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  1. 19 Journal of Physiology and Pharmacology

  2. 5 Acta Biochimica Polonica

  3. 2 Folia Histochemica et Cytobiologica

  4. 2 Journal of Animal and Feed Sciences

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  1. 33 Chlopicki S.

  2. 13 Gryglewski R. J.

  3. 5 Mateuszuk L.

  4. 5 Olszanecki R.

  5. 4 Gajda M.

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  1. 3 2018

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1

Endothelial profiling in vivo: novel approach to experimental pharmacology of endothelium

100%
Chlopicki S.
Acta Biochimica Polonica
|
2018
|
tom 65
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nr S2
2

No-the universal mediator in cardiovascular system

75%
Chlopicki S.
Acta Biochimica Polonica
|
2003
|
tom 50
|
nr Supplement 1
3
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The endothelium-dependent and the endothelium-independent vasodilators in the isolated, perfused guinea pig heart

63%
Chlopicki S., Gryglewski R. J.
Journal of Physiology and Pharmacology
|
1992
|
tom 43
|
nr 4
The endothelium-dependent (acetylcholine, bradykinin, substance P) and the endothelium-independent (gliceryl trinirate, 3-morpholinsydnominine, sodium nitroprusside) vasodilators were studied in the Langendorff-perfused heart of the guinea pig. The involvement of prostanoids and EDRF in the endothelium-dependent responses were assessed by using indomethacin, an inhibitor of cyclooxygenase, and NG -nitro-L-Arginine, an inhibitor of NO synthase. The endothelium-independent agents were used as reference compounds. Both indomethacin and NG -nitro- L-Arginine elevated significantly baseline coronary perfusion pressure, indicating that prostanoids (most likely PGI₂ and PGE₂ ) and EDRF modulate the resting tone of the guinea pig coronary circulation. NG-nitro-L-Arginine, but not indomethacin, considerably reduced receptor-stimulated responses. It is concluded that acetylcholine, bradykinin or substance P-induced vasodilation is mediated by EDRF. In contrast, prostanoids do not contribute to endothelium-dependent responses. In addition, short-term tachyphylaxis to bolus injection of gliceryl trinitrate but not of sodium nitroprusside was demonstrated, suggesting that this preparation may be of value for studying nitrate tolerance.
4
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Endotoxaemia in rats: role of NO, PAF and TXA2 in pulmonary neutrophil sequestration and hyperlactataemia

63%
Olszanecki R., Chlopicki S.
Journal of Physiology and Pharmacology
|
1999
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tom 50
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nr 3
5

Ocena czynności globalnej lewej komory serca w mysim modelu Tgalfaq*44 przy pomocy obrazowania magnetyczno-rezonansowego

51%
Jablonska M., Tyrankiewicz U., Skorka T., Chlopicki S.
Annals of Warsaw University of Life Sciences - SGGW. Animal Science
|
2011
|
tom 48
6
Content available remote

Ultrastructure of immediate microvascular lung injury induced by bacterial endotoxin in the isolated, no-deficient lung perfused with full blood

