No abstract

1. The leucocyte-mediated inflammatory response plays a pivotal role in ischaemia-reperfusion injury. P-Selectin and CD11b are important mediators for the recruitment of leucocytes into the endothelium. However, the time-course of changes in P-selectin and CD11b expression during reperfusion is not defined. Magnesium has been shown to have a protective role in reperfusion injury, but the mechanism of its action is not yet clear. 2. In the present study, 90 male Sprague-Dawley rats were randomized into three groups, namely a sham-operated group, an IR group (subjected to 45 min of coronary occlusion followed by reperfusion for up to 6 h) and an MgSO(4)-treated group, which received an infusion of MgSO(4) starting 30 min before occlusion and continuing until the onset of reperfusion. The expression of P-selectin on platelets and CD11b on leucocytes, endothelial P-selectin on cardiac microvessels and P-selectin mRNA in myocardial tissue were measured by flow cytometry, immunohistochemistry and reverse transcription-polymerase chain reaction, respectively, at different time points during reperfusion. The degree of myocardial necrosis and arrhythmia was assessed. 3. The present study shows that P-selectin expression on platelets and cardiac microvessels, P-selectin mRNA in myocardial tissue and CD11b expression on leucocytes in the IR group were significantly upregulated compared with the sham-operated group in a time-dependent manner during reperfusion. Treatment with MgSO(4) attenuated the upregulation of P-selectin expression, in addition to inhibiting myocardial necrosis and arrhythmia, but had no effect on CD11b expression on leucocytes. 4. These results suggest that the expression of P-selectin and CD11b is upregulated after reperfusion and magnesium pretreatment plays a cardioprotective role in ischaemia-reperfusion injury, possibly by inhibiting the upregulation of P-selectin expression.

Abstract:Objective: This study aims to determine the mechanisms underlying restenosis and ischemia-reperfusion injury of the myocardium after percutaneous coronary intervention (PCI). Methods: The present study examined serial changes (5 min, 30 min, 2 h, 6 h, and 24 h after PCI) in circulating P-selectin, plasminogen activator inhibitor-1 (PAI-1), magnesium (Mg), and creatine kinase-myocardial band fraction (CK-MB) levels, which may be associated with restenosis and myocardial injury in patients undergoing PCI. The occurrence rates of major adverse cardiovascular events were collected over a six-month follow-up. Results: PCI induced an early elevation of P-selectin, which correlated positively with the inflation pressure used in the PCI procedure. PCI also caused a significant and sustained decrease in serum Mg in PCI patients, without an effect on PAI-1. An increase in CK-MB was observed in PCI patients, although values were within normal reference range. In addition, elevated P-selectin and decreased Mg measured shortly after the coronary angioplasty procedure were associated with recurrent treatment and heart failure, respectively. Conclusions: Our study demonstrates that PCI induces temporal changes of P-selectin, Mg, and CK-MB, which may be involved in restenosis and ischemia-reperfusion injury. These findings highlight the need for using antiplatelet therapy and Mg to reduce the risks associated with PCI.