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1882. Chronic and acute effects of different antihypertensive drugs on femoral artery relaxation of L_NAME hypertensive rats
- Creator:
- Sládková, M., Kojšová, S., Lýdia Jendeková, and Oľga Pecháňová
- Format:
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- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, hypertenze, hypertension, L_NAME-induced hypertension, indapamide, hydrochlorothiazide, captopril, femoral artery, vasorelaxation, 14, and 612
- Language:
- English
- Description:
- We aimed to compare the effects of chronic and acute administration of structurally different antihypertensives, diuretics - indapamide and hydrochlorothiazide, ACE inhibitor - captopril and indapamide+captopril combination on endothelium-dependent relaxation of femoral artery isolated from nitric oxide (NO)-deficient rats. In the chronic experiment, femoral artery was isolated from Wistar rats receiving L-NAME (40 mg/kg/day) solely or with indapamide (1 mg/kg/day), hydrochlorothiazide (10 mg/kg/day), captopril (10 mg/kg/day), and indapamide+captopril combination for seven weeks. In the acute in vitro experiment, the incubation medium with femoral artery isolated from L-NAMEhypertensive rats was supplemented with investigated antihypertensives in the same concentration 10-4 mol/l. Interestingly, chronic L-NAME treatment did not cause a reduction of vasorelaxation. Indapamide+captopril elevated relaxation above the control level and completely prevented blood pressure increase induced by L-NAME. Acute incubation with captopril only or indapamide+captopril improved relaxation of femoral artery isolated from L-NAMEhypertensive rats, while the incubation with all antihypertensives increased vasorelaxation of femoral artery isolated from control Wistar rats. In conclusion, NO might be involved in the indapamide- and hydrochlorothiazide-induced improvement of vasorelaxation, while different vasorelaxing factors (prostacyclin, EDHF) contribute to the captoprilinduced improvement of vasorelaxation. During the chronic treatment additive and synergic effects of indapamide and captopril may contribute to the prevention of hypertension and increase of vasorelaxation., M. Sládková, S. Kojšová, L. Jendeková, O. Pecháňová., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
1883. Chronic atropine administration diminishes the contributon of vasoactive intestinal polypeptide to heart rate regulation
- Creator:
- Jitka Kuncová, Faitová, Š., Capouch, J., Milan Štengl, and Jana Slavíková
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Experimentální medicína, fyziologie, polypeptidy, srdeční síně, potkan, physiology, polypeptides, atria of heart, Rattus norvegicus, vasoactive intestinal polypeptide, atropine, vagus nerve stimulation, 14, and 616-092
- Language:
- English
- Description:
- Vasoactive intestinal polypeptide (VIP) is implicated in the modulation of vagal effects on the heart rate. In this study, the impact of acute and chronic atropine administration on VIP levels in rat heart atria was investigated in relation to heart rate in the course of vagus nerves stimulation. Anaesthetised control and atropinised (10 mg/kg/day for 10 days) rats pretreated with metipranolol and phentolamine that were either given or not a single dose of atropine were subjected to bilateral vagus nerve stimulation (30 min: 0.7 mA, 20 Hz, 0.2 ms). VIP concentrations in the atria were determined afte reach stimulation protocol. In control rats with or without single atropine administration, the heart rate upon vagal stimulation was higher than in atropinised animals with or without single atropine dose, respectively. VIP concentrations in the control atria were significantly decreased after the stimulation; the decrease was comparable both in the absence and presence of a single dose of atropine. Compared to controls, VIP levels were significantly decreased after chronic atropine treatment and they were not further reduced by vagal stimulation and single atropine administration. Administration of VIP antagonist completely abolished the differences in the heart rate upon vagal stimulation between control and atropinised groups. In conclusion, the data indicate that chronic atropine administration affects VIP synthesis in rat heart atria and consequently it modifies the heart rate regulation., J. Kuncová, Š. Faitová, J. Capouch, M. Štengl, J. Slavíková., and Obsahuje bibliografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
