Myocardial protection against reperfusion injury: The cGMP pathway

David Garcia-Dorado; Luis Agulló; Carmem Lluisa Sartorio; Marisol Ruiz-Meana

doi:10.1160/TH08-11-0764

Thrombosis and Haemostasis, Inhaltsverzeichnis

Thromb Haemost 2009; 101(04): 635-642
DOI: 10.1160/TH08-11-0764

Theme Issue Article

Schattauer GmbH

Myocardial protection against reperfusion injury: The cGMP pathway

David Garcia-Dorado

¹Laboratorio de Cardiología Experimental, Area del Cor, Hospital Universitari Vall d’Hebron, Barcelona, Spain

,

Luis Agulló

¹Laboratorio de Cardiología Experimental, Area del Cor, Hospital Universitari Vall d’Hebron, Barcelona, Spain

,

Carmem Lluisa Sartorio

¹Laboratorio de Cardiología Experimental, Area del Cor, Hospital Universitari Vall d’Hebron, Barcelona, Spain

,

Marisol Ruiz-Meana

¹Laboratorio de Cardiología Experimental, Area del Cor, Hospital Universitari Vall d’Hebron, Barcelona, Spain

› Institutsangaben

Abstract

Summary

Reperfusion injury may cause myocardial cell death and limit the benefit achieved by restoration of coronary artery patency in patients with acute myocardial infarction. The mechanism includes altered Ca²⁺ handling with cytosolic and mitochondrial Ca²⁺ overload, Ca²⁺- and ATP-dependent hypercontraction, cytoskeletal fragility, mitochondrial permeability transition and gap junction-mediated propagation of cell death, as well as alterations in non-cardiomyocyte cells, in particular platelets and endothelial cells. cGMP modulates favorably all these mechanism, mainly through PKG-mediated actions, but cGMP synthesis is altered in reperfused cardiomyocytes and endothelial cells by mechanisms that are only partially understood. Stimulation of cGMP synthesis during initial reperfusion by means of natriuretic peptides has been found protective in different animal models and in patients. Moreover, increasing evidence indicates that cGMP is an important step in signal transduction of endogenous cardioprotection. Thus, the cGMP pathway appears as a key element in the pathophysiology of myocardial ischaemiareperfusion and as a promising therapeutic target in patients with acute myocardial infarction.

Keywords

Ischaemic heart disease - platelet physiology - acute myocardial infarction

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Referenzen

References
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