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142. Can the gold standard be beaten? How reliable are various modifications of the Synacthen test compared to the insulin tolerance test
- Creator:
- Mikuláš Kosák, Michaela Dušková, Luboslav Stárka, Jandikova, H., Pospisilova, H., Sramkova, M., Václav Hána, Martin Krsek, Drahomíra Springer, and Kateřina Šimůnková
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- Type:
- article, články, journal articles, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, inzulin, fyziologie, insulin, physiology, 14, and 612
- Language:
- English
- Description:
- M. Kosak, M. Duskova, L. Starka, H. Jandikova, H. Pospisilova, M. Sramkova, V. Hana, M. Krsek, D. Springer, K. Simunkova. and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
143. Captopril Fails to Reverse Hypertrophy of the Left Ventricle Induced by Aortic Insufficiency in Rabbits
- Creator:
- Fedor Šimko, Václav Pelouch, and Ján Kyselovič
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- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie člověka, human physiology, Aortic insufficiency, Hypertrophy regression, Fibrosis, Cardiac hypertrophy, 14, and 612
- Language:
- English
- Description:
- Angiotensin converting enzyme (ACE) inhibition has been reported to induce regression of hypertrophy in several models of hemodynamic pressure overload. The aim of the present study was to determine whether the ACE inhibitor captopril can reduce hypertrophy of the left ventricle induced by a chronic volume overload and modify collagen composition of the hypertrophied myocardium. Rabbits with four months lasting aortic insufficiency were divided into two groups: treated with captopril (20 mg/kg/day) for five weeks and treated with placebo. The respective control groups were represented by sham-operated animals. Aortic insufficiency induced a decrease of diastolic pressure, an increase of systolic and pulse pressure, hypertrophy of the left and right ventricle, and an increase of hydroxyproline content in the left ventricle without a change of hydroxyproline concentrations in either ventricle. Captopril treatment further enhanced pulse pressure by decreasing diastolic blood pressure. Hypertrophy of the left ventricle, hydroxyproline content and concentration in both ventricles were unaffected by captopril treatment. It is concluded that ACE inhibition did not reverse the left ventricular hypertrophy developed as a result of overload induced by aortic insufficiency. We suggest that mechanisms different from activation of the renin-angiotensin system may play a decisive role in the maintenance of hypertrophy in this particular model of volume hemodynamic overload., F. Šimko, V. Pelouch, J. Kyselovic., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
144. Captopril partially decreases the effect of H2S on rat blood pressure and inhibits H2S-induced nitric oxide release from S-nitrosoglutathione
- Creator:
- Drobná, M., Misak, A., Holland, T., Kristek, F., Grman, M., Tomasova, L., Berenyiova, A., Cacanyiova, S., and Ondrias, K.
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- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, sulfan, oxid dusnatý, krevní tlak, srdeční rytmus, hydrogen sulphide, nitric oxide, blood pressure, heart rate, captopril, H2S, 14, and 612
- Language:
- English
- Description:
- We studied the effects of the H2S donor Na2S on the mean arterial blood pressure (MAP) and heart and breathing rates of anesthetized Wistar rats in the presence and absence of captopril. Bolus administration of Na2S (1-4 μmol/kg) into the right jugular vein transiently decreased heart and increased breathing rates; at 8-30 μmol/kg, Na2S had a biphasic effect, transiently decreasing and increasing MAP, while transiently decreasing heart rate and increasing and decreasing breathing rate. These results may indicate independent mechanisms by which H2S influences MAP and heart and breathing rates. The effect of Na2S in decreasing MAP was less pronounced in the presence of captopril (2 μmol/l), which may indicate that the renin-angiotensin system is partially involved in the Na2S effect. Captopril decreased H2S-induced NO release from S-nitrosoglutathione, which may be related to some biological activities of H2S. These results contribute to the understanding of the effects of H2S on the cardiovascular system., M. Drobná, A. Misak, T. Holland, F. Kristek, M. Grman, L. Tomasova, A. Berenyiova, S. Cacanyiova, K. Ondrias., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
145. Carbohydrate-modified magnetic nanoparticles for radical scavenging
- Creator:
- Moskvin, M. and Daniel Horák
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- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, glukóza, kyselina askorbová, glucose, ascorbic acid, magnetic nanoparticles, silica, radical, scavenging, 14, and 612
- Language:
- English
- Description:
- Maghemite (γ-Fe2O3) nanoparticles, 12 nm in size, were prepared by co-precipitation of Fe(II) and Fe(III) chlorides with ammonium hydroxide and oxidation with hydrogen peroxide. To achieve stability and biocompatibility, obtained particles were coated with silica, to which glucose and ascorbic acid were bound by different mechanisms. The composite particles were thoroughly characterized by transmission electron microscopy, dynamic light scattering, elemental analysis, and FT-Raman and fluorescence spectroscopy to determine composition, morphology, size and its distribution, ζ-potential, and scavenging of peroxyl and hydroxyl radicals. As the particles showed promising antioxidative properties, they may have a possible application as a stable magnetically controlled scavenger of reactive oxygen species., M. Moskvin, D. Horák., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
