Phenytoin can accelerate the healing process after experimental myocardial infarction?

Zhou, Xin; Li, Yuming; Ji, Wenjie; Jiang, Tiemin; Sun, Xiulian; Zhu, Yuanfeng; Shi, Rui

doi:10.1016/j.ijcard.2004.12.098

Cited by 11 publications

(16 citation statements)

References 38 publications

(35 reference statements)

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“…To encompass the whole part of the infarcted free wall, a ϫ1 objective lens was used. The transmural thickness of the anterior free wall containing the scar was measured at four to five widely spaced locations and averaged (57). Due to the existence of viable myocardium in the infarcted LV free wall (especially in the T-infarct group), we applied another method to calculate infarct size, the fibrosis fraction in the infarcted segment (see Fig.…”

Section: Methodsmentioning

confidence: 99%

Postinfarction healing dynamics in the mechanically unloaded rat left ventricle

Zhou

Yun

Han

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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The healing process is a key determinant for postinfarction left ventricular (LV) remodeling and the development of heart failure, which could be influenced by mechanical (pressure and/or volume) load. So far, limited information exists regarding an indepth characterization of the postinfarct healing process in the mechanically unloaded state. In the present work, we performed isogenic Lewis-to-Lewis rat abdominal heterotopic heart transplantation, which is characterized by hemodynamic unloading in the left ventricle, and simultaneously ligated the left anterior descending coronary artery (T-infarct group). Pathological evolution was dynamically compared with that of in situ infarcted Lewis hearts (I-infarct group) on days 3, 7, 14, and 35. There was a remarkable myocardial salvage in the unloaded heart, as shown by the improvement in infarct size (T-infarct group: 25.47% ± 4.31% vs. I-infarct group: 38.46% ± 4.82%, P < 0.01) and the smaller fraction of fibrosis in infarct segments (T-infarct group: 42.12% ± 8.40% vs. I-infarct group: 75.65% ± 10.51%, P < 0.01). In addition, there was a progressive disorganization of the two-dimensional collagen fiber alignment as well as retarded collagen fiber maturation in the T-infarct group. We also observed enhanced angiogenesis, lymphangiogenesis, and inflammatory cell retention in the infarct region during mechanical unloading. Moreover, capillary density and collagen deposition were significantly increased in the noninfarcted area of the unloaded heart compared with the same region in the in situ infarcted heart. In conclusion, ischemic insult in the mechanically unloaded heart elicits an altered inflammatory and healing response, which is characterized by myocardial salvage, delayed resolution of inflammation, and disorganization of the collagen orientation in the infarcted region. These findings could provide novel insights into the contribution of hemodynamic load in the postinfarction healing process. Further studies are warranted to elucidate its potential mechanism.

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Section: Methodsmentioning

confidence: 99%

Postinfarction healing dynamics in the mechanically unloaded rat left ventricle

Zhou

Yun

Han

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…After measuring body weight and LV weight, the left ventricle was sliced into three transverse sections parallel to the atrioventricular ring from the apex to the base. The middle section was fixed in 10% buffered formalin, embedded in paraffin, cut into 5 μm-thick sections, and stained with Sirius red (Direct Red 80; Sigma Aldrich, St. Louis, MO, USA) [28]. Random images were captured in five fields (100× magnification) for each LV section by a digital CCD camera (Pro 150ES; Pixera Corporation, Los Gatos, CA, USA) connected to a polarized microscope (E600POL; Nikon, Tokyo, Japan) equipped and modified with a commercially available circular polarizer (Kenko, Tokyo, Japan).…”

Section: Tissue Preparation and General Pathologymentioning

confidence: 99%

“…Image analysis was performed with Image Pro Plus software V4.5 (Media Cybernetics, Silver Spring, MD, USA). Infarct size was determined as the percentage of infarcted epicardium and endocardium of the LV circumference as described previously [28]. The mean thicknesses of the LV free wall (LVFWT) and the septum were measured to evaluate the degree of ventricular dilation.…”

Section: Tissue Preparation and General Pathologymentioning

confidence: 99%

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Disassociation Between Left Ventricular Mechanical and Electrical Properties in Ischemic Rat Heart After G-CSF Treatment

Li¹,

Luo²,

Zhou³

et al. 2011

Cardiovasc Drugs Ther

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“…Moreover, Nakaya et al [8] have also shown the beneficial effects of provastatin in preventing ventricular remodeling by decreasing the levels of matrix metalloproteinase-2. Recently, Zhou et al [9] have reported that phenytoin can attenuate the adverse ventricular remodeling after myocardial infarction in rat, possibly by facilitating and strengthen extracellular matrix deposition. The findings of McGavigan et al [3] may be considered to be compatible with these previously reported data.…”

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confidence: 99%