1884. Chronic disturbances in NO production results in histochemical and subcellular alterations of the rat heart
- Creator:
- Narcisa Tribulová, Ľudmila Okruhlicová, Iveta Bernátová, and Oľga Pecháňová
- Format:
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- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, oxid dusnatý, hypertenze, histochemie, nitric oxide, hypertension, histochemistry, ultrastructure, captopril, 14, and 612
- Language:
- English
- Description:
- The mechanisms and myocardial alterations associated with NO-deficient hypertension are still far from clear. The aim of the present study was to focus on the enzyme histochemical and subcellular changes in the heart of L-NAME treated rats, as well as to examine the influence of captopril treatment. Wistar rats were administered either L-NAME (40 mg/kg/day) alone or together with captopril (100 mg/kg/day) for a period of 4 weeks. A significant increase of blood pressure confirmed the reliability of the model. The results showed that long-lasting L-NAME administration was accompanied by a decrease of endothelial NO-synthase activity and by a significant local decrease of the following enzyme activities: capillary-related alkaline phosphatase, 5’-nucleotidase and ATPase (but not dipeptidyl peptidase IV) and cardiomyocyte-related glycogen phosphorylase, succinic dehydrogenase, ß-hydroxybutyrate dehydrogenase and ATPases. No activity of these enzymes was found in the scar, whereas a marked increase of alkaline phosphatase and dipeptidyl peptidase IV activities was found in the foci of fibrotization. Histochemical changes correlated with subcellular changes, which were characterized by 1) apparent fibroblast activation associated with interstitial/perivascular fibrosis, 2) heterogeneous population of the normal, hypertrophic and injured cardiomyocytes, 3) enhancement of the atrial granules and their translocation into the sarcolemma, and 4) impairment of capillaries as well as by induction of angiogenesis. Similar alterations were also found in the heart of captopril co-treated rats, despite of the significant suppression of blood pressure. The results indicate that NO-deficient hypertension is accompanied by metabolic disturbances and ultrastructural alterations of the heart and these changes are probably not induced by the renin-angiotensin system only., N. Tribulová, Ľ. Okruhlicová, I. Bernátová, O. Pecháňová., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
1885. Chronic effects of somatotropin treatment in Vivo and in Vitro on lipogenic activity of goat adipose tissue in a glucose-free buffer during acute incubation
- Creator:
- Josef Škarda
- Format:
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- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, kozy, tuková tkáň, kortizol, goats, adipose tissue, cortisol, somatotropin, lipogenesis, 14, and 612
- Language:
- English
- Description:
- Young castrated male goats (n = 8) were used to investigate the effect of long-term treatment with recombinant methionyl bovine somatotropin in a sustained release vehicle (bST; 100 mg at seven-day intervals in a 147-day experiment) and chronic culture (24 h) of omental adipose tissue in the presence of various hormones on lipogenic responses to catecholamines during acute incubation (2 h) in a sodium acetate supplemented glucose-free buffer. The rate of fatty acid synthesis in freshly-prepared adipose explants was low and did not differ from those cultured in the absence of hormones for 24 h. Hormonal combination of insulin (17 nmol.l-1) plus cortisol (138 nmol.l-1) or insulin plus recombinant enterokinase linker bST (4.5 nmol.l-1) increased lipogenesis (P<0.05). Further addition of bST or cortisol decreased lipogenesis significantly (P<0.05) in the controls but not significantly in bST-treated animals. Cultured explants from either control or bST-treated animals showed significant inhibition of lipogenesis by both norepinephrine (10 m mol.l-1) and isoprenaline (10 m mol.l-1). BST treatment in vivo did not increase the responsiveness of cultured explants to norepinephrine in vitro, however, the responsiveness to isoprenaline(inhibition of lipogenesis) was greater in bST-treated animals than in the controls., J. Škarda., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
