HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Hao Zhang Permission Requests Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Zhang, H. Articles by Hu, S.-S. Search for Related Content PubMed Articles by Zhang, H. Articles by Hu, S.-S. Related Collections Myocardial infarction

J Thorac Cardiovasc Surg 2009;137:216-222
© 2009 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology

Intramyocardial injection of tannic acid attenuates postinfarction remodeling: A novel approach to stabilize the breaking extracellular matrix

^a Research Center for Cardiac Regenerative Medicine, the Ministry of Health, Cardiovascular Institute and Fu Wai Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China
^b Department of Cardiac Surgery, Cardiovascular Institute and Fu Wai Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China

Received for publication January 18, 2008; revisions received June 10, 2008; accepted for publication July 6, 2008.

^_* Address for reprints: Sheng-Shou Hu, MD, Cardiovascular Institute and Fu Wai Hospital, Chinese Academy of Medical Science, Department of Cardiac Surgery, Beilishilu Rd 167A, Beijing 100037, P.R. China. (Email: shengshouhu{at}yahoo.com).

Objective: Myocardial infarction is associated with early matrix metalloproteinase activation and extracellular matrix degradation. We tested the hypothesis that stabilizing the original extracellular matrix of the infarcted left ventricle with local injection of tannic acid would preserve cardiac structure and function.

Methods: In vitro cytotoxicity of tannic acid was performed first; myocardial infarction model was induced by ligation of the left anterior descending branch in rats. Tannic acid was intramyocardially injected into infarcted site 24 hours after myocardial infarction (n = 30), and saline solution was injected in the same way as in the control (n = 30). The matrix metalloproteinase activity from tannic acid/saline solution–treated tissues was assayed by gelatin zymography 24 hours and 1 week after the treatment. The collagen content in the infarcted area was evaluated by hydroxyproline colorimetry assay 1 and 4 weeks after the treatment. Left ventricular structure and function were also evaluated with echocardiography, hemodynamics, and histologic examination.

Results: Tannic acid at a concentration of 0.05% had minimal cytotoxic effects on cultured cardiomyocytes and thus was subsequently chosen as the optimal concentration for injection. Compared with the saline solution injection group, tannic acid treatment inhibited the matrix metalloproteinase-2/-9 activity and increased the collagen content at the early post–myocardial infarction stage (48.6 ± 7.2 vs 37.3 ± 6 µg/mg dry weight). Tannic acid treatment also significantly reduced infarct expansion (infarct expansion index: 1.04 ± 0.15 vs 1.42 ± 0.21) and left ventricular dilatation at 4 weeks after infarction. Although tannic acid treatment improved fractional shortening (26% ± 2.4% vs 23.3% ± 3.2%), it failed to alter blood pressure (systolic blood pressure: 93.8 ± 8.2 vs 90.6 ± 8.5 mm Hg) and rate of pressure rise.

Conclusions: Local delivery of tannic acid prevents collagen matrix degradation via cross-linking fibrous collagen and inhibiting matrix metalloproteinase activity but does not improve the intrinsic contractile function of myocardium. This treatment may be helpful to attenuate the adverse topographic remodeling after acute myocardial infarction.