Physiological research最新文献

Combination of chronic kidney disease (CKD) and heart failure (HF) results in extremely high morbidity and mortality. The current guideline-directed medical therapy is rarely effective and new therapeutic approaches are urgently needed. The study was designed to examine if renal denervation (RDN) will exhibit long-standing beneficial effects on the HF- and CKD-related morbidity and mortality. Fawn-hooded hypertensive rats (FHH) served as a genetic model of CKD and fawn-hooded low-pressure rats (FHL) without CKD served as controls. HF was induced by creation of aorto-caval fistula (ACF). RDN was performed 28 days after creation of ACF and the follow-up period was 70 days. ACF FHH subjected to sham-RDN had survival rate of 34 % i.e. significantly lower than 79 % observed in sham-denervated ACF FHL. RDN did not improve the condition and the final survival rate, both in ACF FHL and in ACF FHH. In FHH basal albuminuria was markedly higher than in FHL, and further increased throughout the study. RDN did not lower albuminuria and did not reduce renal glomerular damage in FHH. In these rats creation of ACF resulted in marked bilateral cardiac hypertrophy and alterations of cardiac connexin-43, however, RDN did not modify any of the cardiac parameters. Our present results further support the notion that kidney damage aggravates the HF-related morbidity and mortality. Moreover, it is clear that in the ACF FHH model of combined CKD and HF, RDN does not exhibit any important renoprotective or cardioprotective effects and does not reduce mortality. Key words Chronic kidney disease, Heart failure, Renal denervation, Fawn-hooded hypertensive rats.

Arterial compliance (AC) is an important cardiovascular parameter characterizing mechanical properties of arteries. AC is significantly influenced by arterial wall structure and vasomotion, and it markedly influences cardiac load. A new method, based on a two-element Windkessel model, has been recently proposed for estimating AC as the ratio of the time constant T of the diastolic blood pressure decay and peripheral vascular resistance derived from clinically available stroke volume measurements and selected peripheral blood pressure parameters which are less prone to peripheral distortions. The aim of this study was to validate AC estimation using a virtual population generated by in silico model of the systemic arterial tree. In the second part of study, we analysed causal coupling between AC oscillations and variability of its potential determinants - systolic blood pressure and heart rate in healthy young human subjects. The pool of virtual subjects (n=3818) represented an extensive AC distribution. AC was estimated from the peripheral blood pressure curve and by the standard method from the aortic blood pressure curve. The proposed method slightly overestimated AC set in the model but both ACs were strongly correlated (r=0.94, p<0.001). In real data, we observed that AC dynamics was coupled with basic cardiovascular parameters variability independently of the autonomic nervous system state. In silico analysis suggests that AC can be reliably estimated by noninvasive method. The analysis of short-term AC variability together with its determinants could improve our understanding of factors involved in AC dynamics potentially improving assessment of AC changes associated with atherosclerosis process. Key words Arterial compliance, Cardiovascular model, Arterial blood pressure, Causal analysis, Volume-clamp photoplethysmography.

The global COVID-19 pandemic, caused by SARS-CoV-2, has led to significant morbidity and mortality, with a profound impact on cardiovascular health. This review investigates the mechanisms of SARS-CoV-2's interaction with cardiac tissue, particularly emphasizing the role of the Spike protein and ACE2 receptor in facilitating viral entry and subsequent cardiac complications. We dissect the structural features of the virus, its interactions with host cell receptors, and the resulting pathophysiological changes in the heart. Highlighting SARS-CoV-2's broad organ tropism, especially its effects on cardiomyocytes via ACE2 and TMPRSS2, the review addresses how these interactions exacerbate cardiovascular issues in patients with pre-existing conditions such as diabetes and hypertension. Additionally, we assess both direct and indirect mechanisms of virus-induced cardiac damage, including myocarditis, arrhythmias, and long-term complications such as 'long COVID'. This review underscores the complexity of SARS-CoV-2's impact on the heart, emphasizing the need for ongoing research to fully understand its long-term effects on cardiovascular health. Key words: COVID-19, Heart, ACE2, Spike protein, Cardiomyocytes, Myocarditis, Long COVID.

