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The role of platelet activating factor in the mechanism of nitric oxide synthases after regional myocardial ischemia-reperfusion injury

University of British Columbia

Myocardial infarction is one of the leading-causes of death in North America. Standard treatment for myocardial infarction consists of reperfusion of the ischemic area. However, several lifethreatening events occur after reperfusion is established. Evidence suggests that platelet activating factor and nitric oxide, two inflammatory mediators, have a main role during this myocardial ischemia-reperfusion injury. However, the mechanism through which these mediators exert their effects as well as a potential relationship between both, during regional myocardial ischemia-reperfusion injury, need to be investigated. The effect of PAF in modulation of NO-releasing enzymes (iNOS, eNOS), severity of cardiac contractile depression and myocardial infraction lesion in the late (48 h post-ischemic reperfusion) phase of MIR injury were investigated. An in-vivo rabbit model underwent 30 min of regional myocardial ischemia followed by 48 h of reperfusion and treated, during the ischemic period, with a PAF antagonist (TCV-309). It was found that PAF up-regulates iNOS expression and down-regulates eNOS expression in the ischemic-reperfused heart. Furthermore, PAF induced myocardial contractile depression and a more severe infarct lesion at 48 hours postischemia reperfusion. These effects were associated to iNOS expression, indicating that NO is an important mechanism through which PAF exerts its negative effects on myocardial infraction and cardiac contractility.

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2009-12-11

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http://hdl.handle.net/2429/16619

Surgery

University of British Columbia

UBCV

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