Cíl práce: Podat přehled o diagnostických metodách a doporučených postupech pro vcestné cévy (vasa praevia) v těhotenství. Typ studie: Souhrnný článek. Metodika: Analýza dostupných literárních zdrojů. Závěr: Vasa praevia patří mezi závažné těhotenské komplikace s nízkou incidencí. Pokud nejsou vcestné cévy diagnostikovány prenatálně, představují vysoké riziko pro plod. Včasná prenatálně stanovená diagnóza významně snižuje perinatální morbiditu a mortalitu novorozence. Diagnostickou metodou volby je ultrasonografické vyšetření s použitím barevného dopplerovského zobrazení. V případě stanovení diagnózy vasa praevia prenatálně je doporučováno ukončení těhotenství elektivním císařským řezem dříve, než dojde k nástupu porodní činnosti nebo odtoku plodové vody., Objective: To report up–to date knowledge on diagnostic methods and recommended practices for vasa praevia in pregnancy. Study design: Review. Methods: Analysis of available literature resources. Conclusion: Vasa praevia is among the major pregnancy complications with a low incidence. If they are not diagnosed prenatally, pose a high risk to the fetus. Early prenatally established diagnosis significantly decrease perinatal morbidity and mortality of the newborn. The diagnostic method of choice is ultrasound scan using colour Doppler image. In the case of diagnosis of vasa praevia prenatally, it is recommended termination of the pregnancy by elective cesarean section before the onset of labor activity or rupture of membranes., and Andrea Galčíková
Present study investigated the effect of red wine polyphenolic compounds (ProvinolsTM) on blood pressure (BP), nitric oxide synthase (NOS) activity and vascular function in Wistar-Kyoto (WKY) rats exposed to chronic social stress produced by crowding. Adult male rats were divided into four groups: control (480 cm2/rat), ProvinolsTM-treated (20 mg/kg/day, 480 cm2/rat), crowded (200 cm2/rat) and crowded treated with Provinols
TM (20 mg/kg/day, 200 cm2/rat) for 8 weeks. No differences in BP were observed among the groups at the end of experiment, however, reduced BP was observed in ProvinolsTM-treated rats after 3 weeks of treatment. NOS activity in the aorta was significantly elevated in crowded rats, while ProvinolsTM alone had no effect on nitric oxide (NO) production. Acetylcholine-induced relaxation of the femoral artery was significantly improved in stressed and ProvinolsTM-treated rats vs. control, without significant changes in their noradrenaline-induced vasoconstriction. Interestingly, ProvinolsTM blunted the elevation of NO production and vasorelaxation during crowding. Increased endothelium-dependent vasorelaxation and NO synthesis in crowded rats may represent the adaptation mechanisms, resulting in unaltered blood pressure in stress-exposed normotensive rats. This study further demonstrated that elevated release of NO during chronic stress may be prevented by ProvinolsTM. Thus, Provino TM might maintain equilibrium between endothelium-derived vasoconstrictor and vasodilator factors in stress.
The purpose of this study was to determine the role of lipotoxicity in vascular smooth muscle (VSM). C1-BODIPY 500/510 C12 used to assess the ability of VSM A7r5 cells to transport long-chain fatty acids showed that lipid transport did not appear to limit metabolism. Thin layer chromatography revealed that storage of transported fatty acid occurred primarily as mono- and diglycerides and fatty acids but not as triglycerides. We used lipid-induced apoptosis as a measure of lipotoxicity and found that 1.5 mM palmitate (6.8:1) bound to albumin resulted in a 15-fold increase in the number of apoptotic cells compared to the control at 24 hours. This apoptosis did not seem to be due to an increase in reactive oxygen species (ROS) since VSM cells incubated in palmitate showed less ROS production than cells incubated in albumin only. Similar exposure to oleate did not significantly increase the number of apoptotic cells compared to the control. Oleate actually significantly attenuated the apoptosis induced by palmitate, suggesting that unsaturated fatty acids have a protective effect on cells undergoing palmitate-induced apoptosis. These results suggest that vascular smooth muscle is vulnerable to lipotoxicity and that this lipotoxicity may play a role in the development of atherosclerosis., H. M. Mattern, C. D. Hardin., and Obsahuje bibliografii a bibliografické odkazy
