The events which follow a cerebral ischemia-reperfusion injury are complex but are mediated by an inflammatory response involving the activation of leukocytes and platelets. The formation of leukocyte-platelet aggregates (LPA) may amplify immunologic functions and increase the severity of reperfusion injury following ischemic stroke. However prior to this study it was unknown whether LPA could be detected in peripheral blood following ischemic stroke and reperfusion (ISR).
Using a rat model LPA in peripheral blood was detected following ischemic stroke and early reperfusion, and also the effect that LPA inhibitors have on LPA formation was studied. Separate groups used tirofiban and fucoidan. Tirofiban is a platelet GPIIb/IIIa inhibitor and fucoidan is a selectin adhesion molecule inhibitor. Since there is also little known about nonadhered polymorphonuclear neutrophilic (PMN) leukocytes following ISR, PMN CD11b adhesion molecule expression and ROS were measured. Following 4 hours of ischemia and 1 hour of reperfusion there was an increase in LPA following ISR, and both tirofiban and fucoidan decreased LPA formation. CD11b showed a small nonsignificant increase and ROS had a significant increase during both ischemia and reperfusion in the SHAM animals. (SHAM animals were the control group that did not undergo placement of the occluding filament.) This may have resulted due to the PMNs in the ISR group being rapidly activated and unable to produce ROS.
Although this study provides evidence that LPA are increased in peripheral blood during early reperfusion following an acute ischemic stroke, there is still very little known of LPA occurence and significance. However the findings of this study may lead to future developments in therapies that target decreasing leukocyte-platelet aggregates to avoid reperfusion injury following ischemic stroke.
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3 comments:
so i know that you summarized the article but what are your personal views on LPA? did you think that there findings in the study provided enough substantial evidence of LPA?
I thought the article did a great job of describing how the experiment was conducted, and the effect of different LPA inhibitors on LPA formation. I think the results they found were easily depicted throughout the charts and based on their observations and other clinical experiments they referred to, there seems to be a correlation with leukocyte-platelet aggregate formation and ischemic stroke. The study in the article involved LPA levels in peripheral blood during early reperfusion however they mention it is still an area that hasn't been fully explored so more research in this area would be needed to determine a definate correlation.
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