Data/hora: 01/06/2024 04:24:44

Provedor de dados: | Brazilian Journal of Medical and Biological Research
País: | Brazil
Título: | Coronary endothelial dysfunction after ischemia and reperfusion: a new therapeutic target?
Autores: | Laude,K.; Thuillez,C.; Richard,V.
Data: | 2001-01-01
Ano: | 2001
Palavras-chave: | Coronary endothelium; Ischemia/reperfusion; Preconditioning.
Resumo: | Although cardiac ischemia is usually characterized as a disease of the myocyte, it is clear that the vasculature, and especially endothelial cells, is also a major target of this pathology. Indeed, using a rat model of ischemia/reperfusion, we were able to detect severe endothelial dysfunction (assessed as a decreased response to acetylcholine) after acute or chronic reperfusion. Given the essential role of the endothelium in the regulation of vascular tone, as well as platelet and leukocyte function, such a severe dysfunction could lead to an increased risk of vasospasm, thrombosis and accelerated atherosclerosis. This dysfunction can be prevented by free radical scavengers and by exogenous nitric oxide. Endothelial dysfunction can also be prevented by preconditioning with brief periods of intermittent ischemia, thus extending to coronary endothelial cells the concept of endogenous protection previously described at the myocyte level. Experiments performed on cultured cells showed that the endothelial protection induced by free radical scavengers or by preconditioning was due to a lesser expression of endothelial adhesion molecules such as intercellular adhesion molecule-1, leading to a lesser adhesion of neutrophils to endothelial cells. Identification of the mechanisms of this protection may lead to the development of new strategies aimed at protecting the vasculature in ischemic heart diseases.
Tipo: | Info:eu-repo/semantics/article
Idioma: | Inglês
Identificador: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2001000100001
Editor: | Associação Brasileira de Divulgação Científica
Relação: | 10.1590/S0100-879X2001000100001
Formato: | text/html
Fonte: | Brazilian Journal of Medical and Biological Research  v.34 n.1 2001
Fonte: | info:eu-repo/semantics/openAccess