动物造模,血栓模型 z-bio 2023-10-11 1656

　　1. Animal modeling materials: Healthy male SD rats, weighing around 200-250g; Medication: 20% Ulatan, 30% FeCl3; Instrument: Physiological multi-channel instrument.

　　2. Method of modeling: Rats fasted for 8 hours, drank freely, and were anesthetized by intraperitoneal injection of 20% urethane (5ml/kg). Femoral artery blood pressure was monitored on a physiological multi-channel instrument through a transducer. A median abdominal incision was made, and a 2cm long abdominal aorta was freed. Filter paper soaked in 30% FeCl3 (1cm) was used × Carefully wrap the abdominal aorta (1cm) (carefully protect surrounding tissues), remove the filter paper strip after 30 minutes, and observe for 10 minutes before ending the experiment.

　　3. Modeling principle: Cover the abdominal aorta of rats with a filter paper strip soaked in 30% FeCl3. Through the production of oxygen free radicals, cause lipid peroxidation damage to the vascular intima, activate the endogenous coagulation system, and promote the formation of intravascular thrombosis.

　　4. Changes in femoral artery blood pressure in the model group animals after thrombus replication (5.19 ± 1.29) kPa decreased by 60% compared to before thrombus replication (13.33 ± 1.26) kPa, indicating severe occlusion of the abdominal aorta. Thrombosis rich in protein, with a wet weight of (28.63 ± 0.98) mg, a dry weight of (7.27 ± 0.98) mg, and a protein quantification of (926.79 ± 73.23) μ g. Pro/mg · DW. Thrombosis (model group) activated both plasminogen activator inhibitors and tissue plasminogen activator, with higher levels of tPA and PAI compared to the control group, while PAI/tPA significantly decreased.