1886. Chronic low-dose L-NAME treatment increases nitric oxide production and vasorelaxation in normotensive rats
- Creator:
- Iveta Bernátová, Kopincová, J., Angelika Púzserová, Pavol Janega, and Pavel Babál
- Format:
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- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, hypertenze, krevní tlak, acetylcholin, hypertension, blood pressure, acetylcholine, cardiac and vascular structure, negative feedback regulation, serotonin, 14, and 612
- Language:
- English
- Description:
- NG-nitro-L-arginine methyl ester (L-NAME) is a non-specific nitric oxide (NO) synthase inhibitor, commonly used for the induction of NO-deficient hypertension. The aim of this study was to investigate the effect of chronic low-dose administration of L-NAME on NO production, vascular function and structure of the heart and selected arteries of rats. Adult male Wistar rats were treated with L-NAME in the dose of approximately 1.5 mg/kg/day in drinking water for 8 weeks. Basal blood pressure (BP) of rats (determined by tail-cuff) was 112±3 mm Hg. The low-dose administration of L-NAME significantly elevated BP measured on the third and sixth week of treatment vs. controls by approximately 9 % and 12 %, respectively. After this period, BP of L-NAME-treated rats returned to the control values. The relative left ventricular mass, heart fibrosis and collagen III/collagen I ratio were not affected by L-NAME. Similarly, there were no alterations in the cross-sectional area and wall thickness/diameter ratio of the aorta and the femoral artery of LNAME- treated rats. NO synthase activity (determined by conversion of [3H]-L-arginine to [3H]-L-citrulline) was not altered in the hypothalamus of L-NAME-treated rats. Interestingly, chronic low-dose L-NAME treatment significantly elevated NO synthase activity in the left ventricle and aorta, increased endothelium-dependent acetylcholine-induced vasorelaxation and reduced serotonin-induced vasoconstriction of the femoral artery. The data suggest that chronic lowdose L-NAME treatment can increase NO production and vasorelaxation in normotensive rats without negative structural changes in the cardiovascular system., I. Bernátová, J. Kopincová, A. Púzserová, P. Janega, P. Babál., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
1887. Chronic oral administraton of beta-adrenoceptor agonist clenbuterol affects myosin heavy chain (MHC) expression in adult mouse heart
- Creator:
- Patiyal, Som N. and Sharma, S.
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- Type:
- article, články, model:article, and TEXT
- Subject:
- Biologické vědy, fyziologie, srdce, physiology, heart, clenbuterol, myosin heavy chain isoforms, left ventricle, actomyosin ATPase, cardiac muscle contraction, 2, and 57/59
- Language:
- English
- Description:
- The aim of this study was to analyze the effects of chronic administration of the β-adrenoceptor agonist clenbuterol (2 mg/kg body weight/day for a period of 30 days) on the major contractile protein (myosin) in the left ventricular muscle of the adult mouse heart. Separation of myosin heavy chain (MHC) isoforms on 7.5 % glycerol SDS-PAGE and subsequent quantification of the gels by laser densitometry showed a 6.5-fold increase in the β-isoform of MHC in the clenbuterol-treated group. The α: β ratio of these two isoforms in the control group was 98.16±0.14 %: 1.83±0.14 %, whereas in the treated group it was 88.05±1.15 %: 11.95±1.15 %. Actomyosin ATPase activity assay demonstrated a significant (20 %) decline in ATPase activity of the tissue in the β-agonist-treated group. These results suggest that chronic clenbuterol treatment is capable to induced the transformation of MHC isoforms increasing the slow β-MHC isoform, which may contribute to the altered contractile mechanics of clenbuterol-treated hearts., S. N. Patiyal, S. Sharma., and Obsahuje bibliografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
1888. Chronic poverty in Kazakhstan
- Creator:
- Kudebayeva, Alma
- Publisher:
- CERGE-EI
- Format:
- electronic, bez média, svazek, and 37 stran : tabulky, grafy.
