ArticleMolecular and cellular biochemistry2000
Acute diabetes modulates response to ischemia in isolated rat heart.
Article in Molecular and cellular biochemistry, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 59 citations in OpenAlex.
- Glycation proteomics identifies creatine kinase as a mediator of the effects of methylglyoxal on mitochondrial permeability transition.bioRxiv : the preprint server for biology · 2026Article
- Article
- mPTP Proteins Regulated by Streptozotocin-Induced Diabetes Mellitus Are Effectively Involved in the Processes of Maintaining Myocardial Metabolic Adaptation.International journal of molecular sciences · 2020Article
- Myocyte membrane and microdomain modifications in diabetes: determinants of ischemic tolerance and cardioprotection.Cardiovascular diabetology · 2017Review
- Mitochondria as a target of cardioprotection in models of preconditioning.Journal of bioenergetics and biomembranes · 2017Review
- Ischemic preconditioning: Interruption of various disorders.Journal of the Saudi Heart Association · 2017Review
- Glucose and fatty acid metabolism in infarcted heart from streptozotocin-induced diabetic rats after 2 weeks of tissue remodeling.Cardiovascular diabetology · 2015Article
- Diabetic hyperglycemia attenuates sympathetic dysfunction and oxidative stress after myocardial infarction in rats.Cardiovascular diabetology · 2014Article
- Inhibition of mitochondrial permeability transition pore restores the cardioprotection by postconditioning in diabetic hearts.Journal of diabetes and metabolic disorders · 2014Article
- Article
- Autophagy, myocardial protection, and the metabolic syndrome.Journal of cardiovascular pharmacology · 2012Review
- Hyperoxic preconditioning fails to confer additional protection against ischemia-reperfusion injury in acute diabetic rat heart.EXCLI journal · 2012Article
- Hyperglycemia can delay left ventricular dysfunction but not autonomic damage after myocardial infarction in rodents.Cardiovascular diabetology · 2011Article
- Short-term diabetes attenuates left ventricular dysfunction and mortality rates after myocardial infarction in rodents.Clinics (Sao Paulo, Brazil) · 2011Article
- Is hyperglycemia bad for the heart during acute ischemia?The Journal of thoracic and cardiovascular surgery · 2010Article
- Involvement of GSK-3β in attenuation of the cardioprotective effect of ischemic preconditioning in diabetic rat heart.Molecular and cellular biochemistry · 2010Article
- Subcellular mechanisms of adaptation in the diabetic myocardium: Relevance to ischemic preconditioning in the nondiseased heart.Experimental and clinical cardiology · 2010Article
- Protection of the abnormal heart.Heart failure reviews · 2007Review
- Hypercholesterolemia abrogates an increased resistance of diabetic rat hearts to ischemia-reperfusion injury.Molecular and cellular biochemistry · 2007Article
- Mitogen-activated protein kinases in the acute diabetic myocardium.Molecular and cellular biochemistry · 2003Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic hearts are suggested to exhibit either increased or lower sensitivity to ischemia. Detrimental effects of prolonged ischemia can be attenuated by preconditioning, however, relatively little is known about its effects in the diseased myocardium. This study was designed to test the susceptibility to ischemia-induced arrhythmias and the effect of preconditioning in the diabetic heart. Rats were made diabetic with streptozotocin (45 mg/kg, i.v.). After 1 week, isolated Langendorff-perfused hearts were subjected to 30 min occlusion of LAD coronary artery without or with preceding preconditioning induced by one cycle of 5 min ischemia and 10 min reperfusion. Glycogen and lactate contents were estimated in the preconditioned and non-preconditioned hearts before and after ischemia. Diabetic hearts were more resistant to ischemia-induced arrhythmias: incidence of ventricular tachycardia (VT) decreased to 42% and only transient ventricular fibrillation (VF) occurred in 17% of the hearts as compared to the non-diabetic controls (VT 100% and VF 70% including sustained VF 36%; p < 0.05). Preconditioning effectively suppressed the incidence and severity of arrhythmias (VT 33%, VF 0%) in the normal hearts. However, this intervention did not confer any additional protection in the diabetic hearts. Despite higher glycogen content in the diabetic myocardium and greater glycogenolysis during ischemia, production of lactate in these hearts was significantly lower than in the controls. Preconditioning caused a substantial decrease in the accumulation of lactate in the normal hearts, whereby in the diabetic hearts, this intervention did not cause any further reduction in the level of lactate. In conclusion, diabetic rat hearts exhibit lower susceptibility to ischemic injury and show no additional response to preconditioning. Reduced production of glycolytic metabolites during ischemia can account for the enhanced resistance of diabetic hearts to ischemia as well as for the lack of further protection by preconditioning.
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