Effects of Prolonged Propranolol Treatment on Left Ventricular Remodeling and Oxidative Stress After Myocardial Infarction in Rats

Mansuy, Pascale; Mougenot, Nathalie; Ramirez‐Gil, Juan Fernando; Bonnefont‐Rousselot, Dominique; Raillecove, Françoise; Komajda, Michel; Lechat, Philippe

doi:10.1097/00005344-200005000-00019

Cited by 16 publications

(15 citation statements)

References 27 publications

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“…In addition to its b-adrenergic antagonist activity, propranolol has antioxidant and anti-inflammatory properties, that are in part linked to the protection of membranes against lipid peroxidation (11). Propranolol reduces intracellular Ca 2 þ overload and attenuate mitochondrial dysfunction by its action on electron mitochondrial membrane transport and also by inhibiting Bax-mediated cytochrome C release (12,13). It also inhibits NADPH oxidase and protein kinase C activity (14) and decreases VEGF/(bFGF) basic fibroblast growth factor genes expression (15,16).…”

Section: Introductionmentioning

confidence: 99%

Effect of Long-term Propranolol Treatment on Hepatocellular Carcinoma Incidence in Patients with HCV-Associated Cirrhosis

N’Kontchou

Aout

Mahmoudi

et al. 2012

Cancer Prevention Research

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Propranolol bears antioxidant, anti-inflammatory, and antiangiogenic properties and antitumoral effects and therefore is potentially active in the prevention of hepatocellular carcinoma (HCC). We retrospectively assessed the impact of propranolol treatment on HCC occurrence in a cohort of 291 patients with compensated viral C (HCV) cirrhosis, prospectively followed and screened for HCC detection.Of ; platelet count, 137 AE 59 Giga/L) did not. Among patients with OV, 50 received treatment by propranolol. During a median follow-up of 54 months interquartile range (32-82), 61 patients developed an HCC. The 3-and 5-year HCC incidence was 4% and 4%, and 10% and 20% for patients treated and not treated by propranolol, respectively (Gray test, P ¼ 0.03). In multivariate analysis, propranolol treatment was associated with a decrease risk of HCC occurrence [HR, 0.25; 95% confidence interval (CI), 0.09-0.65; P ¼ 0.004], and was the only independent predictive factor of HCC occurrence in patients with OV (HR, 0.16; CI, 0.06-0.45; P ¼ 0.0005). The benefit of propranolol was further supported by propensity scores analyses.Conclusion: This retrospective long-term observational study suggests that propranolol treatment may decrease HCC occurrence in patients with HCV cirrhosis. These findings need to be verified by prospective clinical trial. Cancer Prev Res; 5(8);

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Section: Introductionmentioning

confidence: 99%

Effect of Long-term Propranolol Treatment on Hepatocellular Carcinoma Incidence in Patients with HCV-Associated Cirrhosis

N’Kontchou

Aout

Mahmoudi

et al. 2012

Cancer Prevention Research

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“…Propranolol or pindolol did not show free radical scavenging properties relevant for cardioprotection in a coronary occlusion model of isolated hearts of rabbit [660]. However, long-term in vivo treatment with propranolol abolished the increase of oxidative stress and reduced the cardiac sensitivity to catecholamine-induced arrhythmias in infarcted rats [658].…”

Section: Catecholamines and Oxidative Stress: A Complex Talk With Sevmentioning

confidence: 82%

“…I/R is probably the most studied cardiac disease and several drugs have been evaluated using I/R models. The antioxidant properties of propranolol and other -adrenoceptor antagonists are controversial, as some in vitro and in vivo studies support them [421,657,658] while others do not [651,659,660]. Propranolol or pindolol did not show free radical scavenging properties relevant for cardioprotection in a coronary occlusion model of isolated hearts of rabbit [660].…”

Section: Catecholamines and Oxidative Stress: A Complex Talk With Sevmentioning

confidence: 99%

Contribution of Catecholamine Reactive Intermediates and Oxidative Stress to the Pathologic Features of Heart Diseases

