The aim of the work is to ascertain the character of changes in the hormonal profile (concentrations of corticosterone, insulin, and adrenocorticotropic hormone) in conjunction with metabolic alterations and elevated blood pressure, which are induced in rats by restraint stress at 6th, 15th and 21st weeks of environmental space restriction. Materials and methods. A total of 55 normotensive male Wistar rats, aged 6–10 months, were assigned into 4 experimental groups (1 – intact control (10 rats); 2, 3 and 4 (15 rats each exposed to restricted space allowance)). All the animals were subjected to blood pressure (BP), blood glucose level and body weight measurements twice: at the stage of forming groups and at the 6th, 15th and 21st weeks. Plasma hormone concentrations (insulin, corticosterone, and ACTH) were examined by the immunoenzymatic method using commercial kits (Monobind, USA). Results. The body weight of the animals was significantly reduced by 20.72 % after 6 weeks of space allowance restriction, it was restored to baselines by the 15th week and exceeded control values by 26.1 % at the 21st week. BP levels showed an increasing trend, a dynamic increase in systolic pressure by 7 %, 17 % and 26 % was detected, respectively, as well as diastolic from the 15th week to the 21st week by 21.4 % and 37.0 %, respectively. Glucose concentration was within the euglycemic range. Changes in the hormonal profile showed an increase in the concentration of ACTH by more than 50 % and a decrease in insulin – by 34 % at the 6th week with a subsequent twofold decrease in the insulin concentration (at week 15) and a further more than twofold increase in ACTH at the 21st week. As for changes in the concentration of corticosterone, a peak increase of 3.77 times was noticed at the 15th week, followed by a decrease and restoration to the normative values by the 21st week. Conclusions. Even minor and unremarkable continuously acting stressors, which cannot be coped, become important triggers for hormonal profile and carbohydrate metabolism alterations as well as for a persistent increase in blood pressure, which manifest first by hypoinsulinemia, an increase in the level of ACTH, and a constant concentration of corticosterone. Long-term stress exposure contributes to a transient “peak” increase in the corticosterone level, a significant increase in insulin and a sustained increase in ACTH. Multidirectional changes in the levels of the studied hormones occur amidst a gradual increase in blood pressure and a stable increase in the level of glycemia.
The aim of the work is to review the professional literature sources from the scientific database PubMed mainly for the last 20 years analyzing the modern view on approaches to experimental modeling of cognitive impairment. Materials and methods. A review of the scientific literature over the past 20 years was performed. The lack of requisite knowledge about the pathogenesis of cognitive impairment and the wide range of risk factors for these conditions continue to be major challenges in the development of guidelines on early diagnosis and treatment. The literary analysis suggests that all modeling approaches to experimental cognitive impairment are currently divided into two groups: cell culture and animal models. Conclusions. Experimental modeling of cognitive impairment remains important in addition to clinical and population-based studies. In recent years, the problem of selecting an adequate model to study cognitive impairment, which is a central clinical manifestation of various neurological diseases (Alzheimer’s and Parkinson’s diseases, traumatic brain injury, vascular, demyelinating, and infectious diseases, metabolic aberrations and hormonal imbalance, neurodegenerative diseases of the central nervous system) is becoming increasingly relevant. The choice of model and experimental material – animals or cultures (invertebrate and mammalian cells) is based on a clear understanding of the study design and depends on the ultimate goal of research.
Intermittent hypoxia has been studied for many years as a promising non-pharmacological method of cardiovascular disease prevention. Hypoxic effects are accompanied by structural and functional changes in the myocardium. There is a direct link between the duration of hypoxic exposures and the severity of left ventricular myocardial remodeling. A range of histochemical markers of myocardial remodeling (cardiotrophin-1, titin, collagen type 1, annexin V) characterizing parenchymal-stromal relationships in the myocardium has shown high informativeness and prognostic value. The aim of the study was to examine cardiotrophin-1, titin, collagen type 1, annexin V and the morphofunctional state of the left ventricle of the heart in experimental rats exposed to intermittent 15-day (IH15) and 60-day hypoxia (IH60). Materials and methods. Intermittent hypoxia was modeled using 30 normotensive male Wistar rats, 7–8 months old, which were randomly assigned to 3 experimental groups of 10 animals each: 1) INT – a control group – intact animals (196.3 ± 6.8 g); 2) IH15 – 15-day hypoxia (205.6 ± 4.1 g); 3) IH60 – 60-day hypoxia (201.1 ± 5.5 g). The study compared the effects of intermittent hypoxia of varying duration: 15-day and 60-day hypoxia. Experimental modeling of intermittent hypoxia of 2 terms revealed a number of differences between the effects dependent on this factor duration through functional (blood pressure measurement, echocardiography) and immunofluorescent studies. Results. Blood pressure in rats of both groups was in the normotensive range, but an increase in systolic by 10 % and diastolic by 19 % was found in IH60 group compared to IH15 group (p < 0.05). In IH15 group, there was a significant decrease in end-diastolic dimension by 20 %, end-systolic dimension by 22 %, an increase in the thickness of left ventricular posterior wall by 44 % and interventricular septum by 33 % as well as left ventricular mass by 12 %, indicating concentric remodeling of the left ventricle, the development of which was confirmed by a 76 % increase in relative wall thickness compared to that in the control group (p < 0.05). Along with these changes, a decrease in end-diastolic volume by 47 %, end-systolic volume by 48 %, stroke volume by 49 % and cardiac output by 50 % with preserved ejection fraction was revealed (p < 0.05). While the parameters of IH60 rats were characterized by an increase in the thickness of interventricular septum by 33 % and left ventricular posterior wall by 17 %, as well as left ventricle mass by 23 %, relative left ventricular wall thickness was 15 % higher than the control value (p < 0.05). At the same time, diastolic volume was 9 % decreased and systolic volume was 24 % increased (p < 0.05). Also, cardiac output was increased by 58 % compared to that in 15-day hypoxic rats with an 8 % decrease in ejection fraction (p < 0.05). The concentrations of markers in IH60 group exceeded those in IH15, namely: cardiotrophin-1 by 39 %, titin by 70 %, collagen type 1 by 60 % and annexin V by 130 % (p < 0.05). Conclusions. 15-day hypoxia forms concentric left ventricular hypertrophy according to echocardiography findings; the study of marker profile of myocardial remodeling has revealed the development of moderate hypertrophy with increased resilient-elastic properties and decreased intensity of cardiomyocyte death. Remodeling caused by 60-day hypoxia is characterized by the eccentric pattern of changes with severe hypertrophy, significant fibrosis associated with apoptosis of cardiomyocytes. Such morphofunctional state of the myocardium may indicate the initial stages of maladaptation, increasing the risk of heart failure development.
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