The effect of long-term inhibition of nitric oxide synthase on the relaxation and contraction ability of the thoracic aorta, carotid and pulmonary arteries was studied in the early postnatal period. Starting from the fifth day after birth, puppies were administered NG-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg/day subcutaneously) for 6 weeks. After this period, mean blood pressure increased from the control value of 94±14 mm Hg to 168±5 mm Hg (P<0.01) and the heart/body weight ratio from 6.22±0.25 to 8.23±0.45 (PcO.Ol). In control arterial rings precontracted by phenylephrine (10“5 mol/1), acetylcholine caused dose-dependent relaxations; the maximal values were reached in the range of 10 "8 to 10"* mol/1. In arteries from L-NAME treated puppies, acetylcholine also induced dose-dependent relaxations, the maximum values in the thoracic aorta (81.0±2.9 %) and carotid artery (87.2±6.9 %) were significantly reduced, not, however, in the pulmonary artery (76.4±7.8 %). Dose-response curves to acetylcholine in all the examined arteries from L-NAME-treated animals were shifted to the right indicating a decrease in sensitivity to acetylcholine. Neurogenic contractions, induced by electrical stimulation of adrenergic nerves, were not significantly altered in the thoracic aorta and carotid artery. However, in the pulmonary artery the contractions were greater at high frequency of stimulation. The findings that (i) submaximal doses of L-NAME attenuate acetylcholine-induced relaxation only slightly, and (ii) that it does not appreciably influence adrenergic contractions justify the hypothesis that the endothelium of vessels in newborn dogs is very probably endowed with a high content of nitric oxide synthase.
Vascular stenosis is often described only by its percentage in both clinical and scientific praxis. Previous studies gave inconclusive results regarding the effect of stenosis eccentricity on its hemodynamic effect. The aim of this experimental study was to investigate and quantify the effect of stenosis severity and eccentricity on the pressure drop. A combination of pressure and flow measurements by Par ticle Imaging Velocimetry (PIV) method was used. Models of the same stenosis significance but with different levels of eccentricity were studied in vitro by PIV. This study has shown that stenosis asymmetry is associated with more profound pressure drop an d flow volume decrease. On the contrary, pressure drop and flow volume decrease were not further significantly influenced by the level of asymmetry. Hemodynamic changes associated with stenosis eccentricity must be taken into account in both clinical and s cientific studies., L. Novakova, J. Kolinsky, J. Adamec, J. Kudlicka, J. Malik., and Obsahuje bibliografii
Vaskulární demence je druhou nejčastěji se vyskytující demencí (po demenci Alzheimerově). Autoři článku v souhrnném sdělení uvádějí základní epidemiologické údaje týkající se vaskulární demence. Předkládají přehled o klinickém obrazu tohoto onemocnění a shrnují současný pohled na jeho etiopatogenezi, dělení, diagnostiku a terapii., Vascular dementia is second commonest cause of dementia. The authors of the article have ióne a survey of essential epidemiological data concerning vascular dementia. They present a basic review of vascular dementia's picture and summarize the contemporary view of ethiopathogenesis, clinical discrimination. diagnostics and treatment of the disease., Vladimír Kovtun, Jitka Mészarosová, and Lit. 20
The effects of transient and sustained hyperthyroidism on vasoactive intestinal polypeptide-like immunoreactivity (VIP-LI) levels were studied in the heart atria of developing and adult rats. Newborn rats were divided into 5 groups. Neo-T animals were treated with thyroxine (T4) during postnatal days 1-8 and sacrificed at the age of 60 days. Neo-S rats were treated with T4 during postnatal days 1-60 and sacrificed one day later. Adult-1 and Adult-2 animals received T4 during days 52-60 and were sacrificed 5-6 days and 1 day later, respectively. Control animals were injected with saline. VIP-LI concentrations were determined in extracts from the left and right atria separately. In Neo-S and Adult-2 rats, spontaneous heart rate, the weight of both atria and total T4 serum levels were significantly enhanced, while their body weight was decreased. The ratio atria weight to body weight was significantly increased in all groups except for Adult-1 animals. Hyperthyroidism led to a significant decrease in VIP-LI levels in both atria of Neo-S and Neo-T rats. Hyperthyroidism induced in adult rats also decreased VIP-LI levels in both atria. However, this change was only transient. In conclusion, our data have provided new evidence that hyperthyroidism induced during the early neonatal period interferes with the development of VIP-ergic innervation in rat atria. The period of the first few postnatal days seems to be essential for this effect, since VIP-LI concentrations in 60-day-old animals did not significantly differ between Neo-S and Neo-T atria., J. Kuncová, J. Slavíková., and Obsahuje bibliografii