- Type:
- model:monograph and TEXT
- Subject:
- Sociální problémy vyžadující podporu a pomoc. Sociální zabezpečení, chudoba, poverty, Kazachstán, Kazakhstan, 364.662, (574), (048.8), 18, and 364
- Language:
- English and Czech
- Description:
- Alma Kudebayeva., Obsahuje bibliografii a bibliografické odkazy, and České a anglické resumé
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
1889. Chronic stress promotes the progression of pressure overload-induced cardiac dysfunction through inducing more apoptosis and fibrosis
- Creator:
- Liu, W., Wang, X., Mei, Z., Gong, J., Gao, X., Zhao, Y., Ma, J., Xie, F., and Qian, L.
- Format:
- print, bez média, and svazek
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, stres (fyziologie), stress (physiology), chronic stress, pressure overload, cardiac dysfunction, norepinephrine, 14, and 612
- Language:
- English
- Description:
- Stress serves as a risk factor in the etiology of hypertension. The present study was designed to decipher the effect and mechanism of chronic stress on the progression of pressure overload-induced cardiac dysfunction. We used abdominal aortic constriction (AAC) to induce pressure overload with or without chronic restraint stress to establish the animal models. Echocardiographic analysis showed pressure overload-induced cardiac dysfunction was worsened by chronic stress. Compared with the AAC rats, there is a significant increase in cardiac hypertrophy, injury, apoptosis and fibrosis of the AAC + stress rats. Furthermore, we found the secretion of norepinephrine (NE) increased after the AAC operation, while the level of NE was higher in the AAC + stress group. Cardiomyocytes and cardiac fibroblasts isolated from neonatal rats were cultured and separately treated with 1, 10, 100 μM NE. The higher concentration NE induced more cardiomyocytes hypertrophy and apoptosis, cardiac fibroblasts proliferation and collagen expression. These results revealed that high level of NE-induced cardiomyocytes hypertrophy and apoptosis, cardiac fibroblasts proliferation and collagen expression further contributes to the effect of chronic stress on acceleration of pressure overloadinduced cardiac dysfunction., W. Liu, X. Wang, Z. Mei, J. Gong, X. Gao, Y. Zhao, J. Ma, F. Xie, L. Qian., and Obsahuje bibliografii
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
1890. Chronická bolest a strach
- Creator:
- Petr Knotek, Helena Knotková, and Jaroslava Raudenská
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- Type:
- article, články, model:article, and TEXT
- Subject:
- Psychologie, psychologie, psychology, kognice, úzkost, Dynamický model psychologických procesů, cognition, anxiety, Dynamic Model of Psychological Processes, 17, and 159.9
- Language:
- Czech
- Description:
- a1_Bolest je signál ohrožení organizmu. Váže pozornost, narušuje probíhající psychické procesy a vyvolává strach, který neuropsychicky zesiluje bolest, působí hyperestézii a negativní nabuzení (arousal). Kognitivní hodnocení bolesti jako ohrožení vyvolá také strach. Výsledný strach je tedy generovaný neuropsychicky („reflexně“) i kognitivně. Strach, vyvolaný oběma mechanizmy, narušuje zvládání bolesti (coping). Selháváním procesu zvládání vzniká úzkost, zlost a deprese a dále nepříznivé hodnocení vlastní schopnosti zvládat bolest a spokojeně žít. Na předpokladu těchto procesů, jejichž podstatné segmenty byly testované strukturálním modelem EQS, je založen Dynamický model psychologických procesů při chronické bolesti (DM). Původní DM, podobně jako další současné modely chronické bolesti lze považovat za modely lokálně nezávislé (tedy vysvětlené „ze sebe sama“). V této práci jsou analyzovány „spouštějící“ procesy DM, pocit bolesti a kognitivní zpracovávání bolesti, a oběma procesy vyvolaný strach. Protože tyto procesy probíhají v rámci osobnosti jako vyššího psychologického celku, autoři rozšiřují původní předpoklad DM o rys