Preconditioning ischemia attenuates molecular indices of platelet activation‐aggregation

Background: Previous studies have shown that ischemic preconditioning (PC) not only limits infarct size, but also improves arterial patency in models of recurrent thrombosis. We hypothesize that this enhanced patency is presumably because of a PC‐induced attenuation of platelet‐mediated thrombosis....

Full description

Saved in:
Bibliographic Details
Published in:Journal of thrombosis and haemostasis 2006-12, Vol.4 (12), p.2670-2677
Main Authors: LINDEN, M. D., WHITTAKER, P., FRELINGER, A. L., BARNARD, M. R., MICHELSON, A. D., PRZYKLENK, K.
Format: Article
Language:English
Subjects:
Animals
Blood Flow Velocity
Blood Platelets - metabolism
Coronary Circulation
Coronary Thrombosis - blood
Coronary Thrombosis - pathology
Coronary Thrombosis - physiopathology
Coronary Thrombosis - prevention & control
Coronary Vessels - pathology
Coronary Vessels - physiopathology
Disease Models, Animal
Dogs
fibrinogen
Fibrinogen - metabolism
heterotypic aggregates
ischemia
Ischemic Preconditioning, Myocardial
Myocardial Reperfusion Injury - blood
Myocardial Reperfusion Injury - pathology
Myocardial Reperfusion Injury - physiopathology
Myocardial Reperfusion Injury - prevention & control
P-Selectin - metabolism
Platelet Activation
Platelet Adhesiveness
Platelet Aggregation
platelets
P‐selectin
Random Allocation
thrombosis
Vascular Patency
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Background: Previous studies have shown that ischemic preconditioning (PC) not only limits infarct size, but also improves arterial patency in models of recurrent thrombosis. We hypothesize that this enhanced patency is presumably because of a PC‐induced attenuation of platelet‐mediated thrombosis. However, there is, at present, no direct evidence that PC acts on the platelets per se and favorably down‐regulates platelet reactivity. Objectives: Our goal was to test the concept that PC ischemia attenuates molecular indices of platelet activation‐aggregation. Methods: Anesthetized dogs were randomly assigned to receive 10 min of PC ischemia followed by 10 min of reperfusion or a time‐matched control period. Spontaneous recurrent coronary thrombosis was then initiated in all dogs by injury + stenosis of the left anterior descending coronary artery. Coronary flow was monitored for 3 h poststenosis, and molecular indices of platelet activation‐aggregation were quantified by whole blood flow cytometry. Results: Coronary patency was, as expected, better‐maintained following injury + stenosis in the PC group vs. controls (53% ± 5%* vs. 23% ± 5% of baseline flow, respectively; *P 
ISSN:1538-7933
1538-7836
1538-7836
DOI:10.1111/j.1538-7836.2006.02228.x