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. Author manuscript; available in PMC: 2012 Sep 1.
Published in final edited form as: J Cell Physiol. 2011 Sep;226(9):2235–2243. doi: 10.1002/jcp.22559

Table 1.

Myocardial function and cardiomyocyte morphology in sedentary (SED) and exercise trained (TR) sham-operated (SHAM) and post-myocardial infarction (MI) rats, including MI rats treated with the angiotensin II type 1 receptor antagonist losartan.

SHAM MI MI Losartan


SED TR SED TR SED TR


LVEDP (mmHg) 3.8±2.4 4.1±2.1 25.7±1.3a 21.9±1.5a 18.2±1.2ad 17.7±1.1ad
LVPSP (mmHg) 114.3±5.8 120.0±5.1 100.3±3.1a 98.3±3.1a 87.6±4.5a 88.1±5.2a
+dP/dtmax (mmHg · ms−1) 8.9±1.1 8.4±1.1 3.4±1.2a 3.9±1.2a 4.0±0.9a 3.7±1.4a
−dP/dtmax (mmHg · ms−1) 8.8±1.3 8.7±1.1 3.2±1.2a 3.5±1.1a 4.3±1.3a 3.8±1.3a
Cell Length (μm) 100.9±2.6 110.8±4.2b 130.1±8.1a 115.0±4.5ac 117.5±3.2ac 113.2±3.1ac
Cell Width (μm) 22.8±1.3 24.4±0.7b 30.7±2.6a 26.7±1.6ac 28.0±1.7ac 26.9±1.9ac
Cell Volume (pL) 17.7±1.3 20.5±0.8b 30.4±2.9a 23.4±2.1ac 25.5±1.9ac 23.3±1.8ac

LVEDP: left ventricle end-diastolic pressure, LVPSP: left ventricle peak systolic pressure, (+dP/dtmax: peak rate of left ventricle pressure rise, −dP/dtmax: peak rate of left ventricle pressure fall. Note that SHAM TR rats developed physiologic hypertrophy, and that post-MI rats developed heart failure as defined by LVEDP >15 mmHg; presented with reduced LVPSP and rates of contraction and relaxation of the heart, and developed pathologic hypertrophy, which was reversed by exercise training as well as losartan.

a

difference from SHAM groups, p<0.01;

b

difference between SHAM SED and SHAM TR, p<0.01;

c

difference from MI SED, p<0.01.

d

difference from MI SED without losartan, p<0.01.

Data are mean±SEM with 8 animals/group.