Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 1 de 1
Filtrar
Mais filtros

Bases de dados
Ano de publicação
Tipo de documento
Assunto da revista
Intervalo de ano de publicação
1.
Cell Mol Life Sci ; 80(11): 341, 2023 Oct 29.
Artigo em Inglês | MEDLINE | ID: mdl-37898977

RESUMO

Following myocardial ischemic injury, the most effective clinical intervention is timely restoration of blood perfusion to ischemic but viable myocardium to reduce irreversible myocardial necrosis, limit infarct size, and prevent cardiac insufficiency. However, reperfusion itself may exacerbate cell death and myocardial injury, a process commonly referred to as ischemia/reperfusion (I/R) injury, which primarily involves cardiomyocytes and cardiac microvascular endothelial cells (CMECs) and is characterized by myocardial stunning, microvascular damage (MVD), reperfusion arrhythmia, and lethal reperfusion injury. MVD caused by I/R has been a neglected problem compared to myocardial injury. Clinically, the incidence of microvascular angina and/or no-reflow due to ineffective coronary perfusion accounts for 5-50% in patients after acute revascularization. MVD limiting drug diffusion into injured myocardium, is strongly associated with the development of heart failure. CMECs account for > 60% of the cardiac cellular components, and their role in myocardial I/R injury cannot be ignored. There are many studies on microvascular obstruction, but few studies on microvascular leakage, which may be mainly due to the lack of corresponding detection methods. In this review, we summarize the clinical manifestations, related mechanisms of MVD during myocardial I/R, laboratory and clinical examination means, as well as the research progress on potential therapies for MVD in recent years. Better understanding the characteristics and risk factors of MVD in patients after hemodynamic reconstruction is of great significance for managing MVD, preventing heart failure and improving patient prognosis.


Assuntos
Insuficiência Cardíaca , Infarto do Miocárdio , Traumatismo por Reperfusão Miocárdica , Humanos , Células Endoteliais/metabolismo , Infarto do Miocárdio/metabolismo , Miocárdio/metabolismo , Traumatismo por Reperfusão Miocárdica/metabolismo , Insuficiência Cardíaca/metabolismo
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA