In a rat chronic infarction model, the infarcted left ventricular (LV) wall was injected with the hydrogel or phosphate buffered saline (PBS).
In a rat infarction model, the infarcted left ventricle was injected with PBS, hybrid hydrogels, BMSCs or BMSC-encapsulating hybrid hydrogels.
This was a result of less pronounced virtual electrodes in the infarction model, and delayed propagation in the peri-infarct tissue.
Transplantation of the cells was carried out 10 days after the development of myocardial infarction model in order to allow local inflammatory response to subside in the infarcted heart.
For in vivo studies, acute myocardial infarction model was developed in Fischer-344 rats (n = 38).
The functional outcomes of microfibrous, elastomeric, biodegradable cardiac patches have been evaluated in a rat chronic infarction model.
Furthermore, using polymerase chain reaction, peak expression of CD13 was shown 7 days after MI in a mouse myocardial infarction model [15].
Subsequently, the same group [70] used the coronary artery ligation myocardial infarction model of rats to measure the myocardial infarction scope and vasoactive effect of diosgenin.
This study was designed o analyze the cell distribution after ICI in variations of heart status in a swine myocardial infarction model.
βARKct modification of CPCs increased survival and proliferation following adoptive transfer in an acute myocardial infarction model concomitant with increased expression of β-AR.
Myocardial perfusion is one of the key parameters to e.g., determine the area-at-risk in the infarction model (ligature of left anterior descending coronary artery) and to assess therapeutic effects such as after interventional, pharmaceutical, or stem cell therapies.
