Objective -Beneficial effects of natural grape polyphenols on human health have been known for a long time and still attract more and more interest of many researchers. The aim of research was to reveal cardioprotective properties of polyphenols contained in grape concentrate "Fenocor" in rats exposed experimental histotoxic hypoxia.Material and Methods -The study was conducted on 21 adult male Wistar rats divided into 3 groups, 2 of which were administered CoCl 2 water solution in 60 mg/kg dose for 7 days. The control group consisted of 5 non-exposed animals. The rats of the second group (n=8) after the administration of cobalt chloride did not receive any treatment, the animals of the third group (n=8) after administration of cobalt chloride were additionally given Fenocor -a grape polyphelols water solution at a dose of 2.5 ml/kg diluted in 0.05 ml of water. Morphological study was performed using light and electron microscopy. During the experiment the following biochemical parameters such as contents of malondialdehyde, oxidative modification of proteins were estimated. Results -The outcome of the cobalt toxic exposure on the heart of animals in experiments resulted in the development of severe cardiomyopathy which lead to the need for timely cardioprotection. Histological structure of myocardium observed in the second group of male rats after cobalt intoxication on the background of grape polyphenol concentrate generally reflected a tendency to minimize of the damage extent which was manifested in the form of normalization of cell structures and muscle fibers. Conclusion -Administration of Fenocor has demonstrated its antioxidant and cytoprotective properties, promoted myocardial structure preservation in rats exposed to histotoxic hypoxia.

Abstract:The heart is a target of injury for many chemical compounds, both medically prescribed and not. Pathophysiological mechanisms underlying development of chemical-induced cardiomyopathies vary depending on the inciting agent, and can include: direct toxic effects, neurohormonal activation, altered calcium homeostasis, and oxidative stress. The fact that drug-induced heart disease, and in particular cobalt-induced cardiomyopathy, does not occur more often, as would be expected from the diversity of various mechanisms, is perhaps surprising. In spite of this, cardiotoxicity remains a major problem of hundreds of pharmaceutical agents, industrial chemicals and naturally occurring products and is often a limiting factor in treatment of certain diseases. Hence, it must be taken in account in the process of clinical decision making and treatment as well as in the process of drug research and development. The primary morphological alteration is mitochondrial damage that possibly reflects an enzymatic block of oxidative decarboxylation at pyruvate and ketogluterate levels. Due to that myofibrils of the myocardial cells were affected highlighting that the main cause of myofibril reduction could be a lower oxygen intake in the perinuclear area. The reduction of the contractile support of myocardial cells can explain the possible myocardial dysfunction. Nuclear changes were consistent with sarcoplasmic alterations, our study showing deformed, twisted, hyperchromatic nuclei with heterogeneous chromatin and even disintegrating nuclei. Changes of the interstitial connective tissue were sometimes extensive and sometimes barely noticeable. The most common alteration of this structure was the onset and development of a mainly perivascular collagen fibrillogenetic process.

Polyphenols of grapes and their beneficial effects on human health have been known for a long time and still attract more and more research interest. The aim of the research was to reveal cardioprotective properties of polyphenols contained in grape concentrate "Fenokor" in terms of experimental histotoxic hypoxia. Materials and methods. The study was conducted on 21 adult male Wistar rats divided into 3 groups, 2 of which were administered CoCl 2 aqueous solution in a dose of 60 mg/kg for 7 days intragastrically. The control group consisted of 5 intact animals. The rats of the second group (n = 8) after the introduction of the cobalt did not receive any treatment, the animals of the third group (n = 8) after the administration of cobalt chloride intragastrically, were given Fenokor aqueous solution at a dose of 2,5 ml/kg along with 0,05 ml of water orally. Morphological study was performed using light and electron microscopy. During the experiment the following biochemical parameters such as contents of malondialdehyde, oxidative modification of proteins were estimated. The results. The result of the influence of cobalt on the heart of animals in experiments is the development of severe cardiomyopathy that requires cardio-protection. Histological structure of myocardium observed in the second group of male rats after cobalt intoxication on the background of grape polyphenol concentrate generally reflected a tendency to minimize the damage extent which was manifested in the form of normalization of cell structures and muscle fibers. Application of Fenokor has demonstrated its antioxidant and cytoprotective properties, which contributed to myocardial structure preservation in rats exposed to histotoxic hypoxia.

Objective -Quantitative morphological studies of myocardial cellular elements. Aim of research is to study myocardial interstitial matrix with and without succinic acid treatment in the rats exposed to intermittent hypobaric hypoxia.Material and Methods -The study was conducted on 26 adult males of Wistar rats weighing 220-310 g, divided into 3 groups. The first control group consisted of 6 intact animals. The second group included 10 rats which were exposed to hypobaric hypoxia without medication for 30 days. Third group was composed of 10 rats, which were medicated by succinic acid solution which was injected intraperitoneally once a day at the rate of 0.5 ml/100 g of animal body weight 15 minutes before hypoxic exposure for 30 days.Results -In the second group almost the entire stroma was consisting of the thickened collagen fibers and proliferating cells of the connective tissue. Their total number increased relatively to the control by 31% initiating the processes of collagenases. An increase in the number of myofibroblasts which was observed in the hypoxic rat heart in the second group followed by high MPP-9 expression. Hypoxic effects in the third group were not significantly different from control according to the observed changes in the stroma. In rats of the third group the capillary diameter exceeded the indicator of the second group, but was significantly lower than the control indicator. Accordingly, compared with the series without correction, the cross-sectional area of the capillaries was increased -28.44±0.14 μm 2 against 24.53±0.20 μm 2 . The total cross-sectional area of the capillaries is 0.77±0.10 x10 3 μm 2 . The relative surface area of the vascular area was lower than the control by 21.8%. Conclusion -Fibrosis in the myocardium inevitably leads to increased myocardial stiffness, resulting in systolic and diastolic dysfunction, neurohormonal activation and, ultimately, heart failure caused by hypobaric hypoxia. Reduced oxygen delivery by microvascular damage, increased perivascular fibrosis may contribute to contractile failure. Succinic acid combined with inosine acts as a high-energy phosphate reserve, to maintain adenosine triphosphate at levels sufficient to support contractile function.

Cobalt is widespread in the natural environment and can be formed as an effect of anthropogenic activity. The ionic cobalt can be transported by blood in the body, causing adverse effects by the generation of reactive oxygen species. The aim of this research was to describe the changes of myocardial cells during experimental cobalt induced cardiomyopathy. Summarizing the in vivo experiments, it can be stated that severe histotoxic cardiomyopathy occurred in male rats treated with cobalt chloride. Long-term oral administration of cobalt resulted in diminished dietary intake and growth inhibition in the exposed rats compared to the control group. The primary morphological alteration of cardiomyocytes is mitochondrial damage that possibly reflects an enzymatic block of oxidative decarboxylation. Due to that myofibrils of the myocardial cells were affected highlighting that the main cause of myofibril reduction could be a lower oxygen intake in the perinuclear area. The reduction of the contractile support of myocardial cells can the disease and allow a correct therapeutic approach.