[Animal modeling] - Animal model of myocardial infarction and blood stasis syndrome caused by coronary artery ligation

  (1) Reproduction method: Adult dogs were anesthetized and subjected to tracheal intubation for artificial respiration. The chest was opened in the fourth intercostal space on the left edge of the sternum, the heart was exposed, and a pericardial bed was sewn. After stabilizing for 30 minutes, blood flow was blocked above the second branch of the left anterior descending coronary artery. Lidocaine was injected at a dose of 8mg/kg body weight before blocking. 1-3 minutes after blocking, the color of the outer membrane of the ischemic zone of the myocardium darkened, and the degree of myocardial ischemia was continuously monitored by electrocardiogram. Local blood collection from the right atrium before and after coronary artery occlusion was performed to detect platelet aggregation rate, platelet count, TxB2, 6-keto-PGF1a. After 6 hours of coronary artery occlusion, animals were euthanized and their hearts were taken out for pathological examination.

  (2) When acute myocardial ischemia is caused by blocking the coronary artery, the platelet aggregation rate shows a progressive increase, and it is most obvious 60 minutes after ischemia. The platelet count gradually decreases and reaches its lowest value at 60 minutes. After 5 minutes of coronary artery occlusion, TxB2 began to increase and reached its maximum value at 60 minutes. The 6-keto-PG1a orifice decreased at 5 minutes after ischemia and gradually increased thereafter, but did not return to pre occlusion levels. At 60 minutes after ischemia, 6-keto-PGF1a decreased again, and the TxB2/6-keto-FGF1a ratio gradually increased at 5 minutes after ischemia and reached its maximum value at 60 minutes after ischemia.

  (3) After acute coronary artery occlusion in comparative medicine, significant abnormalities in platelet function can occur in the circulating blood. Abnormal changes in platelet aggregation function have the effect of increasing vasoconstriction, reducing the amount of blood flowing from coronary collateral into the peripheral ischemic zone, and expanding the scope of ischemic injury.