51%
Chlopicki S., Walski M., Bartus J. B.
Journal of Physiology and Pharmacology. Supplement
|
2005
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tom 56
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nr 4
47-64
NOS-2-derived NO is involved in hypotension, vasoplegia, metabolic disorders and lung injury in endotoxic shock. On the other hand, NOS-3-derived NO protects against LPS-induced lung injury. We have previously shown that NO limits lung injury in the isolated blood-perfused rat lung. Here we characterize the ultrastructure of microvascular lung injury induced by LPS in the absence of endogenous NO and summarize our data on the mechanisms of immediate lung response to LPS in the presence and absence of endogenous NO. Injection of LPS (from E.Coli, 300 µg/ml) into the isolated blood-perfused rat lung induced an immediate transient constriction of airways and vessels that was not associated with lung edema and pulmonary microcirculation injury. In contrast, in the presence of the NOS inhibitor L-NAME (300 µg/ml), LPS produced an enhanced constriction of airways and vessels, which was accompanied by profound lung edema and capillary-alveolar barrier injury, as evidenced by optic and electron microscopy. Microvascular lung injury was confirmed by the following findings: edema of pulmonary endothelium with low electronic density of endothelial cytoplasm, presence of protein-rich fluid and numerous erythrocytes in alveolar space, concentric figures of damaged tubular myelin of surfactant (myelin-like bodies), edema of epithelium type I cells with low electronic density of their cytoplasm and alterations in ultrastructure of basal membrane of vascular-alveolar barrier. Interestingly, epithelial type II cells did not show signs of injury. It is worth noting that capillary-alveolar barrier injury induced by L-NAME+LPS was associated with sequestration of platelets and neutrophils in pulmonary microcirculation and internalization of LPS by neutrophils. In conclusion, in the absence of endogenous nitric oxide LPS induces injury of microvascular endothelium and vascular-alveolar barrier that leads to fatal pulmonary edema. Mechanisms of immediate lung response to LPS in presence of NO and those leading to acute microvascular lung injury in response to LPS in absence of NO are summarized. In our view, immediate lung response to bacterial endotoxin represents a phylogenetically ancient host defence response involving complement-dependent activation of platelets and neutrophils and subsequent production of lipid mediators. This response is designed for a quick elimination of bacterial endotoxin from the circulation and is safeguarded by endothelial NO.
7
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NO-dependent vasodilation induced by nebivolol in coronary circulation is not mediated by beta-adrenoceptors or by 5 HT 1A-receptors

51%
Chlopicki S., Kozlovski V. I., Gryglewski R. J.
Journal of Physiology and Pharmacology
|
2002
|
tom 53
|
nr 4,1
Nebivolol is a unique ß1-adrenoceptor antagonist which possesses peripheral vasodilator properties dependent on endothelial NO. Nebivolol-induced release of NO was attributed to its L stereoisomer and to its ability to stimulate endothelial ß2, ß3 adrenoceptors or 5-HT1A receptors. Here, in the isolated guinea pig heart we analysed coronary vasodilator potency of L- and D-nebivolol and a possible role of ß2, ß3 adrenoceptors and 5-HT1A receptors in nebivolol-induced vasodilation. Surprisingly, we found that not only L-nebivolol (3-30x10-6 M) but also D-nebivolol (3-30x10-6 M) induced coronary vasodilation, and both responses were inhibited by L-NAME (10-4 M). In contrast with the stereoisomers of nebivolol, atenolol at the equimolar concentrations did induce slight vasoconstriction. The nonselective ß1/ß2- adrenoceptor antagonist - nadolol (10-5 M), the selective ß3-adrenoceptor antagonist - L 748337 (10-6 M) and the 5 HT1A receptor antagonist - NAN 190 (5 x 10-6 M), none of them inhibited coronary vasodilation induced by D- and L-nebivolol. In summary, in the isolated guinea pig heart both D- and L-nebivolol act as coronary vasodilators. Coronary vasodilation induced by stereoisomers of nebivolol is mediated by endothelium-derived NO and does not depend on ß2, ß3 adrenoceptors or 5 HT1A receptors.
8
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Reversal of the postischaemic suppression of coronary function in perfused guinea pig heart by ischaemic preconditioning

51%
Chlopicki S., Lomnicka M., Gryglewski R. J.
Journal of Physiology and Pharmacology
|
1999
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tom 50
|
nr 4
9
Content available remote

The involvement of adhesion molecules and lipid mediators in the adhesion of human platelets to eosinophils

