Prostate Tissue-Induced Platelet Activation and Platelet-Neutrophil Aggregation Following Transurethral Resection of
Po-An Lin1, Hsiang-Han Huang1, Mei-Hua Hu2,3,4
1Department of Anesthesiology, Tri-Service General Hospital, National Defense Medical Center, Taipei 114202, Taiwan.
Abstract:
Background: This study aimed to investigate the effects of prostate tissue on platelet activation markers, primarily assessed through P-selectin expression, and to assess the formation of platelet-leukocyte aggregations in response to prostate tissue exposure. Furthermore, we compared platelet activation induced by prostate tissue homogenates with that induced by thrombin stimulation. These processes may play a role in the development of disseminated intravascular coagulation (DIC) following transurethral resection of the prostate (TURP). Methods: We collected prostate tissue samples from 12 patients undergoing TURP. The samples were homogenized and used to stimulate platelet-rich plasma in vitro. Flow cytometry was used to measure platelet P-selectin expression and platelet-leukocyte aggregation. Additionally, four experimental groups were established: (A) saline control, (B) thrombin stimulation, (C) phosphate-buffered saline (PBS) control, and (D) prostate tissue homogenate. Data were analyzed to assess the impact of prostate tissue and thrombin on platelet activation and platelet-leukocyte interactions. Results: Prostate tissue homogenates significantly increased platelet P-selectin expression and platelet-neutrophil aggregation compared with the control groups (p < 0.05). Overall, platelet-leukocyte aggregation was not significantly different between the thrombin and prostate tissue groups. However, prostate tissue exposure did not significantly affect platelet-monocyte and platelet-lymphocyte aggregations. Conclusions: Prostate tissue exposure during TURP induces platelet activation, particularly platelet P-selectin expression and platelet-neutrophil aggregation, suggesting a potential mechanism for DIC development. These findings highlight the importance of monitoring platelet activity in patients undergoing TURP and indicate that interventions targeting platelet P-selectin expression and platelet-neutrophil interactions may help mitigate DIC risk.
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