动物造模,药效评价,心肌病 z-bio 2024-09-23 424

　　1. Experimental animals: Wistar rats, weighing 170-200g, male or female not limited. Rabbit modeling 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, followed by 1 week for a total of 6 times, with a total dose of 15mg/kg. After the last injection was completed, the rats were observed for 4 weeks.

　　3. Experimental observation content determination method: Ultrasound monitoring of cardiac function, measuring the M2 curve of left ventricular long axis section and left ventricular papillary muscle level, continuously measuring the 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) for three cardiac cycles, taking their average values, and calculating the left ventricular ejection fraction and left ventricular shortening fraction (LVEF, LVFS) using Simpson's method. The calculation formula is LVEF=L (LVDV-LVSV)/LVDV * 100%, LVFS=[(LVDD-LVSD)/LVDD * 100%, as follows: Cardiac function parameter indicators.

　　4. Reference results: From the beginning of injection of doxorubicin, Wistar rats showed no increase in body weight, reduced food intake, and low response. As the injection dose increased, the above symptoms gradually worsened. After complete injection of doxorubicin, the body weight of rats showed a significant negative increase (body weight decreased by 40-50g), indicating poor response. During the 4-week observation period, the mortality rate was highest 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 myocardial disease group showed a reduction in heart cavity size, thickening of the left ventricular posterior wall, decreased left ventricular posterior wall motion, significant decrease in LVEF and LVFS, decrease in LVDD and LVDV, and increase in LVSD in myocardial disease mice.