动物造模,心肌病模型 z-bio 2023-11-07 883

　　1. Experimental animal: Wistar rats, 170-200g, regardless of gender. Rabbit models can also be used.

　　2. Experimental method: Wistar rats were intraperitoneally injected with doxorubicin at a dose of 2.5mg/(kg · time), 3 times per week, with an interval of 2 weeks. The rats were then used for another 1 week, with a total dose of 15mg/kg. After the last injection was completed, the rats were observed for 4 weeks.

　　3. Experimental observation content measurement method: Ultrasound monitoring of cardiac function. M2 type curves were measured at the left ventricular long axis section and left ventricular papillary muscle level. Left ventricular end diastolic diameter (LVDD, mm), left ventricular end systolic diameter (LVSD, mm), left ventricular end diastolic volume (LVDV), and left ventricular end systolic volume (LVSV) were continuously measured for three cardiac cycles, and their average values were taken, The Simpson method was used to convert left ventricular ejection fraction and left ventricular shortening fraction (LVEF, LVFS). The calculation formula is: LVEF=L (LVDV LVSV)/LVDV] × 100%, LVFS=[(LVDD LVSD)/LVDD] × 100%, as a cardiac function parameter indicator.

　　4. Reference results: From the beginning of the injection of doxorubicin, Wistar rats showed no increase in body mass, decreased food intake, and low response. As the injection dose increased, the above symptoms gradually worsened. After the completion of doxorubicin injection, the rats showed a significant negative increase in body mass (a decrease of 40-50g in body mass) and poor response. During the 4-week observation period, the highest mortality rate was observed at 2-3 weeks (58%), with a 1-week mortality rate of 16.7% and a 4-week mortality rate of 21.5%. Microscopic examination: Changes such as swelling of myocardial cells, narrowing of gaps, localized rupture of myocardial fibers, and dilation of blood vessels in the myocardial interstitium can be observed. Ultrasound: The cardiomyopathy group showed a narrowing of the heart cavity, thickening of the left ventricular posterior wall, decreased left ventricular posterior wall motion, and a significant decrease in LVEF and LVFS, as well as a decrease in LVDD and LVDV, and an increase in LVSD in cardiomyopathy mice.