A Inibição do Sistema Renina-Angiotensina e o Bloqueio Beta Adrenérgico podem ser Úteis para Atenuar a Cardiotoxicidade por Antraciclinas

Neves, Mário Fritsch

doi:10.36660/abc.20230280

Cited by 2 publications

(1 citation statement)

References 11 publications

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“…β2 receptors are predominant in smooth muscle and cause visceral relaxation. Among some known functions are: smooth muscle relaxation, for example, in the bronchi and histamine release by mast cells (ERASMUS et al, 2019;ALMONFREY et al, 2020;NEVES et al, 2023).…”

Section: β-Adrenergic Receptorsmentioning

confidence: 99%

Evaluation of Pulmonary Changes Caused by Induced Sepsis and the Use of Propranolol in Endothelial Dysfunction in Wistar Rats

Vargas,

Antunes,

Leandro

et al. 2023

JHS

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Objective: To evaluate the potential effect of propranolol as a possible lung protector on endothelial dysfunction in cases of induced sepsis in Wistar rats. Methods: The animals were divided into 3 groups: Group 1, intraperitoneal propranolol administration 30 minutes before sepsis induction; Group 2, administration of intraperitoneal propranolol 30 minutes after sepsis induction; Group 3, SHAM (control), septic animals without propranolol administration. For evaluation, hemorrhage, edema, atelectasis and pneumonia scores were used as tissue damage criteria. Results: Propranolol was found to protect against pneumonia and atelectasis, but increased bleeding while edema remained mild in all groups. Final considerations: The results showed that the treated groups showed clinical improvement in different aspects during the sepsis period, with a survival of treated animals when compared to untreated ones.

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Section: β-Adrenergic Receptorsmentioning

confidence: 99%

Evaluation of Pulmonary Changes Caused by Induced Sepsis and the Use of Propranolol in Endothelial Dysfunction in Wistar Rats

Vargas,

Antunes,

Leandro

et al. 2023

JHS

View full text Add to dashboard Cite

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Cardio-Oncology’s Modern Approaches to Prevent Doxorubicin-Induced Cardiotoxicity: A Systematic Review

Palvia,

Damera,

Nandi

et al. 2024

Cureus

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Advances in the field of oncology have led to the advent of doxorubicin (DOX), an anthracycline chemotherapeutic agent, through which cancer survival rates have remarkably improved. There has, however, been a rise in adverse effects from the use of DOX, most notably cardiotoxicity. DOX-induced cardiotoxicity is thought to arise through the generation of reactive oxygen species (ROS), causing mitochondrial dysfunction in the cardiomyocytes. This systematic review followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) standards and focused on cancer patients undergoing DOX therapy. The research question addressed interventions aimed at preventing DOX-induced cardiotoxicity. Google Scholar, PubMed, and ScienceDirect databases were used to conduct a systematic search. Next, screening was carried out by reviewing the title and abstract of various articles to exclude irrelevant studies, followed by the retrieval of full-text articles. Scale for the assessment of narrative review articles 2 (SANRA 2) for narrative reviews, a measurement tool to assess systematic reviews (AMSTAR) checklist for systematic reviews, and the Cochrane risk of bias tool for randomized controlled trials (RCTs) were the tools employed for quality assessment. This systematic review provides convincing evidence about preventive interventions to counteract DOX-induced cardiotoxicity. Primary prevention strategies against DOX-induced cardiotoxicity include pharmacological and non-pharmacological measures. Dexrazoxane reduces cardiotoxicity without therapeutic compromise. Beta-blockers showed mixed results in preserving cardiac function. The research on renin-angiotensin-aldosterone system (RAAS) inhibitors suggests that most of these agents can reduce the risk of DOX-induced cardiotoxicity. The liposomal formulation of DOX decreases cardiotoxicity without sacrificing effectiveness. Chemotherapy regimens should be supplemented with cardioprotective medications to increase therapeutic efficacy and lower cardiac risks. Exercise is an essential non-pharmacological strategy for decreasing DOX-induced cardiotoxicity. It acts by lowering oxidative stress, maintaining mitochondrial function, and averting apoptosis. Other non-pharmacological interventions through antioxidative, anti-apoptotic, and mitochondrial protective mechanisms, such as resveratrol, vitamin E, curcumin, and visnagin, show promise in lowering DOX-induced cardiotoxicity and may be useful as supplementary therapy during cancer treatment. In conclusion, this review highlights the need for a multimodal strategy that incorporates different tactics, as well as the need for additional research and strong clinical trials, with the ultimate goal of protecting cardiac health in patients receiving chemotherapy with DOX.

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A Inibição do Sistema Renina-Angiotensina e o Bloqueio Beta Adrenérgico podem ser Úteis para Atenuar a Cardiotoxicidade por Antraciclinas

Cited by 2 publications

References 11 publications

Evaluation of Pulmonary Changes Caused by Induced Sepsis and the Use of Propranolol in Endothelial Dysfunction in Wistar Rats

Evaluation of Pulmonary Changes Caused by Induced Sepsis and the Use of Propranolol in Endothelial Dysfunction in Wistar Rats

Cardio-Oncology’s Modern Approaches to Prevent Doxorubicin-Induced Cardiotoxicity: A Systematic Review

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