51%
Jawien J., Lomnicka M., Korbut R., Chlopicki S.
Journal of Physiology and Pharmacology
|
2005
|
tom 56
|
nr 4
Platelet-leukocyte interactions represent an important determinant of the inflammatory response. Although mechanisms of platelet-neutrophil adhesion were studied extensively, little is known on the mechanisms of platelet-eosinophil interactions. The aim of the present study was to analyze the involvement of adhesion molecules and lipid mediators in platelet-eosinophil adhesion as compared to platelet-neutrophil adhesion. For that purpose human platelets, eosinophils and neutrophils were isolated and platelet-eosinophil and platelet-neutrophil adhesion induced by thrombin (30 mU/ml), LPS (0.01 µg/ml) and fMLP (1 µM) was quantified using the "rosettes" assay. The involvement of adhesion molecules such as selectin P, glycoprotein IIb/IIIa (GPIIb/IIIa) and lipid mediators such as of thromboxane A2 (TXA2), platelet activating factor (PAF) and cysteinyl leukotrienes (cysLTs) were studied using monoclonal antibodies and pharmacological inhibitors, respectively. Thrombin (30 mU/ml), LPS (0.01 µg/ml) and fMLP (1 µM) each of them induced platelet-eosinophil adhesion that was even more pronounced as compared with platelet-neutrophil adhesion induced by the same stimulus. Anti-CD62P antibody (1 µg/ml) and anti-GP IIb/IIIa antibody (abciximab - 3 µg/ml) strongly inhibited platelet-eosinophil as well as platelet-neutrophil adhesion. Aspirin inhibited platelet-eosinophil adhesion, while MK 886 - a FLAP inhibitor (10 µM), or WEB 2170 - a PAF receptor antagonist (100 µM) were less active. On the other hand aspirin, MK 886 and WEB 2170 all three of them inhibited platelet-neutrophil adhesion. In summary, platelets adhered avidly to eosinophils both after activation of platelets by thrombin, eosinophils by fMLP or simultaneous activation of platelets and eosinophils by LPS. Similarly to platelet-neutrophil interaction adhesion of platelets to eosinophils involved not only adhesion molecules (selectin P, GPIIb/IIIa), but also lipid mediators such as TXA2. The involvement of PAF and cysteinyl leukotrienes in platelet-eosinophil adhesion was less pronounced as compared to platelet-neutrophil adhesion.
10
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Clonidine-induced coronary vasodilatation in isolated guinea pig heart is not mediated by endothelial alpha2 adrenoceptors

51%
Chlopicki S., Kozlovski V. I., Gryglewski R. J.
Journal of Physiology and Pharmacology
|
2003
|
tom 54
|
nr 4
Functional role of endothelial alpha2-adrenoceptor in coronary circulation remains unclear. Clonidine, an agonist of alpha2-adrenoceptors, was reported to induce coronary vasodilatation via stimulation of endothelial alpha2-adrenoceptors or coronary vasoconstriction involving vascular smooth muscle alpha2-adrenoceptors. Moreover, H2 receptor-dependent responses to clonidine were described. Here, we reassess the contribution of endothelial alpha2-adrenoceptor and H2 receptors to coronary flow and contractility responses induced by clonidine in the isolated guinea pig heart. We found that clonidine (10-9 - 10-6 M) produced concentration-dependent coronary vasoconstriction without a significant change in contractility. This response was inhibited by the alpha1/alpha2-adrenoceptor antagonist - phentolamine (10-5 M) and the selective alpha2-adrenoceptor antagonist yohimbine (10-6 M), but it was not changed by the selective alpha1-adrenoceptor antagonist prazosin (10-6 M). In the presence of nitric oxide synthase inhibitor, L-NAME (10-4 M) the clonidine-induced vasoconstriction was potentiated. Clonidine at high concentrations of 10-5 – 3 x 10-5 M produced coronary vasodilatation, and an increase in myocardial contractility. These responses were abolished by a selective H2-receptor antagonist, ranitidine (10-5 M), but not by phentolamine (10-5 M). We conclude that in the isolated guinea pig heart, clonidine-induced vasoconstriction is mediated by activation of smooth muscle alpha2-adrenoceptors whereas clonidine-induced coronary vasodilatation is mediated by activation of vascular H2 histaminergic receptors. Accordingly, endothelial alpha2-adrenoceptors does not seem to play a major role in coronary flow response induced by clonidine.
11

