Representative histological findings of epicardial vessels evaluation at 35^th day post-infarction after long-term oral treatment (6^th– 35^th day) with captopril (2 × 25 mg/kg) or M-2 (4 mg/kg) (hematoxylin and eozine-stained).

<p>(A) Captopril group, (B) M-2 group (scanned with 20× objective, magnification 30×, bar represents 50 μm). </p><p></p><p>(A)</p><p>Small vessels composed of flattened endothelial cells observed inside fibrotic area.</p><p></p><p>(B)</p><p>Multiple, small capillary vessels composed of enlarged endothelial cells. Predominant part of endothelial cells reveals basophilic cytoplasm suggesting progressive neovascularization process.</p><p></p><p></p> <p></p> <p>Small vessels composed of flattened endothelial cells observed inside fibrotic area.</p> <p>Multiple, small capillary vessels composed of enlarged endothelial cells. Predominant part of endothelial cells reveals basophilic cytoplasm suggesting progressive neovascularization process.</p

The influence of long-term oral treatment (6^th– 35^th day) with captopril (2 × 25 mg/kg) and M-2 (4 mg/kg) after experimental myocardial infarction (MI) on: (A) heart rate (HR), (B) preload pressure (PP), (C) aortic systolic pressure (AoS), (D) aortic diastolic pressure (AoD), (E) aortic maximum rise of the first pressure derivative (+d<i>P</i>/d<i>t</i>) and (F) aortic maximal fall of the first pressure derivative (-d<i>P</i>/d<i>t</i>), tested in working heart setup.

<p>Data are expressed as mean values for each minute. For simplicity sake, standard error of the mean is presented only in control group. Non-parametric Kruskal-Wallis ANOVA test was used for all comparisons.</p> <p>Values marked with ✩<i>P</i><0.05, ✩✩<i>P</i><0.01 or ★<i>P</i><0.001 are significantly different from control group.</p> <p>Values marked with ○<i>P</i><0.05 or ○○<i>P</i><0.01 are significantly different from DMSO group.</p> <p>Values marked with ^<i>#</i><i>P</i><0.05 or ^<i>##</i><i>P</i><0.01 are significantly different between captopril and M-2 group.</p

Inflammatory infiltrations in studied material.

<p>Inflammatory infiltrations in studied material.</p

The influence of long-term oral treatment (6^th– 35^th day) after experimental myocardial infarction with captopril (2 × 25 mg/kg) or M-2 (4 mg/kg) on biochemical parameters measured in rats’ blood serum.

<p>The influence of long-term oral treatment (6^th– 35^th day) after experimental myocardial infarction with captopril (2 × 25 mg/kg) or M-2 (4 mg/kg) on biochemical parameters measured in rats’ blood serum.</p

Incidence of cardiomyopathy development in rats treated orally with captopril (2 × 25 mg/kg) or M-2 (4 mg/kg) from 6^th to 35^th day after experimental myocardial infarction.

<p>Incidence of cardiomyopathy development in rats treated orally with captopril (2 × 25 mg/kg) or M-2 (4 mg/kg) from 6^th to 35^th day after experimental myocardial infarction.</p

Schedule of the protocol study in the model of experimental myocardial infarction in rats.

<p>LH indicates Langedorff mode and WH the working heart mode. Aortic systolic pressure (<i>AoS</i>), aortic diastolic pressure (<i>AoD</i>), aortic flow (<i>AF</i>), coronary flow (<i>CF</i>), maximum rate of aortic systolic pressure increase (+<i>dP/dt</i>), maximum rate of aortic systolic pressure decrease (-<i>dP/dt</i>), oxygen partial pressure (<i>pO</i>_<i>2</i>) and carbon dioxide partial pressure (<i>pCO</i>_<i>2</i>) and pH values in pulmonary effluent, myocardial oxygen consumption (<i>MVO</i>_<i>2</i>), preload pressure (<i>PP</i>), heart rate (<i>HR</i>).</p