The history of the Czech and Slovak experimental cardiology describes a completely unusual curve. The personality of J.E. Purkynje caused this field to reach unprecedented peak at the very beginning of its modern history. The development of experimental cardiology after the death of the great scholar was certainly not linear. Just when it seemed to be raising its head, the German occupation came. Its second hopeful awakening was delayed for a long time by forty years of isolation. The significant limitation of foreign contacts gradually led to the loss of hopefully developing contacts, to professional isolation and lagging behind the stormy development of world science. At the moment of greatest depression, in 1971, in Prague there was created a professional forum that was supposed to enable its intellectual survival and reduce the negative consequences of the "splendid isolation". The Society of Experimental Cardiology (SEC) was founded at the Czechoslovak Physiological Society of the Czechoslovak Medical Society J.E. Purkynje, with the main task of introducing theoretical and clinical cardiologists to the advances in world cardiology. The first meeting was held in 1973 and in 2023 we celebrated already the 50th anniversary of SEC. Moreover, nowadays we see the increasing interest of the young researchers, both experimental and clinical cardiologists, who consider SEC a very attractive platform for their education and professional growth. Key words: Experimental cardiology, Czech and Slovak Society, History, Relationship to clinical cardiology.

Mitochondria represent pivotal cellular organelles endowed with multifaceted functionalities encompassing cellular respiration, metabolic processes, calcium turnover, and the regulation of apoptosis, primarily through the generation of reactive oxygen species (ROS). Perturbations in mitochondrial dynamics have been intricately linked to the etiology of numerous cardiovascular pathologies, such as heart failure, ischemic heart disease, and various cardiomyopathies. Notably, recent attention has been directed towards the detrimental impact of micro- and nanoplastic pollution on mitochondrial integrity, an area underscored by a paucity of comprehensive investigations. Given the escalating prevalence of plastic particle contamination and the concomitant burden of cardiovascular disease in aging populations, understanding the interplay between mitochondria within the cardiovascular system and micro- and nanoplastic pollution assumes paramount importance. This review endeavors to elucidate the current albeit limited comprehension surrounding this complex interplay. Key words Mitochondria, Nanoplastics, Microplastics, Cardiovascular system, Endothelial function, Oxidative phosphorylation.

Disproportion between reactive oxygen species (ROS) production and the body's antioxidant system can cause oxidative stress, which is considered a common denominator in various pathological conditions, including cardiovascular diseases, aging, and cognitive disorders. The generation of free radicals, which occurs through partial reduction of oxygen, can quickly overwhelm the endogenous antioxidant system capacity of the cell. This causes lipid, protein, DNA and RNA damage, inflammation, and overall cell degeneration, which can be mitigated by various antioxidants. However, their use in human medicine did not bring the expected effect. Molecular hydrogen (H2), due to its unique physical and chemical properties, provides a number of benefits for alleviating oxidative stress. H2 is superior to conventional antioxidants as it can selectively reduce (.)OH radicals while preserving important ROS that are otherwise used for normal cell signaling. Key words Oxidative stress, Cardiovascular diseases, Molecular hydrogen, ROS, Inflammation.

An important part of the side effects of combined oral contraceptives (COC) usage is its psychological impact, which includes mood changes, anxiousness and depression. The psychological impacts are expected to be caused by physiological fluctuations of sex hormone levels during the menstrual cycle; this cycling is, however, suppressed in COC users. In our study, we assessed the differences in emotional awareness and anxiousness between women long term users of anti-androgenic COC (AA) and women with no COC use in their medical history (C). We also searched for intraindividual differences by comparing the results of both groups for the follicular and luteal phase of their cycle. A total of 45 women aged 18 to 22 participated in this study. The respondents were given our battery of questionnaires at the beginning of their follicular phase - this battery included two State-Trait Anxiety Inventory questionnaires (STAI-I, STAI-II), as well as a Levels of Emotional Awareness Scale (LEAS) test. The respondents were given only STAI-I in their luteal phase. We also analyzed the hormonal profile of our respondents. Our results show a significant difference in the LEAS analysis, implying the possibility of altered emotional awareness in AA group. STAI-I and STAI-II analysis did not yield any significant results, showing that anxiety levels of COC users probably do not differ from the general female population. We therefore discovered lower emotional awareness in COC using women (AA). Key words LEAS, STAI, Combined oral contraceptives, Anxiety, Hormonal profile.

