Search results for "Protection"
showing 10 items of 1623 documents
Improving the preclinical models for the study of chemotherapy-induced cardiotoxicity: a Position Paper of the Italian Working Group on Drug Cardioto…
2015
Although treatment for heart failure induced by cancer therapy has improved in recent years, the prevalence of cardiomyopathy due to antineoplastic therapy remains significant worldwide. In addition to traditional mediators of myocardial damage, such as reactive oxygen species, new pathways and target cells should be considered responsible for the impairment of cardiac function during anticancer treatment. Accordingly, there is a need to develop novel therapeutic strategies to protect the heart from pharmacologic injury, and improve clinical outcomes in cancer patients. The development of novel protective therapies requires testing putative therapeutic strategies in appropriate animal model…
Intracoronary application of C1 esterase inhibitor improves cardiac function and reduces myocardial necrosis in an experimental model of ischemia and…
1997
Background Myocardial injury from ischemia can be aggravated by reperfusion of the jeopardized area. The precise underlying mechanisms have not been clearly defined, but proinflammatory events, including complement activation, leukocyte adhesion, and infiltration and release of diverse mediators, probably play important roles. The present study addresses the possibility of reducing reperfusion damage by the application of C1 esterase inhibitor (C1-INH). Methods and Results Cardioprotection by C1-INH 20 IU/kg IC was examined in a pig model with 60 minutes of coronary occlusion, followed by 120 minutes of reperfusion. C1-INH was administered during the first 5 minutes of coronary reperfusion…
Differential responses to docosahexaenoic acid in primary and immortalized cardiac cells
2013
Abstract The importance of dietary polyunsaturated fatty acids (PUFAs) in the reduction of cardiovascular disease has been recognized for many years. Docosahexaenoic acid (22:6n3, DHA) is an n-3 PUFA known to affect numerous biological functions and provide cardioprotection; however, the exact molecular and cellular protective mechanism(s) remain unknown. In contrast, DHA also possesses many anti-tumorgenic properties including suppressing cell growth and inducing apoptosis. In the present study, we investigated the effect of DHA toward H9c2 cells (an immortalized cardiac cell line) and neonatal primary cardiomyocytes (NCM). Cells were treated with 0 μM, 10 μM or 100 μM DHA for upto 48 h. C…
HERS study disturbs hormonal replacement therapy
2000
Cardiovascular protection of hormonal replacement therapy was considered a fact. The effects of estrogens on lipid levels and vascular health gave biological support to estrogen cardioprotection. The recently published HERS study showing no protective effects of estrogen and progesterone replacement therapy on the risk of myocardial infarction or coronary deaths is provoking perplexity. These surprising results may have several causes such as the use of progesterone, the associated use of cardioprotective agents or the short observation period. However, the study results scope is rectricted to secondary prevention. These cannot be extrapolated to frequent conditions of postmenopausal women …
Nitroglycerin-induced cardioprotection is endothelial nitric oxide synthase- dependent
2015
Purpose We sought to evaluate the contribution of the endogenous NO pathway to the cardioprotective action of nitroglycerin (NTG). Methods and Results Anesthetized rabbits were subjected to 30-min myocardial ischemia (isc) and 3-h reperfusion (rep) and randomized into: Control group (no further intervention); PostC group (application of 8 cycles 30-sec isc/rep) and NTG treated group (2 μg/kg-1/min-1 IV bolus) for 65 min starting 10 min prior to rep. In additional groups, pharmacological inhibitors of NOS, nNOS, iNOS, PI3K, adenosine receptors and PKG were administrated with or without NTG. The infarcted (I) to risk (R) ratio was estimated. In a second experimental series tissue samples were…
Inorganic Nitrate Therapy Improves Doxorubicin-Induced Cardiomyopathy
2011
The anthracycline doxorubicin (DOX) is a potent and effective antineoplastic antibiotic agent widely used in the treatment of a broad range of forms of cancer. The clinical use of DOX is limited by cardiotoxicity, which increases dose dependently and may lead to dilated cardiomyopathy and clinical
Heart Failure and Left Ventricular Dysfunction
2018
Heart failure (HF) and left ventricular (LV) dysfunction are the most concerning and serious cardiovascular complications of cancer therapies and cause an increase in morbidity and mortality. Some cancer treatments induce left ventricular dysfunction that appears early after exposure and therefore may adversely affect oncological therapy, while others generate cardiac injuries resulting in clinical problems only years later.
Cardioprotection by gene therapy
2015
Ischemic heart disease remains the leading cause of death worldwide. Ischemic pre-, post-, and remote conditionings trigger endogenous cardioprotection that renders the heart resistant to ischemic-reperfusion injury (IRI). Mimicking endogenous cardioprotection by modulating genes involved in cardioprotective signal transduction provides an opportunity to reproduce endogenous cardioprotection with better possibilities of translation into the clinical setting. Genes and signaling pathways by which conditioning maneuvers exert their effects on the heart are partially understood. This is due to the targeted approach that allowed identifying one or a few genes associated with IRI and cardioprote…
C1-esterase inhibitor in ischemia and reperfusion.
2002
Summary Myocardial injury from ischemia can be aggravated by reperfusion of the jeopardized area. The precise underlying mechanisms have not been clearly defined, but proinflammatory events including complement activation play important roles. Cardioprotection by complement inhibition inter alia C1-esterase-inhibitor (C1-INH) was examined in several experimental models and under clinical conditions with ischemia and reperfusion. C1-INH reduced local anaphylatoxin release revealing the importance of the classical complement pathway. Inhibition of local complement activation was accompanied by improvement of myocardial function and perfusion of the previously ischemic myocardium. Leukocyte en…
Cardioprotection by gene therapy: A review paper on behalf of the Working Group on Drug Cardiotoxicity and Cardioprotection of the Italian Society of…
2015
Ischemic heart disease remains the leading cause of death worldwide. Ischemic pre-, post-, and remote conditionings trigger endogenous cardioprotection that renders the heart resistant to ischemic-reperfusion injury (IRI). Mimicking endogenous cardioprotection by modulating genes involved in cardioprotective signal transduction provides an opportunity to reproduce endogenous cardioprotection with better possibilities of translation into the clinical setting. Genes and signaling pathways by which conditioning maneuvers exert their effects on the heart are partially understood. This is due to the targeted approach that allowed identifying one or a few genes associated with IRI and cardioprote…