Abstract
Objective:To evaluate the effects of ischemic postconditioning on expressions of pentraxin-related protein 3 (PTX3) and neutrophil CD11b in the plasma of patients with acute myocardial infarction (AMI) after percutaneous coronary intervention (PCI).Methods:Fifty-six patients who had AMI with ST-segment elevation were randomly divided into a control group and an ischemic postconditioning group (n=28). Both groups received emergency PCI. After recanalization of infarct-related arteries, the control group did not receive intervention within three minutes, while the ischemic postconditioning group was treated by low-pressure filling and emptying of balloon within one minute. The plasma expressions of PTX3 before and 24 hour after PCI were detected by ELISA, and those of neutrophil CD11b were detected by flow cytometry.Results:PTX3 and neutrophil CD11b expressions of the two groups were similar before PCI, but those of the ischemic postconditioning group significantly decreased 24 hour after PCI (P<0.05).Conclusion:Ischemic postconditioning lowered the expressions of PTX3 and neutrophil CD11b in AMI patients after PCI, inhibited inflammatory response, reduced the adhesion between leukocytes and endothelial cells, and protected the ischemic-reperfused myocardium.
Highlights
Ischemic postconditioning, which refers to several cycles of reperfusion-ischemia performed immediately after reperfusion, can protect the myocardium by decreasing infarct area and1
PTX3 and neutrophil CD11b expression levels: PTX3 and neutrophil CD11b expressions of the two groups were similar before percutaneous coronary intervention (PCI) (P>0.05), but those of the ischemic postconditioning group significantly decreased 24 h after PCI (P
By establishing a canine model of ischemia-reperfusion, Zhao et al.[1] found that ischemic postconditioning protected the myocardium from reperfusion injury, which has been verified in many other animal models
Summary
Ischemic postconditioning, which refers to several cycles of reperfusion-ischemia performed immediately after reperfusion, can protect the myocardium by decreasing infarct area and. Ya Li, 1-4: Department of Cardiology, Affiliated Hospital of Hebei University, Baoding 071000, China. Correspondence: November 26, 2015 January 15, 2016 relieving reperfusion-induced arrhythmias.[1,2,3] On the other hand, inflammatory response plays an important role in the onset and progression of AMI. Whether ischemic postconditioning affects pentraxin-related protein 3 (PTX3) and CD11b as crucial inflammatory mediators has never been reported. We aimed to assess the influence of ischemic postconditioning on PTX3 and CD11b expressions
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