The pulmonary vasodilator action of an S-nitrosothiol, S-nitroso acetylpenicillamine (SNAP), was investigated in the rat pulmonary vasculature. The influence of its nitric oxide donator property was studied by comparison with the effect of acetylpenicillamine (AP), SNAP minus the nitroso group, and the blockade of nitric oxide release by the L-arginine analogue, L-NAME. In the isolated rat lung perfused with autologous blood at a constant flow rate (1PL), changes in pulmonary artery pressure (Ppa) reflect changes in pulmonary vascular resistance. Dose-response relationships to both SNAP and AP (0.1, 1, 10 and 100 /ug) were established both during normoxic ventilation (air + 5 % CO2; low Ppa) and when Ppa was raised by alveolar hypoxic vasoconstriction (2 % O2 + 5 % CO2). SNAP caused small dose-dependent fall in normoxic Ppa (mean±S.D. 17.4±3.0 mm Hg). in 11 rat IPL % fall of Ppa was 1, 3 and 4 % for 1, 10 and 100 ¡ug, respectively (p<0.01). This fall was more obvious when Ppa was raised by hypoxia (mean Ppa rise (HPV) 11.5±3.8 mm Hg); there was a 22, 55 and 79 % fall in HPV for 1,10 and 100 /ug in 11 rat IPL. The dilatation after 10 /ig SNAP was not consistently affected by 100/rg L-NAME (% fall in HPV pre L-NAME 45±22 % vs 42±23 % post L-NAME). AP had no significant effect on Ppa, causing only small falls in Ppa, equivalent to solvent (saline). There was occasionally a small rise in Ppa with 10 and 100 /tg AP. Thus, the dilator action of SNAP is most likely due to its NO donator property, and is not consistently affected by blockade of endogenous NO release.
Pathophysiological mechanisms underlying the development of renal dysfunction and progression of congestive heart failure (CHF) remain poorly understood. Recent studies have revealed striking differences in the rol e of epoxyeicosatrienoic acids (EETs), active products of cytochrome P-450-dependent epoxygenase pathway of arachidonic acid, in the progression of aorto-caval fistula (ACF)-induced CHF between hypertensive Ren-2 renin transgenic rats (TGR) and transgene-negative normotensive Hannover Sprague-Dawley (HanSD) controls. Both ACF TGR and ACF HanSD strains exhibited marked intrarenal EETs deficiency and impairment of renal function, and in both strains chronic pharmacologic inhibition of s oluble epoxide hydrola se (sEH) (which normally degrades EETs) normalized EETs levels. However, the treatment improved the survival rate and attenuated renal function impairment in ACF TGR only. Here we aimed to establish if the reported improved renal function and attenuation o f progression of CHF in ACF TGR observed after sEH blockade depends on increased vasodilatory responsiveness of renal resistance arteries to EETs. Therefore, we examined the responses of interlobar arteries from kidneys of ACF TGR and ACF HanSD rats to EET-A, a new stable 14,15-EET analog. We found that the arteries from ACF HanSD kidneys rats exhibited greater vasodilator responses when compared to the ACF TGR arteries. Hence, reduced renal vasodilatory responsiveness cannot be responsible for the lack of beneficial effects of chronic sEH inhibition on the development of renal dysfunction and progression of CHF in ACF HanSD rats., A. Sporková, Z. Husková, P. Škaroupková, N. Rami Reddy, J. R. Falck, J. Sadowski, L. Červenka., and Obsahuje bibliografii
Previous studies have substantiated the antipyretic role played by extrahypothalamic limbic system (EXHY-LS) AVP during fever. Repeated attempts to elucidate other thermoregulatory functions of this hormone have failed. Circumstantial evidence, however, suggest central role for this hormone in thermoregulation under hypohydration. Hypohydration, hyperosmolarity and hypovolaemia induce upward shifts in temperature thresholds for activation of heat dissipating mechanisms. When hypovolaemia is superimposed on hyperosmolarity these shifts are additive. Analogously, these two stressors when combined, decrease the osmotic threshold for AVP release. In rats, the elevated temperature thresholds for evaporative cooling and peripheral vasodilation occurring with hypohydration are positively correlated with lower Hypothalamic/EXHY-LS AVP ratio. Reciprocal relations between limbic system and blood AVP contents suggest competitive interaction between central and peripheral demands. Hypothesis for the possible mode of action of central AVP in thermoregulation under hypohydration is discussed.