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The body surface potential mapping of the heart during the period of ventricular depolarization and the inotropic function of the ventricles were studied in rats under conditions of a translational model of post-infarction chronic heart failure developed by us. We revealed a statistically significant (p<0.001) correlation between the left-ventricular ejection fraction and the values of the maximum positive and negative extrema of the cardioelectric field on the body surface of rats with post-infarction chronic heart failure caused by anterior transmural myocardial infarction. The calculated linear regression equations have high predictive efficiency, which makes it possible to use the amplitude characteristics of the heart cardioelectric field as a marker of the development of chronic heart failure. [ABSTRACT FROM AUTHOR]

We studied some features of blood and lymph microcirculation in the brain, heart, and liver of female rats with developed alcoholic cardiomyopathy. In female rats after 24-week forced consumption of 10% ethanol solution, the size and inotropic function of the heart were measured by echocardiography. Microcirculation in the brain, myocardium, and liver was assessed by laser Doppler flowmetry using LAKK-OP2 and LAZMA-D computerized laser analyzers. Using spectral wavelet analysis, we determined the absolute and normalized to total perfusion amplitudes of microcirculation oscillations reflecting various regulatory mechanisms. Intact animals served as controls. In rats of the experimental group, alcoholic cardiomyopathy completely developed. Under these conditions, the index of microcirculation in the brain, myocardium, and liver significantly decreased. At the same time, there was a redistribution in the brain between shunting and nutritive blood flow in favor of the latter. In the myocardium and liver, this ratio did not change. [ABSTRACT FROM AUTHOR]

Cardioprotective effect of 1-({4 [(4 chlorobenzoyl)amino]phenyl}sulfonyl-L-proline (compound AL-828) was studied in rats with modeled acute myocardial infarction. The test compound was administered intragastrically in a dose of 30 mg/kg/day for 3 days prior to infarction modeling. Metalloproteinase inhibitor antibiotic doxycycline served as the reference drug and was administered in a dose of 40 mg/kg/day by the same schedule. It was shown that AL-828 similar to doxycycline significantly reduced the intensity of myocardial remodeling and maintained the inotropic function of the myocardium in the acute phase of myocardial infarction. By the 20th minute of ischemia, the end-systolic dimension of the left ventricle in control animals increased from 1.98±0.12 to 3.84±0.16 mm, while in animals treated with AL-828, this increase was significantly (p=0.007) less pronounced (from 1.84±0.07 and 2.87±0.21 mm, respectively). The ejection fraction characterizing the inotropic status of the left ventricle in animals treated with AL-828 was significantly higher (p=0.02). By its cardioprotective activity, AL-828 was not inferior to the reference drug doxycycline. It can be assumed that the cardioprotective activity of compound AL-828 is related to suppression of MMP-9 expression and/or inhibition of its activity as was previously demonstrated by us. [ABSTRACT FROM AUTHOR]

A translational rat model of chronic heart failure was employed to examine the cardioprotective effect of fabomotizole hydrochloride. Fabomotizole therapy for 28 days (15 mg/kg/day intraperitoneally) restored inotropic function of the left ventricle and increased ejection fraction from 54±3 to 65±3% (p=0.001). The inotropic function returned to normal against the background of significantly reduced myocardial expression of angiotensin (p=0.01) and glucocorticoid (p=0.03) receptors and significant increased expression of sigma-1 receptors (p=0.04). Inhibition of abnormal expression of angiotensin and glucocorticoid receptors responsible for activation of the pathological cascades underlying the postinfarction remodeling of the left ventricle as well as activation of the expression of cytoprotective sigma-1 receptors are viewed as the key features of the cardioprotective action of fabomotizole hydrochloride. [ABSTRACT FROM AUTHOR]

We created a translational model of chronic heart failure in rats that developed in 3 months after reproducing experimental anterior transmural myocardial infarction. The model simulated the basic clinicodiagnostic criteria of this disease: impaired contractility and dilatation of heart ventricles, signs of venous congestion, elevated plasma content of biochemical markers, and abnormal overexpression of AT1aR and β-adrenoceptors. [ABSTRACT FROM AUTHOR]

Original translational rat model of chronic heart failure provoked by experimental anterior transmural myocardium infarction was employed to examine the preventive action of anxiolytic Afobazole (15 mg/kg/day administered intraperitoneally during the first 15 days after coronary occlusion) on the development of the heart failure assessed in 3 months after infarction. Afobazole prevented the development of pathologic remodeling of the myocardium, maintained its inotropic function, and decreased the plasma level of brain natriuretic peptide known as a biochemical marker of chronic heart failure. In the myocardium, Afobazole down-regulated overexpression of the genes induced in chronic heart failure and assessed by corresponding RNA levels, which code angiotensin (AT1A-R), vasopressin (V1A-R), and glucocorticoid (GR) receptors as well as Epac2 protein. The revealed biochemical changes are consistent with the data on cardioprotective action of Afobazole. [ABSTRACT FROM AUTHOR]

Echocardiography in control narcotized rats ( n = 12) revealed that acute single-stage ligation of coronary artery induced a rapid and significant decrease in systolic function of the heart, which attained minimum to postischemic minutes 10-20 and then gradually restored during 60 min after coronary occlusion. Matrix proteinase inhibitor doxycycline (40 mg/kg/day intragastrically for 3 days prior to the experiment) prevented dramatic impairment of systolic function in the left ventricle during first 20 min of ischemia and then all the indices characterizing the state of pumping function of the left ventricle in the experimental (doxycycline) group ( n = 9) surpassed the control. Thus, matrix proteinase inhibitor doxycycline prevented early postischemic remodeling of the heart during the most acute phase of experimental myocardial infarction. [ABSTRACT FROM AUTHOR]