Costa

Carvalho

Bastos

et al. 2011

CMC

100

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Pathologic heart conditions, particularly heart failure (HF) and ischemia-reperfusion (I/R) injury, are characterized by sustained elevation of plasma and interstitial catecholamine levels, as well as by the generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS). Despite the continuous and extensive research on catecholamines since the early years of the XX(th) century, the mechanisms underlying catecholamine-induced cardiotoxicity are still not fully elucidated. The role of catecholamines in HF, stress cardiomyopathy, I/R injury, ageing, stress, and pheochromocytoma will be thoroughly discussed. Furthermore and although the noxious effects resulting from catecholamine excess have traditionally been linked to adrenoceptors, in fact, several evidences indicate that oxidative stress and the oxidation of catecholamines can have important roles in catecholamine-induced cardiotoxicity. Accordingly, the reactive intermediates formed during catecholamine oxidation have been associated with cardiac toxicity, both in in vitro and in vivo studies. An insight into the influence of ROS, RNS, and catecholamine oxidation products on several heart diseases and their clinical course will be provided. In addition, the source and type of oxidant species formed in some heart pathologies will be referred. In this review a special focus will be given to the research of cardiac pathologies where catecholamines and oxidative stress are involved. An integrated vision of these matters is required and will be provided along this review, namely how the concomitant surge of catecholamines and ROS occurs and how they can be interconnected. The concomitant presence of these factors can elicit peculiar and not fully characterized responses on the heart. We will approach the existing data with new perspectives as they can help explaining several controversial results regarding cardiovascular diseases and the redox ability of catecholamines.

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“…Nevertheless, the true relationship between oxidative stress, endothelial damage and CHF is still unknown, although there is ample evidence that oxidative stress is involved in the pathogenesis of atherosclerosis, endothelial damage, platelet aggregation and CHF [32,33]. It is currently thought that excessive production of superoxide may reduce synthesis of endothelium-derived relaxation factor (EDRF) or nitric oxide (NO), while stimulating the release of endothelins [34][35][36][37]. Recent data have also shown a close link between apoptosis and oxidative stress [18].…”

Section: Discussionmentioning

confidence: 99%

“…Kukin et al [34] recently reported that both carvedilol and metoprolol reduced oxidative stress significantly and equally after 6 months therapy. Other β-blockers, such as propanolol [35], have also been shown to reduce oxidative stress indirectly, although propanolol possesses neither cytotoxic nor superoxide-scavenging properties and its membranestabilizing effects may even lead to inhibition of superoxide generation [36].…”

Section: Discussionmentioning

confidence: 99%

Neither carvedilol nor bisoprolol in maximally tolerated doses has any specific advantage in lowering chronic heart failure oxidant stress: implications for β-blocker selection

et al. 2003

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We hypothesized that abnormal oxidative stress in chronic heart failure (CHF) could be related to endothelial damage and platelet activation, and that the vasodilating beta-blocker carvedilol would have beneficial effects on these processes compared with a selective non-vasodilating cardioselective beta-blocker, bisoprolol. We therefore assessed the effects of introducing carvedilol and bisoprolol in a prospective manner on indices of oxidative stress [lipid hydroperoxides (LHP)], endothelial damage [von Willebrand factor (vWf)], platelet activation (soluble P-selectin) and coagulation (fibrinogen) and their inter-relationships in stable outpatients with CHF in sinus rhythm. We recruited 46 patients [23 male; age 64 +/- 13 years (mean +/- S.D.); range 38-85 years] with CHF. Baseline levels of serum LHP (P<0.002), plasma vWf (P<0.001) and soluble P-selectin (P=0.02), but not fibrinogen (P=0.16), were higher in CHF patients compared with 22 age- and sex-matched healthy controls. After treatment for 2 months, systolic blood pressure fell in both arms of the study (both P<0.01), but there were no statistically significant (defined as P<0.01) decreases in LHP, vWf, fibrinogen or soluble P-selectin levels with either carvedilol or bisoprolol. In conclusion, patients with CHF have increased levels of plasma LHP and vWf, indicating increased oxidative stress and endothelial damage respectively. Contrary to the proposed antioxidative effects of carvedilol, initiating and titrating such therapy did not result in a reduction in levels of LHP in CHF.

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Effects of Prolonged Propranolol Treatment on Left Ventricular Remodeling and Oxidative Stress After Myocardial Infarction in Rats

Cited by 16 publications

References 27 publications

Effect of Long-term Propranolol Treatment on Hepatocellular Carcinoma Incidence in Patients with HCV-Associated Cirrhosis

Effect of Long-term Propranolol Treatment on Hepatocellular Carcinoma Incidence in Patients with HCV-Associated Cirrhosis

Contribution of Catecholamine Reactive Intermediates and Oxidative Stress to the Pathologic Features of Heart Diseases

Neither carvedilol nor bisoprolol in maximally tolerated doses has any specific advantage in lowering chronic heart failure oxidant stress: implications for β-blocker selection

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