Cardiovascular disease (CVD) and depressive disorders (DD) are two of the most prevalent health problems in the world. Although CVD and depression have different origin, they share some common pathophysiological characteristics and risk factors, such as the increased production of proinflammatory cytokines, endothelial dysfunction, blood flow abnormalities, decreased glucose metabolism, elevated plasma homocysteine levels, oxidative stress and disorder in vitamin D metabolism. Current findings confirm the common underlying factors for both pathologies, which are related to dramatic dietary changes in the mid-19th century. By changing dietary ratio of omega-6 to omega-3 fatty acids from 1:1 to 15-20:1 some changes in metabolism were induced, such as increased pro-inflammatory mediators and m odulations of different signaling pathways following pathophysiological response related to both, cardiovascular diseases and depressive disorders., J. Trebatická, A. Dukát, Z. Ďuračková, J. Muchová., and Obsahuje bibliografii
Gasotransmitters represent a subfamily of the endogenous gaseous signaling molecules that include nitric oxide (NO), carbon monoxide
(CO), and hydrogen sulphide (H2S). These particular gases share many common features in their production and function, but they fulfill their physiological tasks in unique ways that differ from those of classical signaling molecules found in tissues and organs. These gasotransmitters may antagonize or potentiate each other’s cellular effects at the level of their production, their downstream molecular targets and their direct
interactions. All three gasotransmitters induce vasodilatation, inhibit apoptosis directly or by increasing the expression of anti-apoptotic genes, and activate antioxidants while inhibiting inflammatory actions. NO and CO may concomitantly participate in vasorelaxation, anti-inflammation and angiogenesis. NO and H2S collaborate in the regulation of vascular tone. Finally, H2S may upregulate the heme oxygenase/carbon monoxide
(HO/CO) pathway during hypoxic conditions. All three gasotransmitters are produced by specific enzymes in different cell types that include cardiomyocytes, endothelial cells and smooth muscle cells. As translational research on gasotransmitters has exploded over the past years, drugs that alter the production/levels of the gasotransmitters themselves or
modulate their signaling pathways are now being developed. This review is focused on the cardiovascular effects of NO, CO, and H2S. Moreover, their donors as drug targeting the cardiovascular system are briefly described.
Chronic renal failure (CRF) is associated with high incidence of cardiovascular complications. To clarify pathogenesis of CRF numerous animal models have been developed. The aim of our work was to describe methodology of subtotal surgical renal ablation in rat and to characterize some biochemical and cardiovascular parameters of this animal model. Male rats underwent 5/6 surgical nephrectomy or sham operations in two steps. The following parameters were measured on day 10 and in week 10 after the surgery: plasma concentrations of creatinine and urea, blood pressure, resting heart rate, chronotropic response to atropine and metipranol, heart ventricles weight, contraction parameters and action potential duration in the left ventricle. Increased serum concentrations of creatinine and urea, decreased creatinine clearance, polyuria and alteration of the remnant kidney tissue were found in CRF rats. Changes in cardiovascular parameters identified after subtotal nephrectomy resembled alterations of cardiovascular system in uremic patients and included hypertension, elevated resting heart rate, diminished parasympathetic cardiac tone, hypertrophy of the left ventricle associated with weakened force of contraction, prolonged contraction and relaxation and shortening of action potential duration. These data suggest that the present model can be a useful tool in the study of CRF and its cardiovascular complications., J. Švíglerová ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
Down Syndrome (Ds) is the most common chromosomal cause of intellectual disability that results from triplication of chromosome 21 genes. Individuals with Ds demonstrate cognitive deficits in addition to comorbidities including cardiac defects, pulmonary arterial hypertension (PAH), low blood pressure (BP), and differences in autonomic regulation. Many individuals with Ds are born with heart malformations and some can be surgically corrected. Lower BP at rest and in response to exercise and other stressors are a prevalent feature in Ds. These reduced cardiovascular responses may be due to underlying autonomic dysfunction and have been implicated in lower exercise/work capacity in Ds, which is an important correlate of morbidity, mortality and quality of life. Exercise therapy can be beneficial to normalize autonomic function and may help prevent the development of co-morbidities in Ds. We will review cardiovascular physiology and pathophysiology in individuals with Ds, along with exercise therapy and special considerations for these individuals.
