No abstract

Background: Patients undergoing cardiac surgery are at increased risk of bleeding due to multifactorial coagulopathies. In the present study, we aimed at investigating the changes in platelet count and function during and after surgery as well as determining the association of the platelet dysfunction with bleeding and transfusion requirements in these patients. Methods: A total of 40 adult patients scheduled for elective valve coronary cardiac surgery were included in this prospective observational study. Changes in platelet count and function with ADP, acid arachidonic, and collagen (light transmission aggregometry) were analyzed at three time points: before CPB, after CPB, and 24 hours after end of surgery. Postoperative bleeding and intraoperative transfusion requirements were recorded. Results: There were a significant reverse correlation between CPB time and ADP-induced aggregation, particularly after CPB and postoperative AA-induced aggregation. There was not any significant correlation between platelet count and function at all-time points. Both platelet count and platelet aggregation significantly reduced during CPB. While platelet aggregation increased on postoperative Day 1, platelet count reduced by about 40% after CPB, and remained at this level postoperatively. Patients with abnormal ADP-induced aggregation had significant increased postoperative bleeding and transfusion requirements. Conclusion: The results of this study demonstrate that platelet count and platelet aggregation are reduced during CPB. Our results emphasized the effect of platelet dysfunction on increased postoperative bleeding and transfusion requirements. Perioperative monitoring of platelet function can be considered as a bleeding management strategy for implantation of PBM programs.

Purpose: Mesenchymal stem cells (MSCs) release hematopoietic cytokines, growth factors, and Microvesicles (MVs) supporting the hematopoietic stem cells (HSCs). MVs released from various cells, playing a crucial role in biological functions of their parental cells. MSC-derived MVs contain microRNAs and proteins with key roles in the regulation of hematopoiesis. Umbilical cord blood (UCB) is a source for transplantation but the long-term recovery of platelets is a main problem. Therefore, we intend to show that MSC-MVs are able to improve the differentiation of UCB-derived CD34+ cells to megakaryocyte lineage. Methods: In this descriptive study, MSCs were cultured in DMEM to collect the culture supernatant, which was ultracentrifuged for the isolation of MVs. HSCs were isolated from UCB using MACS method and cultured in IMDM supplemented with cytokines and MVs in three different conditions. Megakaryocyte differentiation was evaluated through the expression of specific markers and genes after 72 hours, and the data was analyzed by t test (P<0.05). Results: The expression of specific megakaryocyte markers (CD41 and CD61) in the presence of different concentrations of MSC-MVs did not show any significant difference. Also, the expression of specific genes of megakaryocyte lineage was compared with control group. The expression of GATA2 and c-Mpl was significantly increased, GATA1 was not significantly decreased, and FLI1 was significantly decreased. Conclusion: MSC-MVs could improve the expression of specific megakaryocyte genes; however, there was no significant expression of CD markers. Further studies, including the evaluation of late stages of megakaryocyte differentiation, are required to evaluate platelet production and shedding