Reduction of oxidative stress by carvedilol: role in maintenance of ischaemic myocardium viability

Cargnoni, Anna; Ceconi, Claudio; Bernocchi, Palmira; Boraso, Antonella; Parrinello, Giovanni; Curello, Salvatore; Ferrari, Roberto

doi:10.1016/s0008-6363(00)00082-1

Cited by 36 publications

(31 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…22,23 In our preliminary study using sham-operated rats, the heart rate reduction induced by the present dose of carvedilol (1 mg/kg) was similar to that of propranolol (1 mg/kg) (19.0±8.9%, n=8 vs 18.5±8.0%, n=8). Therefore, the magnitude of -blocking action of carvedilol might be equivalent to that of propranolol in the present study.…”

Section: Propranolol Vs Carvedilolsupporting

confidence: 60%

“…These effects of carvedilol were not different from those of propranolol, suggesting the primary influence of -adrenoceptor blocking action of carvedilol is on tracer kinetics, but not other mechanisms, such as -blocking or antioxidant effects, that have been implicated previously. 22,23 The present results also imply that the efficacy of cardiac FA imaging for the detection of coronary heart disease would not be decreased by treatment with -blockers.…”

Section: Effects Of -Adrenoceptor Blockade On Cardiac Fa Imagingmentioning

confidence: 50%

See 1 more Smart Citation

Influence of .BETA.-Adrenoceptor Blockade on the Myocardial Accumulation of Fatty Acid Tracer and Its Intracellular Metabolism in the Heart After Ischemia-Reperfusion Injury

Igarashi

Nozawa

Fujii

et al. 2006

Circ J

View full text Add to dashboard Cite

Section: Propranolol Vs Carvedilolsupporting

confidence: 60%

Section: Effects Of -Adrenoceptor Blockade On Cardiac Fa Imagingmentioning

confidence: 50%

Influence of .BETA.-Adrenoceptor Blockade on the Myocardial Accumulation of Fatty Acid Tracer and Its Intracellular Metabolism in the Heart After Ischemia-Reperfusion Injury

Igarashi

Nozawa

Fujii

et al. 2006

Circ J

View full text Add to dashboard Cite

“…37 Carvedilol, a nonspecific ␤-antagonist with ␣-blocking activity, has antioxidant properties. 38 Calcium channel blockers have also been reported to have antioxidant properties, inasmuch as they inhibit lipid peroxidation by scavenging peroxy radicals. 39 Captopril, an ACE inhibitor, has also been reported to be an OH Ϫ scavenger because of its sulfhydryl content in addition to reduced angiotensin II, which is a potent activator of NADPH oxidase.…”

Section: Pharmacological Perspectivesmentioning

confidence: 99%

Heart Failure, Redox Alterations, and Endothelial Dysfunction

2001

View full text Add to dashboard Cite

Abstract-Heart failure is characterized by neurohumoral alterations, such as activation of the sympathetic nervous system, stimulation of the renin-angiotensin system, increased activity of the endothelin system, increased production of norepinephrine, and increased circulating levels of cytokines. Oxidative stress is associated with the formation of reactive oxygen species (ROS). The myocardium has enzymes that stimulate ROS generation and enzymes with antioxidant effects. Several studies have suggested that ROS are increased in the failing heart. ROS may contribute to the pathophysiology of heart failure by initiating myocyte apoptosis and exerting direct negatively inotropic effects through the reduction of cytosolic intracellular free calcium. However, mechanisms such as endothelial dysfunction and inflammation have also been involved in the progression of heart failure. Antioxidants (eg, vitamin C) seem to improve endothelial functionality and reduce the inflammatory response in patients with heart failure. Therefore, in this review, we analyzed the involvement of ROS in the cellular and molecular mechanisms associated with endothelial dysfunction in heart failure.

show abstract

“…The antiapoptotic cardioprotective role of Carv is independent of its antiadrenergic properties (Schwarz et al, 2003). Studies have shown that the antioxidant properties of Carv provide it a unique ability to maintain the viability and inhibit apoptosis in the ischemic myocardium (Cargnoni et al, 2000;Carreira et al, 2006). In addition, experimental studies have shown that Carv treatment alleviates left ventricular remodeling, fibrosis, and cardiac dysfunction in rats (Barone et al, 2007;Yoshikawa et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Carvedilol Enhances Mesenchymal Stem Cell Therapy for Myocardial Infarction via Inhibition of Caspase-3 Expression

Hassan

Meduru

Taguchi

et al. 2012

J Pharmacol Exp Ther

View full text Add to dashboard Cite

Adult stem cells have shown great promise toward repairing infarcted heart and restoring cardiac function. Mesenchymal stem cells (MSCs), because of their inherent multipotent nature and their ability to secrete a multitude of growth factors and cytokines, have been used for cardiac repair with encouraging results. Preclinical studies showed that MSCs injected into infarcted hearts improve cardiac function and attenuate fibrosis. Although stem cell transplantation is a promising therapeutic option to repair the infarcted heart, it is faced with a number of challenges, including the survival of the transplanted cells in the ischemic region, due to excessive oxidative stress present in the ischemic region. The objective of this study was to determine the effect of Carvedilol (Carv), a nonselective ␤-blocker with antioxidant properties, on the survival and engraftment of MSCs in the infarcted heart. MSCs were subjected to a simulated host-tissue environment, similar to the one present in the infarcted myocardium, by culturing them in the presence of hydrogen peroxide (H 2 O 2 ) to induce oxidative stress. MSCs were treated with 2.5 M Carv for 1 h in serum-free medium, followed by treatment with H 2 O 2 for 2 h. The treated cells exhibited significant protection against H 2 O 2 -induced cell death versus untreated controls as determined by 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assays. Likewise, transplantation of MSCs after permanent left coronary artery ligation and treatment of animals after myocardial infarction (MI) with Carv (5 mg/kg b.wt.) led to significant improvement in cardiac function, decreased fibrosis, and caspase-3 expression compared with the MI or MSC-alone groups.

show abstract

Reduction of oxidative stress by carvedilol: role in maintenance of ischaemic myocardium viability

Abstract: Our data show that the anti-oxidant activity of carvedilol is relevant for the maintenance of myocardium viability.

Cited by 36 publications

References 24 publications

Influence of .BETA.-Adrenoceptor Blockade on the Myocardial Accumulation of Fatty Acid Tracer and Its Intracellular Metabolism in the Heart After Ischemia-Reperfusion Injury

Influence of .BETA.-Adrenoceptor Blockade on the Myocardial Accumulation of Fatty Acid Tracer and Its Intracellular Metabolism in the Heart After Ischemia-Reperfusion Injury

Heart Failure, Redox Alterations, and Endothelial Dysfunction

Carvedilol Enhances Mesenchymal Stem Cell Therapy for Myocardial Infarction via Inhibition of Caspase-3 Expression

Contact Info

Product

Resources

About