Qualitative analysis of platelet rich plasma prepared by acute plateletpheresis in patients undergoing heart surgery / 中国实验血液学杂志

This study was aimed to evaluate the efficiency and effectiveness of platelet-rich plasma(PRP) prepared by acute plateletpheresis in patients undergoing open heart surgery, and to analyze the quality of prepared platelet-rich plasma. Whole blood from 20 patients with ASAII-III was collected and PRP was harvested by machine after induction of anesthesia. Platelet count (Plt), mean platelet volume (MPV), platelet distribution width (PDW), plasma pH, plasma lactic acid (LA) concentration, and lactic dehydrogenase (LDH) concentration, germiculture result, CD62p and PAC-1 positive rate of inactivated and activated platelets by ADP in the whole blood before plateletpheresis (T1) , in the PRP after plateletpheresis (T2) and PRP before back-transfusion (T3) were determinated. The results showed that as compared with whole blood the platelet count in the PRP at T2 was (783 ± 184) ×10(9)/L, MPV, PDW and pH significantly decreased (P < 0.01) , while the plasma LDH, LA concentration, CD62p and PAC-1 positive rate of inactivated platelets were not significantly different from the whole blood at T1. In the PRP at T3, the platelet count, MPV, PDW and pH significantly decreased (P < 0.01) , while plasma LDH concentration, CD62p and PAC-1 positive rate of inactivated platelet significantly increased (P < 0.05 or P < 0.01) compared with the whole blood at T1. There were no significant difference among the CD62p and PAC-1 positive rate of activated platelets in the whole blood and PRP. It is concluded that PRP can be efficiently obtained from the patients undergoing open heart surgery by acute plateletpheresis, and the platelets in PRP are not activated during the preparing process. Some platelets in PRP are activated during the preserving process, but the whole activating function of platelets keeps normal.

Heat shock protein 27 regulates oxidative stress-induced apoptosis in cardiomyocytes: mechanisms via reactive oxygen species generation and Akt activation / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Increased reactive oxygen species (ROS) formation, which in turn promotes cardiomyocytes apoptosis, is associated with the pathogenesis and progression of various cardiac diseases such as ischemia and heart failure. Recent studies have shown that over expression of heat shock protein 27 (Hsp27) confers resistance to cardiac ischemia/reperfusion injury. However, not much is known about the regulation of myocyte survival by Hsp27.</p><p><b>METHODS</b>The rat cardiac cell line H9c2, with a stable overexpression of Hsp27, was established, with empty vector transfected H9c2 cells as controls. Following the cells challenged by Hydrogen Peroxide (H2O2), lactate dehydrogenase (LDH) release, apoptosis, intracellular ROS, cell morphology, mitochondrial transmembrane potential and the activation of serine/threonine kinase Akt were determined.</p><p><b>RESULTS</b>Along with marked suppression of H2O2-induced injury by Hsp27 overexpression in H9c2 cells, ROS generation and the loss of mitochondrial membrane potential were also significantly depressed. Furthermore, augmented Akt activation was observed in Hsp27 overexpressed H9c2 cells following H2O2 exposure.</p><p><b>CONCLUSIONS</b>Hsp27 inhibits oxidative stress-induced H9c2 damage and inhibition of ROS generation and the augmentation of Akt activation may be involved in the protective signaling.</p>