TY - JOUR
T1 - Effect of delayed intervention with ACE-inhibitor therapy on myocyte hypertrophy and growth of the cardiac interstitium in the rat model of myocardial infarction
AU - McDonald, Kenneth M.
AU - Chu, Cuixia
AU - Francis, Gary S.
AU - Carlyle, Wenda
AU - Judd, Dianne L.
AU - Hauer, Katherine
AU - Hartman, Malinda
AU - Cohn, Jay N.
PY - 1997/12
Y1 - 1997/12
N2 - The effectiveness of angiotensin-converting enzyme (ACE)-inhibitor therapy in attenuating ventricular remodeling when initiated immediately following myocardial damage is clearly established. Less information, however, is available on the impact of late therapy on the remodeling process, especially its influence on the cellular components of these structural changes. The purpose of this study was to examine the effects of converting enzyme inhibitor therapy commenced 28 days following infarction in the rat on changes in cardiac myocyte dimension and the interstitium. At 28 days following infarction, myocyte cell length (153.9 ± 7.3 v 131.1 ± 5.9 μm, P = 0.0002) and cell volume in the free wall of the left ventricle (38.5 ± 5.0 x 103 v 31.4 ± 3.1 x 103, P = 0.009) had increased compared with sham-operated rats. Similar changes were noted in the septum and right ventricle. Captopril therapy administered between 28 and 56 days attenuated a further increase in cell length noted in an untreated group in the left ventricle (153.5 ± 15.3 v 167.3 ± 13.7 μm, P = 0.02), right ventricle (153.8 ± 20.5 v 173.8 ± 2.3 μm, P = 0.01) and septum (158.0 ± 20.2 v 179.1 ± 16.6 μm, P = 0.004). There was an increase in hydroxyproline content in the right ventricle and a similar trend in the left ventricle in the untreated myocardial infarction groups. These changes were not altered by captopril therapy. In summary, even late therapy with captopril attenuates progressive myocyte remodeling, which may contribute to the ability of ACE-inhibitor therapy to slow progressive chamber enlargement following infarction.
AB - The effectiveness of angiotensin-converting enzyme (ACE)-inhibitor therapy in attenuating ventricular remodeling when initiated immediately following myocardial damage is clearly established. Less information, however, is available on the impact of late therapy on the remodeling process, especially its influence on the cellular components of these structural changes. The purpose of this study was to examine the effects of converting enzyme inhibitor therapy commenced 28 days following infarction in the rat on changes in cardiac myocyte dimension and the interstitium. At 28 days following infarction, myocyte cell length (153.9 ± 7.3 v 131.1 ± 5.9 μm, P = 0.0002) and cell volume in the free wall of the left ventricle (38.5 ± 5.0 x 103 v 31.4 ± 3.1 x 103, P = 0.009) had increased compared with sham-operated rats. Similar changes were noted in the septum and right ventricle. Captopril therapy administered between 28 and 56 days attenuated a further increase in cell length noted in an untreated group in the left ventricle (153.5 ± 15.3 v 167.3 ± 13.7 μm, P = 0.02), right ventricle (153.8 ± 20.5 v 173.8 ± 2.3 μm, P = 0.01) and septum (158.0 ± 20.2 v 179.1 ± 16.6 μm, P = 0.004). There was an increase in hydroxyproline content in the right ventricle and a similar trend in the left ventricle in the untreated myocardial infarction groups. These changes were not altered by captopril therapy. In summary, even late therapy with captopril attenuates progressive myocyte remodeling, which may contribute to the ability of ACE-inhibitor therapy to slow progressive chamber enlargement following infarction.
KW - Angiotensin converting enzyme inhibitor
KW - Mycocyte hypertrophy
KW - Rat myocardial infarction
KW - Ventricular remodeling
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U2 - 10.1006/jmcc.1997.0562
DO - 10.1006/jmcc.1997.0562
M3 - Article
C2 - 9441827
AN - SCOPUS:0031461009
SN - 0022-2828
VL - 29
SP - 3203
EP - 3210
JO - Journal of Molecular and Cellular Cardiology
JF - Journal of Molecular and Cellular Cardiology
IS - 12
ER -