adp-beta-s and Myocardial-Ischemia

Blockage of a coronary artery, usually caused by arteriosclerosis, can lead to life threatening acute myocardial infarction. Opening with PCI (percutaneous coronary intervention), may be lifesaving, but reperfusion might exacerbate the cellular damage, and changes in the endothelium are believed to be involved in this worsened outcome.. The aim of the present study was to compare endothelial dependent and independent vasodilatory effect after experimental myocardial ischemia/reperfusion (I/R).. A well-established rat model of myocardial ischemia with 24 h of reperfusion was applied, followed by a study in a wire myograph.. Endothelial NO dependent relaxation in response to carbachol, was sensitive to arterial depolarization, and was unaffected by I/R. In contrast, endothelial NO dependent ADPβS signalling, which was not sensitive to arterial depolarization, was significantly reduced after I/R. Following I/R, an H

Topics: Adenosine Diphosphate; Animals; Calcitonin Gene-Related Peptide; Carbachol; Coronary Vessels; Endothelium, Vascular; Heart; Hydrogen Peroxide; Male; Myocardial Ischemia; Myocardial Reperfusion Injury; NG-Nitroarginine Methyl Ester; Nitric Oxide Synthase Type III; Purinergic P2Y Receptor Agonists; Rats, Sprague-Dawley; Thionucleotides; Vasodilation