146. Cardiac connexin-43 and PC signaling in rats with altered thyroid status without and with omega-3 fatty acids intake
- Creator:
- Szeiffová Bačová, B., Egan Beňová, T., Viczenczová, C., Tomáš Soukup, Hana Rauchová, Pavelka, S., Knezl, V., Miroslav Barančík, and Narcisa Tribulová
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- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, hormony štítné žlázy, srdeční arytmie, omega-3 mastné kyseliny, thyroid hormones, cardiac arrhythmia, omega-3 fatty acids, connexin-43, omega-3 polyunsaturated fatty acids, 14, and 612
- Language:
- English
- Description:
- Thyroid hormones are powerful modulators of heart function and susceptibility to arrhythmias via both genomic and non-genomic actions. We aimed to explore expression of electrical coupling protein connexin-43 (Cx43) in the heart of rats with altered thyroid status and impact of omega-3 polyunsaturated fatty acids (omega-3) supplementation. Adult male Lewis rats were divided into following six groups: euthyroid controls, hyperthyroid (treated with T3) and hypothyroid (treated with methimazol) with or without six-weeks lasting supplementation with omega-3 (20 mg/100 g/day). Left and right ventricles, septum and atria were used for immunoblotting of Cx43 and protein kinase C (PKC). Total expression of Cx43 and its phosphorylated forms were significantly increased in all heart regions of hypothyroid rats compared to euthyroid controls. In contrast, the total levels of Cx43 and its functional phosphorylated forms were decreased in atria and left ventricle of hyperthyroid rats. In parallel, the expression of PKC epsilon that phosphorylates Cx43, at serine 368, was increased in hypothyroid but decreased in hyperthyroid rat hearts. Omega-3 intake did not significantly affect either Cx43 or PKC epsilon alterations. In conclusion, there is an inverse relationship between expression of cardiac Cx43 and the levels of circulating thyroid hormones. It appears that increased propensity of hyperthyroid while decreased of hypothyroid individuals to malignant arrhythmias may be in part attributed to the changes in myocardial Cx43., B. Szeiffová Bačová, T. Egan Beňová, C. Viczenczová, T. Soukup, H. Rauchová, S. Pavelka, V. Knezl, M. Barančík, N. Tribulová., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public
147. Cardiac effects of endothelin-1 (ET-1) and related C-terminal peptide fragment: increased inotropy or contribution to heart failure?
- Creator:
- Ján Dřímal, Knezl, V., Dřímal, J., Dřímal, D., Bauerová, K., Viktor Kettmann, Doherty, A. M., and Štefek, M.
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- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, endotel, fyziologie, endothelium, physiology, endothelin-1, ETA and ETB receptors, endothelin antagonicst, 14, and 612
- Language:
- English
- Description:
- The contrasting pattern of cardiac inotropy induced by human peptide endothelin-1 (ET-1) has not been satisfactorily explained. It is not clear whether ET-1 is primarily responsible for increased myocardial ET-1 expression and release with resultant inotropic effects, or for the induction of myocardial hypertrophy and heart failure. There are at least two subtypes of endothelin receptors (ETA and ETB) and the inotropic effects of ET-1 differ depending on the receptor involved. Along with some other groups, we reported significant subtype-ETB endothelin receptor down-regulation in human cardiac cells preincubated with endothelin agonists (Dřímal et al. 1999, 2000). The present study was therefore designed to clarify the subtype-selective mechanisms underlying the inotropic response to ET-1 and to its ETB-selective fragment (8-21)ET-1 in the isolated rat heart. The hearts were subjected to (1-21)ET-1 and to (8-21)ET-1, or to 30 min of stop-flow ischemia followed by 40 min of reperfusion, both before and after selective blockade of endothelin receptors.The present study revealed that both peptides, ET-1 and its (8-21)ET-1 fragment, significantly reduced coronary blood flow in nmolar and higher concentrations. The concomitant negative inotropy and chronotropy were marked after ET-1, while the infusion of the ET-1(8-21) fragment produced a slight but significant positive inotropic effect. Among the four endothelin antagonists tested in continuous infusion only the non-selective PD145065 and ETB1/B2-selective BQ788 (in mmolar concentrations) slightly reduced the early contractile dysfunction of the heart induced by ischemia, whereas ETA-selective PD155080 partially protected the rat heart on reperfusion., J. Dřímal, V. Knezl, J. Dřímal Jr , D. Dřímal, K. Bauerová , V. Kettmann, A.M. Doherty , M. Štefek., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
148. Cardiac Troponin T Following Repeated Administration Of Pyridoxal Isonicotinoyl Hydrazone In Rabbits
- Creator:
- Michaela Adamcová, Jarmila Macháčková, Vladimír Geršl, Václav Pelouch, Tomáš Šimůnek, Ivona Klimtová, Radomír Hrdina, and Přemysl Poňka
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- Type:
