ArticleCardiovascular diabetology2013
Angiotensin-converting enzyme inhibition and food restriction restore delayed preconditioning in diabetic mice.
Article in Cardiovascular diabetology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Morphine induces physiological, structural, and molecular benefits in the diabetic myocardium.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Co-morbidities and co-medications as confounders of cardioprotection-Does it matter in the clinical setting?British journal of pharmacology · 2020Review
- Perspectives on the Potential Benefits of Antihypertensive Peptides towards Metabolic Syndrome.International journal of molecular sciences · 2020Review
- Emodin alleviates cardiac fibrosis by suppressing activation of cardiac fibroblastsActa pharmaceutica Sinica. B · 2019Article
- Definition of hidden drug cardiotoxicity: paradigm change in cardiac safety testing and its clinical implications.European heart journal · 2019Review
- Clinical significance of chronic myocardial ischemia in coronary artery disease patients.Journal of thoracic disease · 2019Review
- ACE-inhibition induces a cardioprotective transcriptional response in the metabolic syndrome heart.Scientific reports · 2018Article
- Myocyte membrane and microdomain modifications in diabetes: determinants of ischemic tolerance and cardioprotection.Cardiovascular diabetology · 2017Review
- Sarcolemmal dependence of cardiac protection and stress-resistance: roles in aged or diseased hearts.British journal of pharmacology · 2016Review
- Acute hyperglycemia abolishes cardioprotection by remote ischemic perconditioning.Cardiovascular diabetology · 2015Article
- Type 2 diabetes mellitus and myocardial ischemic preconditioning in symptomatic coronary artery disease patients.Cardiovascular diabetology · 2015Article
- High carbohydrate and high fat diets protect the heart against ischaemia/reperfusion injury.Cardiovascular diabetology · 2014Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundClassical and delayed preconditioning are powerful endogenous protection mechanisms against ischemia-reperfusion damage. However, it is still uncertain whether delayed preconditioning can effectively salvage myocardium in patients with co-morbidities, such as diabetes and the metabolic syndrome. We investigated delayed preconditioning in mice models of type II diabetes and the metabolic syndrome and investigated interventions to optimize the preconditioning potential.
methodsHypoxic preconditioning was induced in C57Bl6-mice (WT), leptin deficient ob/ob (model for type II diabetes) and double knock-out (DKO) mice with combined leptin and LDL-receptor deficiency (model for metabolic syndrome). Twenty-four hours later, 30 min of regional ischemia was followed by 60 min reperfusion. Left ventricular contractility and infarct size were studied. The effect of 12 weeks food restriction or angiotensin-converting enzyme inhibition (ACE-I) on this was investigated. Differences between groups were analyzed for statistical significance by student's t-test or one-way ANOVA followed by a Fisher's LSD post hoc test. Factorial ANOVA was used to determine the interaction term between preconditioning and treatments, followed by a Fisher's LSD post hoc test. Two-way ANOVA was used to determine the relationship between infarct size and contractility (PRSW). A value of p<0.05 was considered significant.
resultsLeft ventricular contractility is reduced in ob/ob compared with WT and even further reduced in DKO. ACE-I improved contractility in ob/ob and DKO mice. After ischemia/reperfusion without preconditioning, infarct size was larger in DKO and ob/ob versus WT. Hypoxic preconditioning induced a strong protection in WT and a partial protection in ob/ob mice. The preconditioning potential was lost in DKO. Twelve weeks of food restriction or ACE-I restored the preconditioning potential in DKO and improved it in ob/ob.
conclusionDelayed preconditioning is restored by food restriction and ACE-I in case of type II diabetes and the metabolic syndrome.
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