From:  Role of angiotensin II in the development of subcellular remodeling in heart failure

Cardiac performance, status of RAS and oxidative stress in control and MI animals with or without ENP and LOS treatments for 4 weeks starting at 3 weeks after induction of MI

ParametersControlMIMI + ENPMI + LOS
A. Hemodynamic parameters
LVEDP (mmHg)4.0 ± 0.215.9 ± 1.3*7.5 ± 0.66.9 ± 0.5
LVSP (mmHg)133 ± 4.9128 ± 3.2131 ± 3.8127 ± 3.9
LV + dP/dt (mmHg/s)9,208 ± 10754,806 ± 745*7,690 ± 6807,544 ± 722
LV − dP/dt (mmHg/s)8,788 ± 9564,326 ± 590*7,248 ± 7027,312 ± 690
B. RAS activity parameters
Plasma ANG II (fmol/mL)8.3 ± 1.4125 ± 6.9*34 ± 3.5192 ± 9.9
Plasma ACE activity (nmol/min per mL)51 ± 3.385 ± 7.1*32 ± 2.4145 ± 7.1
LV ACE activity (nmol/min per mg protein)0.45 ± 0.030.69 ± 0.04*0.23 ± 0.020.84 ± 0.05
C. Oxidative stress levels
LV MDA (nmol/mg tissue lipids)5.9 ± 0.419.1 ± 0.8*12.7 ± 0.310.1 ± 0.4
LV conjugated dienes formation (nmol/mg tissue lipids)33 ± 1.956 ± 4.9*41 ± 3.037 ± 3.3
LV GSH (μmol/g tissue)82 ± 1.636 ± 4.1*74 ± 4.168 ± 3.7
LV GSSG (μmol/g tissue)12.4 ± 0.825.2 ± 2.6*14.2 ± 1.415.3 ± 1.6

Values are mean ± standard error (SE) of 4–6 animals in each group. ENP: enalapril (10 mg/kg per day); LOS: losartan (20 mg/kg per day); MI: myocardial infarction; RAS: renin-angiotensin system; ACE: angiotensin-converting enzyme; LVEDP: LV end diastolic pressure; LVSP: LV systolic pressure; + dP/dt: maximum rate of pressure development; -dP/dt: maximum rate of pressure decay; MDA: malondialdehyde; GSH: reduced glutathione; GSSG: oxidized glutathione. Data are based on the analysis of the information in our papers Shao et al. Am J Physiol Heart Circ Physiol. 2005;288:H2637–46 [116]; and Shao et al. Am J Physiol Heart Circ Physiol. 2005;288:H1674–82 [113]. *P < 0.05 compared with control; P < 0.05 compared with MI group