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• W2514094329 endingPage "50" @default.
• W2514094329 startingPage "14" @default.
• W2514094329 abstract "espanolEsta Revision se centra en la isquemia-reperfusion del miocardio, prestando particular atencion al papel del oxido nitrico (NO) y endothelina-1 (ET-1) en la regulacion de la circulacion coronaria en condiciones normales y tras la isquemia-reperfusion. La ateromatosis coronaria suele estar causada por disfuncion/dano endotelial, y lidera las causas de los sindromes coronarios agudos (p. e., infarto agudo de miocardio, IAM). El tratamiento mas eficaz del IAM es la reperfusion del territorio de miocardio isquemico, pero este procedimiento tambien causa lesion del miocardio (lesion por reperfusion), cuya fisiopatologia y tratamiento siguen siendo inciertos. La interaccion entre el NO y ET-1 es relevante en la regulacion de la circulacion coronaria, y en condiciones normales predomina el NO sobre la ET-1. La circulacion coronaria desempena un papel crucial en la isquemia-reperfusion puesto que ella es la causa y victima de las consecuencias de esta situacion. La isquemia-reperfusion dana no solo el miocardio, sino tambien el lecho vascular coronario, aumenta los niveles plasmaticos de ET-1, induce el predominio de la ET-1 sobre el NO, aumenta la respuesta coronaria alaET-1 y altera el papel de sus receptores en esta respuesta. Todo ello podria contribuir a la disfuncion de la circulacion coronaria y el fenomeno de no-reflujo y, como consecuencia, a la lesion por reperfusion. Asi, la ET-1 podria ocupar un papel destacado en la fisiopatologia de la lesion por reperfusion, y el uso de antagonistas de los receptores ETA/ETB podria proteger al corazon frente a la lesiones por reperfusion. EnglishThis Review focus on the myocardial ischemia-reperfusion, paying particular attention to the role of nitric oxide (NO) and endothelin-1 (ET-1) in the regulation of the coronary circulation under normal conditions and after ischemia-reperfusion. Coronary atheromatosis is usually induced by endothelium dysfunction/damage, and is the main cause of acute coronary syndromes (e. g., acute myocardial infarction, AMI). The assessment of endothelial function of patients with coronary artery disease may provide useful information. The most effective treatment of AMI is timely reperfusion for restoring the blood flow to the ischemic myocardial territory, but this procedure may also damage myocardium (reperfusion injury), of which the pathophysiology and treatment remain uncertain. The interaction between NO and ET-1 may be relevant for regulating the coronary circulation, with predominance of NO over ET-1 under normal conditions. The coronary circulation plays a crucial role in ischemia-reperfusion since it is the cause and victim of consequences of this condition. Ischemia-reperfusion damages not only the myocardium but also coronary vasculature, including the endothelium, increases plasma levels of ET-1, induces functional predominace of ET-1 over NO, augments the coronary response to ET-1, and alters the role of endothelin receptors in this response. All these alterations may lead to dysregulation of coronary vasculature and the non-reflow phenomenon, which may underly reperfusion injury. Thus, ET-1 could be of significance in pathophsysiology of ischemia-reperfusion and reperfusion injury, and the use of antagonists for endothelin ETA/ETB receptors could protect the heart against reperfusion injury." @default.
• W2514094329 created "2016-09-16" @default.
• W2514094329 creator A5048072549 @default.
• W2514094329 date "2016-01-01" @default.
• W2514094329 modified "2023-09-28" @default.
• W2514094329 title "Coronary ischemia-reperfusion: role of nitric oxide and endothelin-1. A Review" @default.
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