Myocardial remodelling involves structural and functional changes in the heart, potentially leading to heart failure. The deoxycorticosterone acetate (DOCA)/salt model is a widely used experimental approach to study hypertension-induced cardiac remodelling. It allows to investigate the mechanisms underlying myocardial fibrosis and hypertrophy, which are key contributors to impaired cardiac function. In this study, myocardial remodelling in rat deoxycorticosterone acetate/salt model was examined over a three-week period. The experiment involved 11 male Sprague-Dawley rats, divided into two groups: fibrosis (n=6) and control (n=5). Myocardial remodelling was induced in the fibrosis group through unilateral nephrectomy, deoxyco-rticosterone acetate administration, and increased salt intake. The results revealed significant structural changes, including increased left ventricular wall thickness, myocardial fractional volume, and development of myocardial fibrosis. Despite these changes, left ventricular ejection fraction was preserved and even increased. ECG analysis showed significant prolongation of the PR interval and widening of the QRS complex in the fibrosis group, indicating disrupted atrioventricular and ventricular conduction, likely due to fibrosis and hypertrophy. Correlation analysis suggested a potential relationship between QRS duration and myocardial hypertrophy, although no significant correlations were found among other ECG parameters and structural changes detected by MRI. The study highlights the advantage of the DOCA/salt model in exploring the impact of myocardial remodelling on electrophysiological properties. Notably, this study is among the first to show that early myocardial remodelling in this model is accompanied by distinct electrophysiological changes, suggesting that advanced methods combined with established animal models can open new opportunities for research in this field. Key words Myocardial fibrosis, Remodelling, Animal model, DOCA-salt, Magnetic resonance imaging.

Obesity is considered an important factor contributing to the development of atherosclerosis. Inflammation plays a key role in endothelial dysfunction (ED), an initial stage of the atherosclerotic process. Several microRNAs (miRNAs) may play an important role in the inflammatory process, but there is a lack of information about their participation in the early stages of atherosclerosis development in patients with obesity. We aimed to assess the relations between plasma concentration of selected miRNAs, ED evaluated by reactive hyperemia index (RHI), inflammatory markers and other factors involved in the pathogenesis of atherosclerosis in adolescents and young adults with obesity. Participants (30 males, 30 females; aged 15 25 years) were divided into two groups: those with overweight/obesity (OW/O) (20 males, 20 females) and controls (C) (10 males, 10 females). The plasma concentrations of inflammatory markers, cytokines, adipocytokines, markers of lipid profile and glucose metabolism and selected miRNAs (miR 92, 126, -146a, -155) were analyzed. No significant differences in any of the miRNAs were found between the groups. MiR-146a correlated positively with RHI. Dividing the group by sex showed more significant associations between miRNA and analyzed parameters (IL-6, fasting glycemia) in men. Several observed correlations indicate a potential role of miRNAs in inflammation, the atherosclerotic process and glycemic control, primarily in male subjects with obesity. The relatively low number of observed associations between assessed parameters related to obesity and the pathogenesis of its complications could be attributed to the early stage of the atherosclerotic process in young subjects with obesity, where only subtle abnormalities are expectedly found. Key words Endothelial dysfunction, Atherosclerosis, Obesity, MicroRNA, Reactive hyperemia index.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been associated with significant cardiovascular complications, including myocardial infection and pulmonary embolism. This study aims to elucidate the relationship between the presence of SARS-CoV-2 RNA in the myocardium of the left ventricle and the levels of IgG and IgM antibodies against the SARS-CoV-2 virus in deceased COVID-19 patients. We conducted a post-mortem examination on 91 individuals who succumbed to COVID-19-related complications. The presence of SARS-CoV-2 RNA in the myocardium of the left ventricle was analyzed reverse transcription real time PCR (RT-qPCR) (EliGene® COVID19 UKV/SAV RT kit, Elisabeth Pharmacon), and antibody levels in serum were analyzed by serological assays (VIDAS SARS-COV-2 IgM and VIDAS SARS-COV-2 IgG II tests, BioMérieux). Of the heart tissue samples, 44 % tested positive for SARS-CoV-2 RNA. Our findings indicate that any detectable level of IgG antibodies against SARS-CoV-2 reduces the risk of viral penetration into the myocardium by more than fourfold. Specifically, individuals with detectable levels of IgG and IgM antibodies exhibited a significantly reduced presence of SARS-CoV-2 RNA in cardiac tissues (p<0.0001 for IgG and p<0.001 for IgM). Notably, all patients who died from pulmonary embolism had elevated levels of IgG antibodies. The study underscores the protective role of IgG and IgM antibodies in preventing SARS-CoV-2 penetration into cardiac tissues. However, high antibody titers were associated with fatal outcomes such as pulmonary embolism, pointing to the intricate balance of immune response in COVID-19 pathology. Key words SARS-CoV-2, Antibody, IgG, IgM, Cardiac damage, qPCR, Pneumonia, Pulmonary embolism, Heart failure.