In this study we set out to understand is sleep fragmentation affects the cardiovascular regulation and circadian variability of core body temperature more or less than sleep deprivation. 50 healthy men (age 29.0±3.1 years; BMI 24.3±2.1 kg/m2) participated in a 3-day study that included one adaptative night and one experimental night involving randomization to: sleep deprivation (SD) and sleep fragmentation (SF). The evaluation included hemodynamic parameters, measures of the spectral analysis of heart rate and blood pressure variability, and the sensitivity of arterial baroreflex function. Core body temperature (CBT) was measured with a telemetric system. SF affects heart rate (61.9±5.6 vs. 56.2±7.6, p<0.01) and stroke index (52.7±11.1 vs. 59.8±12.2, p<0.05) with significant changes in the activity of the ANS (LF-sBP: 6.0±5.3 vs. 3.4±3.7, p<0.05; HF-sBP: 1.8±1.8 vs. 1.0±0.7, p<0.05; LF-dBP: 5.9±4.7 vs. 3.5±3.2, p<0.05) more than SD. Post hoc analysis revealed that after SD mean value of CBT from 21:30 to 06:30 was significantly higher compared to normal night’s sleep and SF. In healthy men SF affects the hemodynamic and autonomic changes more than SD. Sympathetic overactivity is the proposed underlying mechanism., J. Słomko, M. Zawadka-Kunikowska, J. J. Klawe, M. Tafil-Klawe, J. Newton, P. Zalewski., and Obsahuje bibliografii
The altered regulation of autonomic response to mental stress can result in increased cardiovascular risk. The laboratory tests used to simulate the autonomic responses to real-life stressors do not necessarily induce generalized sympathetic activation; therefore, the assessment of regulatory outputs to different effector organs could be important. We aimed to study the cardiovascular sympathetic arousal in response to different mental stressors (Stroop test, mental arithmetic test) in 20 healthy students. The conceivable sympathetic vascular index - spectral power of low frequency band of systolic arterial pressure variability (LF-SAP) and novel potential cardiosympathetic index - symbolic dynamics heart rate variability index 0V% were evaluated. The heart and vessels responded differently to mental stress - while Stroop test induced increase of both 0V% and LF-SAP indices suggesting complex sympathetic arousal, mental arithmetic test evoked only 0V% increase compared to baseline (p<0.01, p<0.001, p<0.01, respectively). Significantly greater reactivity of LF-SAP, 0V%, heart rate (HR) and mean arterial pressure (MAP) were found in response to Stroop test compared to mental arithmetic test potentially indicating the effect of different central processing (0V%, LF-SAP: p<0.001; HR, MAP: p<0.01). The different effectors’ sympathetic responses to cognitive stressors could provide novel important information regarding potential pathomechanisms of stress-related diseases., M. Mestanik, A. Mestanikova, Z. Visnovcova, A. Calkovska, I. Tonhajzerova., and Obsahuje bibliografii
a1_The question was addressed of how nitric oxide synthase (NO synthase) inhibition-induced hypertension in rat parents would affect the cardiovascular system in their offsprings. Two experimental groups were set up: Group I - offsprings of parents who had both been administered NO synthase inhibitor L-nitro-arginine methyl ester (L-NAME 40 mg/kg/day) for 5 weeks, the treatment of dams continued till week 12. Group II - offsprings fed by dams administered L-NAME after delivery only for a period of 4 weeks. Control age-matched offsprings formed the third group. Blood pressure and heart rate in parents and in 3-week-old offsprings were determined noninvasively. In the offsprings, body and heart weight were measured and the heart/body weight ratio (HW/BW) was calculated. The NO synthase activity, and also ornithine decarboxylase activity as a marker of polyamine production, were determined in the heart. The acetylcholine-induced relaxation of aortic rings was also followed. A marked blood pressure increase with a tendency to a decreased heart rate was found in the offsprings of Group I. A significant decrease in heart weight and body weight with a decreased HW/BW ratio indicated cardiac hypotrophy that contrasted with the decrease in NO synthase activity and increase in ornithine decarboxylase activity in the heart. Noteworthy was also the finding of completely preserved relaxation of the aorta to acetylcholine. Offsprings of Group II were similarly characterized by significantly higher blood pressure, a tendency to decreased heart rate, a decrease in heart weight, but not of the HW/BW ratio. The contrasting findings of heart weight decrease on the one hand and NO synthase activity decrease and ornithine decarboxylase increase on the other, were also found in this group. Full relaxation of the aorta to acetylcholine was preserved., a2_It can be concluded that remarkable alterations in the cardiovascular system were found in offsprings of hypertensive NO compromised parents., M. Gerová, I. Bernátová, J. Török, M. Juráni., and Obsahuje bibliografii