Objective To explore the feasibility of establishing a modified mouse model of pressure overload induced left ventricular hypertrophy by transverse aortic constriction(TAC).Methods 55 C57BL/6 female mice were randomly divided into three groups:severe TAC group (n =27),moderate TAC group (n =7) and sham surgery group (n =21),respectively.By ligating the aorta arch between innominate artery and the left common carotid artery with modified techniques in a minimally invasive way,moderate or severe aortic constriction were established successfully and reliably to mimic left ventricular(LV)outflow obstruction; to correctly evaluate the cardiac structural and functional responses to aortic arch banding,2-dimention (2D) and M mode transthoracic echocardiography (TTE) were deployed to monitor the LV contractile function and assess the LV hypertrophic changes induced by pressure overload at 4 weeks after the surgery.Results The mouse model of aortic constriction was established successfully with a post-operative survival rate more than 88％.And all these operated mice were able to survive at least 4 weeks long.Eccentric left ventricular hypertrophic changes were detected with echocardiographic measurement 4 weeks after the banding operation in both mTAC and sTAC group,as dilated left ventricular lumen with enlarged LV end-diastolic dimension (LVEDD) and LV end systolic-dimension (LVESD) were confirmed.Mice with moderate banded aorta exhibited a compensated LV hypertrophy with preserved contractile functions and satisfactory ventricular wall movements to some extent,although left ventricular fractional shorting (LVFS) reduced gradually from 0.403 ± 0.007 to 0.340 ± 0.015 (P＜0.05) ; while in severe banded (sTAC) mice,LVFS reduced more significantly as a sharp decrease from 0.438 ± 0.011 to 0.216 ± 0.012 (P ＜ 0.01) were detected,combined with poor contractile function and stiff ventricular wall movements,exhibiting a de-compensated pathological left ventricular hypertrophy.Conclusion This modified TAC opcration could be easily carried out,and the TAC mouse model mentioned in the present research was an effective pressure overload model with several superiorities including less trauma,improved post-operative survival rate,rapid recovery and satisfactory reproducibility,thus a better and recommended mouse model for specific research purpose concerning LV hypertrophy mechanistic studies.

Objective To explore the inhibitory effect of L-arginine on cardiac allograft vasculopathy (CAV) and its possible mechanisms.Methods The rat cardiac allograft model was used. In the control group (n=26), L-arginine was not administered after heterotopic cardiac transplantation, and the other 21 rats (experimental group) received administration of L-arginine ( 800?mg/kg every day, in drinking water) after heart transplantation. CAV score was evaluated and plasma nitric oxide (NO) was measured at 2 and 3 months after transplantation. Results Graft survival rate 2 months after transplantation was significantly (P

Objective To study the relationship between Cardiac allograft vasculopathy (CAV) and donor heart ischemia time. Methods The rat model of retroperitioneal heterotopic heart transplantation was used. Seventy Wistar rats were divided into 4 groups: group 1 receiving CsA after sham operation; group 2 receiving transplantation directly; group 3 having 3 h-ischemia before transplantation; group 4 having 6?h ischemia before transplantation. After transplantation, all rats in each group were subjected to the gastric lavage of CsA for 20?days. At 20?days after transplantation, the donor heart was removed for observation of changes in pathological lesions and ultrastructues of coronary artery. Results With ischemia time being prolonged, cardiac capillary endothelial cell swelling and coronary intimal proliferation were observed which were similar to the CAV histopathological changes. Conclusion The prolongation of ischemia time can lead to intimal proliferation and hyperplasia which can promote CAV development. So ischemia time is a vital reason for the CAV.

Objective To study the prevention of cardiac allograft vasculopathy (CAV) post-transplant through the expression of iNOS mRNA. Methods Rat model of heterotopic heart transplantation (Abdomen) was developed and recipients were injected with Cyclosporin A at abdomen in the meantime of receiving L-arginine (iNOS mRNA group) and inhibitor of iNOS (L-NAME group) according to grouping. Plasma content of NO_3-, the expression of iNOS mRNA in coronary ~artery of transplanted heart and the radio of tunica intima/tunica media thickness (I/M) were assayed after ~operation . Results The plasma content of NO_3-and the expression of iNOS mRNA in coronary ~artery of transplanted heart in iNOS mRNA group were obviously higher than those in control group and L-NAME group during 2 to 4 weeks after operation. The ratio of I/M in iNOS mRNA group was ~lower than that in control group and L-NAME group 4 weeks after operation. Conclusion The ~expression of iNOS can promote the synthesis of NO and prevent CAV development.

Objective To investigate the effects of perfluorochemical ( PFC) on in vitro long-term hypothermic heart preservation in rats. Methods Thirty Wistar rats were randomly divided into control group ( Celsior solution), Celsior + O_2 group (Celsior solution plus oxygen) and PFC/Celsior + O_2 group (two-layer method plus oxygen) , with 10 rats in each group. Langendorff model of isolated rat heart was prepared. The isolated heart was preserved at 4 ℃ for 8 h, and hemodynamic parameters, coronary effluent flow, and leakage of creatine kinase ( CK), lactate dehydrogenase ( LDH) and aspartate transaminase (AST) were detected after reperfusion. Besides, the myocardial ultrastructure was also observed. Results Compared with control group and Celsior + O_2 group, the left ventricular developed pressure and ± dp/dt in PFC/ Celsior + O_2 group significantly increased ( P < 0.01), while LDH, CK and AST leakage significantly decreased ( P < 0.01). However, there was no significant difference in the above paramters between Celsior + O_2 group and control group (P>0.05). Compared with control group and Celsior + O_2 group, the impairment of myocardial ultrastructure in PFC/ Celsior + O_2 group after hypothermic preservation was alleviated. Conclusion PFC as a supplementation to oxygen in heart preservation solution could enhance myocardial protection during in vitro long-term hypothermic heart preservation in rats via the improvement of energy metabolism.

Objective To establish the swine acute heart failure model for surgical experiment, and evaluate the heart function by continuous cardiac index (CCI). Methods Swine heart failure model was attempted to establish by coronary ligation in six swines. CCI was obtained by Swan-Canz catheters and Vigilance monitor, and hemodynamic, biochemical and ultrasonocardiographic results were utilized to evaluate the changes of heart function. Results Five swines accomplished the experiment. Compared with basic status, there were significant differences in mean arterial pressure (MAP) , pulmonary artery systolic pressure (PASP), mixed venous oxygen saturation ( SVO_2) and CCI for swines with heart failure ( P < 0.05) , there was no significant change in biochemical parameters, while left ventricle ejection fraction ( LVEF) significantly decreased (P<0.05). Conclusion CCI is feasible in monitoring and evaluating heart function of animal model. The swine acute heart failure model established by coronary ligations can meet the needs of surgical experiment in principle.

This article introduces a new method using the servo motor which is controlled by ARM microcontroller to provide power for a pulsatile blood pump to beat. This method is featured with straightforward structure, accurate control, excellent timeliness, stable performance and small noise. And it can adjust the rate of beat, the rate of flow and the compression ratio according to actual demand.
Algorithms ; Heart-Assist Devices ; Models, Cardiovascular ; Pulsatile Flow