动物造模,心肌炎 z-bo 2022-04-25 648

　　(1) Reproduction method For experimental mice weighing 25～30g, first observe the experimental animals for 3 days, select healthy animals for modeling. The modeling method is to pass the diphtheria toxin stock solution through the tail of the mouse at a dose of 7.30μ/g body weight. Intravenous injection. 30min after the injection, the medicine should be injected after the diphtheria is basically absorbed. Observation indicators include ① Body temperature. The rectal temperature was measured 2 days before the experiment, and 4 times every 24 hours after diphtheria toxin was administered until death. ② Respiration and general activity status and food intake are recorded every 6h. ③ ECG, start 2 days before the experiment, do it twice a day. Method: Puncture a needle electrode on each of the extremities and chest. ④Cardiology, after each mouse died, the chest cavity was opened and the heart was taken out to make pathological specimens, and sliced for optical and electron microscope observation. ⑤The time of death shall be observed and recorded every hour.

　　(2) Model characteristics The mouse myocarditis model caused by diphtheria toxin is an acute progressive disease, with a rapid onset, and the survival time of model animals is short, about 2 days. The body temperature of the animals increased 6 hours after the injection of diphtheria toxin, with an average increase of 0.9°C. Compared with the pre-experimental ECG after 24 hours, the PR interval of each group was prolonged, the ST segment was elevated, and the heart rate of all animals was fast and irregular; The main pathological changes are degeneration and necrosis of myocardial cells, sarcoplasmic degeneration and progressive sarcolysis, and inflammatory cell infiltration.

　　(3) Comparative medicine Clinical diphtheria patients often have acute diphtheria toxic myocarditis. Using diphtheria toxin to intravenously inject mice, the acute myocarditis model caused by clinical diphtheria bacillus infection has many similarities in pathogenesis, symptoms, signs and pathological changes. The manifestations are elevated body temperature, abnormal electrocardiogram, degeneration and necrosis of myocardial cells, sarcoplasmic agglutination, progressive sarcolysis and inflammatory cell infiltration.