- article, studie, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie člověka, human physiology, Iron chelators, Cardiotoxicity, Cardiac troponin T, Protein profile, Rabbits, 14, and 612
- Language:
- English
- Description:
- Pyridoxal isonicotinoyl hydrazone (PIH) is a new tridentate Fe-chelating agent that should be very promising in many pathological states resulting from both an iron-overload and formation of free radicals. The aim of our study was to investigate the effect of PIH on the cardiovascular system focusing to the regulatory protein - cardiac troponin T (cTnT). The study was carried out in two groups of Chinchilla male rabbits: 1) PIH (50 mg/kg dissolved in 10 % Cremophor i.p., once a week, 10 administrations, n=8) and 2) Cremophor (2 ml/kg i.p. in the same schedule, n=7). Plasma concentrations of cTnT (as a marker of myocardial damage) were measured using a commercial kit (Roche). cTnT was within the physiological range (i.e. < 0.1 mg/l) during the whole experiment in the Cremophor group. In the PIH group, the cTnT levels were not significantly increased when compared with the control group or with the initial values (except with those before the 5th administration). Furthermore, we analyzed the cytosolic and myofibrillar fraction of cTnT in the left ventricular myocardium. Using SDS-PAGE and Western blot we resolved three isoforms. The profiling of TnT did not differ significantly between the PIH-treated group and the Cremophor-treated group. Our data concerning cTnT support the opinion that the possible cardiotoxicity of PIH is very low., M. Adamcová, J. Macháčková, V. Geršl, V. Pelouch, T. Šimůnek, I. Klimtová, R. Hrdina, P. Poňka., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
149. Cardioprotective effect of chronic hypoxia is blunted by concomitant hypercapnia
- Creator:
- Jan Neckář, Ondrej Szárszoi, Jan Herget, Bohuslav Ošťádal, and František Kolář
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- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, hypoxie, hypoxia, rat heart, chronic hypoxia, hypercapnia, infarction, protection, 14, and 612
- Language:
- English
- Description:
- The effect of chronic hypercapnia on cardioprotection induced by chronic hypoxia was investigated in adult male Wistar rats exposed to isobaric hypoxia (10 % O2) for three weeks. In the first experimental group, CO2 in the chamber was fully absorbed; in the second group, its level was increased to 4.1 %. Normoxic controls were kept in atmospheric air. Anesthetized open-chest animals were subjected to 20-min LAD coronary artery occlusion and 3-h reperfusion for infarct size determination (TTC staining). Chronic hypoxia alone reduced body weight and increased hematocrit; these effects were significantly attenuated by hypercapnia. The infarct size was reduced from 61.9 ± 2.2 % of the area at risk in the normoxic controls to 44.5±3.3 % in the hypoxic group (P<0.05). Hypercapnia blunted the infarct size-limiting effect of hypoxia (54.8±2.4 %; P<0.05). It is concluded that increased CO2 levels in the inspired air suppress the development of the chronic hypoxia-induced cardioprotective mechanism, possibly by interacting with ROS signalling pathways., J. Neckář, O. Szárszoi, J. Herget, B. Ošťádal, F. Kolář., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
150. Cardioprotective effects of quercetin against ischemia-reperfusion injury are age-dependent
- Creator:
- Monika Barteková, Radosinska, J., Dezider Pancza, Miroslav Barančík, and Ravingerova, T.
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- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, věk, srdce, ischemie, age, heart, ischemia, quercetin, ischemia-reperfusion, 14, and 612
- Language:
- English
- Description:
- Quercetin, a polyphenolic compound present in various types of food, has been shown to exert beneficial effects in different cardiac as well as non-cardiac ischemia/reperfusion (I/R) models in adult animals. However, there is no evidence about the effects of quercetin on I/R injury in non-mature animals, despite the fact that efficiency of some interventions against I/R is agedependent. This study was aimed to investigate the effects of chronic quercetin treatment on I/R injury in juvenile and adult rat hearts. Juvenile (4-week-old) as well as adult (12-week-old) rats were treated with quercetin (20 mg/kg/day) for 4 weeks, hearts were excised and exposed to 25-min global ischemia followed by 40-min reperfusion. Functional parameters of hearts and occurrence of reperfusion arrhythmias were registered to assess the cardiac function. Our results have shown that quercetin improved post-ischemic recovery of LVDP, as well as recovery of markers of contraction and relaxation, +(dP/dt)max and -(dP/dt)max, respectively, in juvenile hearts, but not in adult hearts. Quercetin had no impact on incidence as well as duration of reperfusion arrhythmias in animals of both ages. We conclude that the age of rats plays an important role in heart response to quercetin treatment in the particular dose and duration of the treatment. Therefore, the age of the treated subjects should be taken into consideration when choosing the dose of quercetin and duration of its application in prevention and/or treatment of cardiovascular diseases., M. Bartekova, J. Radosinska, D. Pancza, M. Barancik, T. Ravingerova., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/publicdomain/mark/1.0/ and policy:public