RESUMO
Background and aim: Chronic alcohol intoxication (CAI) induces heart damage. One of the promising ways of its treatment involves the administration of herbal medicinal products. The purpose of this study was to explore the effect of solid herbal extract of Primula veris L. (PVSHE) on the morphofunctional changes in rats' myocardium after CAI. Experimental procedure: CAI was simulated for 24 weeks. Loading testing was used to assess the functional condition of the heart, the functional assessment of mitochondria was based on the polarographic determination of oxygen consumption rate and determination of the indices of lipid peroxidation and antioxidant enzymes activity. We performed a microscopic examination of the left ventricle following the standard protocol of histological processing and h&e staining. Results and conclusion: PVSHE restricts the toxic effects of ethanol on the heart which was indicated by a higher rise in the rates of myocardial contraction (by an average of 3.9 times, P < 0.05) and relaxation (2.6 times under volume load, P < 0.05), LVP (by an average of 1.7 times, P < 0.05) and MISP (by an average of 1.5 times, P < 0.05). PVSHE caused an improvement in the functional state of rats' cardiac mitochondria exposed to CAI, which was demonstrated by on average 1.3-1.4 times (P < 0.05) as high RCR as compared to the control group. The histological examination of the myocardium of the animals treated with PVSHE showed the increase in the volume fraction of cardiac myocytes, and a 31.2% (P < 0.05) decline in the interstitial volume. Therefore, PVSHE has a protective effect on the heart after CAI.
RESUMO
Alcohol abuse is a risk factor for heart damage and deterioration of its inotropic function. Currently, there is no pathogenetic pharmacological treatment for alcohol-induced myocardial injury. Therefore, the study of drugs with cardioprotective action is of current interest. Our earlier studies of stress-induced heart damage showed that a new derivative of glutamic acid - glufimet - protects the myocardium's inotropic function and limits lipid peroxidation. Additionally, we found that it increases the activity of antioxidant enzymes and improves mitochondrial respiration. The purpose of our study was to assess the effect of glufimet on the heart after chronic alcohol intoxication (CAI). The comparison drug was mildronate, which possesses cardioprotective properties and is used to treat alcohol withdrawal. We conducted our study using female Wistar rats (10 months old, 280-320 g). CAI was simulated by replacing drinking water with a 10% ethanol solution sweetened with sucrose (50 g/L) over a period of 24 weeks. The day after the animals stopped ethanol solution drinking, the control group was injected intraperitoneally (i.p.) with a saline solution once a day for 14 days, while the experimental groups received glufimet (28.7 mg/kg) and the drug of comparison mildronate (50 mg/kg), respectively. After that, we studied the heart contractility by measuring volume load, adrenergic reactivity, and maximum isometric load. Under CAI, the control group showed significantly lower growth in left ventricular pressure (LVP), myocardium contraction rate, and relaxation rate during functional tests. Higher concentrations of LPO products (malondialdehyde) and low activity of antioxidant enzymes (superoxide dismutase, glutathione peroxidase), indicating a disturbance in mitochondrial respiration compared to the control group, were registered. While being treated with glufimet and mildronate, the animals demonstrated higher growth rates of myocardial contraction, myocardial relaxation, and LVP, compared to the control group. Mitochondrial functioning and activity of the antioxidant enzymes increased in the same group as well.
