Cardioprotective effect and mechanism of post-infarction ventricular remodeling after self-assembling peptide and thermosensitive hydrogel implantation in rat myocardial infarction model

ArticleinZhonghua yi xue za zhi 90(4):259-63 · January 2010with5 Reads
DOI: 10.3760/cma.j.issn.0376-2491.2010.04.014 · Source: PubMed


    To compare the cardioprotective effect of self-assembling peptide (RAD16-II) and thermosensitive hydrogel DPHP (Dex-PCL-HEMA/PNIPAAm) and investigate the optimal property of hydrogel for the treatment of myocardial infarction (MI).
    MI model was induced by left anterior descending (LAD) coronary artery ligation in SD rats. The animals were randomized into three groups to receive RAD16-II hydrogel (n = 15), DPHP hydrogel (n = 15) or PBS (phosphate buffered saline; control group n = 15); sham-operated rats (n = 10), a suture was tied loosely around left coronary artery without ligating it. At Day 20 post-MI, left ventricle function was evaluated by echocardiography and cardiac catheter. Masson's trichrome was used for histological examination; anti-alpha-smooth muscle antigen (alpha-SMA) was applied to label the neovasculature formation in infarct area.
    The rats receiving DPHP hydrogel showed a significantly smaller left ventricle end diastolic diameter (LVEDd) and higher levels of left ventricle fraction shortening (LVFS) and left ventricle end systolic pressure (LVESP) than the rats in RAD16-II group [LVEDd (7.9 +/- 0.9) mm vs (8.9 +/- 0.8) mm]; [LVFS (25.4 +/- 5.1)% vs (21.9 +/- 2.9)%; LVESP (114.0 +/- 7.6) mm Hg vs (99.1 +/- 9.6) mm Hg; P < 0.05]. Histological examination showed uncompleted degraded hydrogel in infarct area of DPHP group but not in RAD16-II group. The animals receiving DPHP hydrogel demonstrated significantly a smaller infarct size, a higher infarct wall thickness and a lower vessel density in infarct than the animals receiving RAD16-II hydrogel (P < 0.05).
    DPHP hydrogel implantation further inhibits the post-MI ventricle remodeling than RAD16-II hydrogel implantation. The mechanism is not correlated with the vascular density in infarct area.