial infarct size and ischemic PC and PostC and discuss perspectives for protection of DM hearts.

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“…The extra-pancreatic cardiovascular effects of glyburide and repaglinide may potentially increase the risk of adverse cardiovascular events. In contrast, gliclazide appears to be more selective for SUR1, which may confer a better cardiovascular prognosis during acute ischemic events (Abdelmoneim et al, 2012;Kristiansen et al, 2011). Indeed, we have shown previously that gliclazide use is associated with a lower risk of acute coronary syndrome-related morbidity and mortality compared to glyburide use (Abdelmoneim et al, 2014).…”

Section: Introductionmentioning

confidence: 86%

“…Some IS, like glyburide and the non-sulfonylurea IS repaglinide, will bind to both SUR1 and SUR2 isoforms when given at usual therapeutic doses and therefore also inhibit K ATP channels located in the myocardium and vascular smooth muscle cells (Abdelmoneim et al, 2012). Animal models have shown that cardiac K ATP channel opening is protective during ischemia-reperfusion injury and that K ATP channel activity is essential for ischemic conditioning, an endogenous protective mechanism that promotes salvage of myocardial tissue during ischemia-reperfusion injury (Kristiansen et al, 2011;Tang et al, 2006). The extra-pancreatic cardiovascular effects of glyburide and repaglinide may potentially increase the risk of adverse cardiovascular events.…”

Section: Introductionmentioning

confidence: 98%