úzkosti, jako další podmínku toho, jak silný bude strach, vyvolaný bolestí a jejím kognitivním zpracováním. Na souboru 272 pacientů s nemaligní bolestí, věk M = 47,93 (SD = 10,73) roků, trvání bolesti v letech = 11,06 (SD = 9,57), byl postupně testován odpovídající regresní model: K původním nezávisle proměnným, faktorům Bolest (Intenzita bolesti, Nepříjemnost bolesti) a Kognitivní zpracovávání bolesti (Očekávání bolesti v budoucnu, Vina druhých aj.), byla nově zavedena „vnější“ proměnná, Rys úzkosti, a vypočítána lineární regrese na Strach z bolesti., a2_Po redukci modelu s 8 měřenými hodnotami (CFI = 0,81) na 5 měřených hodnot (CFI = 0,84) přistoupili autoři k zařazení další proměnné (tj. mimo původní DM), kovariancí mezi (reziduální variancí) Přetrváváním bolesti a Rysem úzkosti. Tento model se dobře shoduje s daty (CFI = 0,95). Předpoklad přímého vztahu mezi Přetrváváním bolesti a Rysem úzkosti tak významně zvyšuje shodu modelu s daty. Strach z bolesti je tedy nejvíce podmíněn kognitivně, a to očekáváním, že bolest potrvá, a přisuzováním viny za bolest druhým. Efekt dispoziční úzkosti je dvojí: a) Strach z bolesti je specifický projev dispoziční úzkosti při bolestivém stavu, b) dispoziční úzkost ovlivňuje nastavení kognitivních procesů a vede k očekávání bolesti v budoucnosti, a tím ke strachu z bolesti. Pocit bolesti, atribut bolestivého stavu, tyto procesy spouští. Efekt intenzity a nepříjemnosti bolesti na strach z bolesti je malý., b1_Pain represents a signal that an organism is in danger. It attracts attention, it disturbs ongoing mental processes and it brings about fear. In addition, cognitive appraisal of the pain brings about fear as well. The resulting fear triggers coping. If the coping fails, it is followed by anxiety, anger, depression and negative evaluation of one‘s ability to cope with the pain and to live well. Assumption of the processes forms the basis of the Dynamic Model of Psychological Processes in Chronic Pain (DM). The original DM, similarly to other recent models of chronic pain, may be considered a locally independent model (i.e., explained “by itself”). The present paper contains an analysis of “triggering” processes of the DM, the feeling and cognitive processing of the pain, as well as the fear caused by both processes. In addition, the DM assumption is expanded by an “external” variable – Trait Anxiety – representing another condition of the fear. In a group of 272 patients with non-malignant pain (age: M=47.9, SD=10.7 years; duration of pain: M=11.1, SD=9.6 years), the authors gradually tested the regression model: together with the original DM factors of Pain (Pain Intensity, Pain Unpleasantness, and Cognitive Processing of Pain) a new “external“ variable Trait Anxiety was entered and the linear regression on the Fear of Pain was calculated. After reducing the model containing 8 measured values (CFI=0.81) to a model having 5 measured values (CFI=0.84), additional variables were included and covariance between Permanence of Pain and Trait Anxiety was computed. Resulting model fits the data very well (CFI=0.95). The assumption of a direct relationship between the Permanence of Pain and Trait Anxiety significantly increases correspondence of the model with the data., b2_ The results show that the fear of pain is primarily cognitively dependent on expectation that pain will last in future and that pain is blamed on the others. Two effects of Trait Anxiety in the Fear of Pain were found: a) the Fear of Pain represents specific manifestation of Trait Anxiety under pain conditions, b) Trait Anxiety influences cognitive setting, which leads to expectation that pain will last and it thus creates Fear of Pain. The effect of Pain Intensity and Pain Unpleasantness on the Fear of Pain is small., Petr Knotek, Helena Knotková, Jaroslava Raudenská., and Obsahuje seznam literatury
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public