By vantal Changes of left ventricular systolic function during the pathological process of heart failure in experimental miceOn the other hand, suture kit It also brings tangible benefits to everyone and feels useful. It is a model of the industry. https://pinnaclemedics.com/
Ejection fraction and short axis shortening rate reflect left ventricular myocardial shortening and left ventricular emptying function respectively, which are two main indexes to evaluate cardiac systolic function as a whole. The results showed that the cardiac ejection fraction and short axis shortening rate were significantly higher than those before modeling, suggesting that the compensatory function of left ventricular systolic function was enhanced due to pressure overload. At 4 weeks, the cardiac ejection fraction and short axis shortening rate decreased significantly compared with those at 2 weeks, but there was no significant difference before modeling, suggesting that the compensatory systolic function of left ventricle gradually lost. When the disease lasted for 8 weeks, the cardiac ejection fraction and short axis shortening rate further decreased, which were significantly different from those in 2 and 4 weeks.
In addition, the cardiac stroke output of the experimental mouse fixator decreased continuously after modeling. To sum up, in the pathological process of heart failure induced by pressure overload in mice, the systolic function of the heart first increased compensatively, and with the development of the disease, the systolic function was continuously lost until it was decompensated. Cardiac ejection fraction and short axis shortening rate at each week after operation.
Experimental mouse fixing frame
2.4 Evaluation of left ventricular diastolic function in the pathological process of heart failure in mice
Left ventricular diastolic function was evaluated by mitral orifice blood flow Doppler combined with mitral annulus tissue Doppler.
The results of blood flow Doppler showed that compared with before modeling, the isovolumic contraction time of mitral valve orifice was prolonged at 2 and 4 weeks, but there was no significant difference, and it was significantly prolonged at 8 weeks, and the isovolumic relaxation time was significantly prolonged at 2, 4 and 8 weeks. There was no significant change in ejection time at each time point. The above results suggest that cardiac function is impaired. Experimental mouse fixing frame.
The peak velocity of E in mitral valve orifice early diastolic period decreased significantly in the 2 nd and 4 th week groups, and it increased in the 4 th week group. There was no significant change in peak velocity of E in the 8-week group. The peak velocity of blood flow a in the late diastolic period decreased significantly only in the 8-week group. By calculating the peak velocity ratio E/A, it can be seen that the peak velocity ratio first decreases, and then increases, in which the 2-week group shows a significant decrease, the 4-week group shows a significant increase, and the 8-week group shows a significant increase (Figure 5B). Tissue Doppler e’ and a’ of mitral annulus represent the velocity of mitral annulus in early and late diastole respectively.
Experimental mouse mouth gag
The results showed that compared with 0 week, e’,a’ and e’/a’ were significantly decreased at 2, 4 and 8 weeks, indicating that the diastolic function of the heart was impaired. Combined with the measurement results of mitral flow Doppler and mitral annulus tissue Doppler, the analysis of E/e’ value shows that the value of this index has changed significantly at 0 week and at 2, 4 and 8 weeks, indicating that the diastolic function of the three heart failure processes is impaired, and suggesting that the E/A value in the 4-week transition period is pseudo-normal.
2.4 Pathological changes of left ventricle in the pathological process of heart failure in experimental mice. The pathological sections of heart were analyzed in 0, 2, 4 and 8 weeks groups. Under low power microscope, the shape of the heart was normal before modeling, the myocardium thickened and the cardiac cavity decreased at 2 weeks, the inner diameter of the heart increased at 4 weeks, and the cardiac cavity continued to expand at 8 weeks, which was consistent with the results of B-mode and M-mode ultrasound. Under high magnification, the myocardial cells showed complete structure and orderly arrangement before modeling. After 2 weeks of modeling, the cells were enlarged, but the complete cell structure could still be seen. After 4 weeks of modeling, myocardial cells were hypertrophy and the cell structure was disordered; After 8 weeks of modeling, the nuclear condensation, cell lysis and cell gap of the heart increased significantly. At the same time, Sirius red staining showed that myocardial fibrosis gradually increased with the process of heart failure in experimental mice.