动物实验,血小板线粒体 z-bo 2020-08-22 630

　　Objective: To explore the changes of platelet mitochondria after ischemia-reperfusion injury of the tourniquet, and to provide guidance for the clinical application of the tourniquet.

　　Method: 30 SD rats were randomly divided into a control group (6) and an ischemia/reperfusion group (24). After reperfusion, the blood samples were divided into 4 groups at 2, 6, 12 and 24 hours. Randomly divided. Detection). A self-made tourniquet was used to surround the bottom of the white rabbit’s thigh (pressure 280 mmHg) to simulate tourniquet ischemia, and it was released 4 hours later. At the corresponding time point, blood was taken to separate platelets. The platelet count was measured with an automatic hemocytometer, and the platelet ATP content was measured with a luciferin-luciferase kit. The JC-1 Mitochondrial Membrane Potential Kit was used to detect the changes in mitochondrial membrane potential (△ym), and the Cytochrome C Apoptosis Kit was used to detect platelets, and the cytoplasmic cytochrome C content and lipid peroxides in the platelets were detected. Lipid peroxidation kit for detection.

　　Results: The platelet ATP content of the ischemia-reperfusion injury group was significantly lower than that of the control group at 2 and 6 hours (P0.05). There was no statistical difference in platelet count between the two groups (P\→0.05).

　　Conclusion: Tourniquet ischemia-reperfusion injury can lead to impaired platelet mitochondrial function, which mainly occurs in the early stage of ischemia-reperfusion (6 hours), and has a significant impact on platelet count.