Kinetics of increased generation of NO in endotoxaemic rats as measured by EPR

51%
Plonka P. M., Chlopicki S., Wisniewska M., Plonka B. K.
Acta Biochimica Polonica
|
2003
|
tom 50
|
nr 3
Ferrous-diethyldithiocarbamate (Fe(DETC)2) chelate is a lipophilic spin trap devel­oped for NO detection by electron paramagnetic resonance (EPR) spectroscopy. Using this spin trap we investigated the kinetics of NO production in endotoxaemia in rats induced by lipopolysaccharide (Escherichia coli, 10 mg/kg). The NO-Fe(DE- TC)2 complex was found to give a characteristic EPR signal, and the amplitude of the 3rd (high-field) component of its hyperfine splitting was used to monitor the level of NO. We found that in blood, kindey, liver, heart and lung NO production starts to in­crease as early as 2 h after LPS injection, reaches the maximum 6 h after LPS injec­tion and then returns to basal level within further 12-18 h. Interestingly, in the eye bulb the maximum of NO production was detected 12 h after LPS, and the signal was still pronounced 24 h after LPS. In brief, the highly lipophilic exogenous spin trap, Fe(DETC)2 is well suited for assessment of NO production in endotoxaemia. We dem­onstrated that the kinetics of increased production of NO in endotoxaemic organs, with the notable exception of the eye, do not follow the known pattern of NOS-2 induc­tion under those conditions. Accordingly, only in early endotoxaemia a high level of NO is detected, while in late endotoxaemia NO detectability is diminished most probably due to concomitant oxidant stress.
12
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Kinins and thrombolysis

51%
Swies J., Chlopicki S., Gryglewski R. J.
Journal of Physiology and Pharmacology
|
1993
|
tom 44
|
nr 2
13
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Permissive effect of molsidomine towards cardioprotective action of iloprost in myocardial ischaemia in cats

51%
Gryglewski R. J., Swies J., Chlopicki S., Niezabitowski P.
Journal of Physiology and Pharmacology
|
1993
|
tom 44
|
nr 3
14
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Role of thromboxane A2 and platelet activating factor in early haemodynamic response to lipopolysaccharide in rats

51%
Bochenski J., Chlopicki S., Gryglewski R. J.
Journal of Physiology and Pharmacology
|
1999
|
tom 50
|
nr 2
15
Content available remote

Involvement of platelet activating factor in immediate heart response to lipopolysaccharide

51%
Jakubowski A., Olszanecki R., Chlopicki S.
Journal of Physiology and Pharmacology
|
2004
|
tom 55
|
nr 2
Although lipopolysaccharide (LPS) is recognized to induce a biphasic cardiovascular response its mechanism is not fully elucidated. In this study we analysed the involvement of PAF, TXA2 and cysteinyl leukotrienes (cysLTs) in the acute cardiovascular effects of LPS in the isolated rat heart as well as in delayed phase of LPS response using a surrogate cellular model of the induction of NOS-2 by LPS in mouse macrophages. Perfusion of rat hearts with LPS resulted, in an immediate fall in heart contractility and coronary flow by 2.5 ± 0.59 ml min-1 and 560 ± 81 mmHg sec-1, respectively. This response was fully blocked by platelet activating factor (PAF) antagonist - WEB 2170 and partially inhibited, by inhibitor of cyclooxygenase (indomethacin) or by inhibitor of thromboxane synthase (camonagrel). The inhibition of leukotriene synthesis (BAY x1005) or cysLTs receptors (BAY x7195) was without effect. Administration of stable PAF analog (methylcarbamyl-PAF - MC-PAF) alone, mimicked heart response to LPS. In cultured mouse macrophages, MC-PAF did not induce NOS-2 expression and when given with LPS it slightly potentiated NOS-2 induction by LPS. However, in presence of WEB 2170 NOS-2 induction by LPS was inhibited in a dose-dependent manner. Inhibition of cyclooxygenase and leukotriene pathways had no effect on NOS-2 induced by LPS. These results indicate that PAF and TXA2 but not cysLTs mediate the instant heart response induced by LPS, while PAF alone mediates a delayed NOS-2 induction by LPS. Accordingly, PAF may constitute the mediator that links acute and delayed phases of LPS-induced cardiovascular response.
16
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Increased pneumotoxicity of lipopolysaccharide from E.coli in nitric oxide deficient blood-perfused rat lungs

51%
Bartus J. B., Chlopicki S., Gryglewski R. J.
Journal of Physiology and Pharmacology
|
1997
|
tom 48
|
nr 4
17
Content available remote

Ultrastructural alterations of endothelium covering advanced atherosclerotic plaque in human carotid artery visualised by scanning electron microscope

51%
Walski M., Chlopicki S., Celary-Walska R., Frontczak-Baniewicz M.
Journal of Physiology and Pharmacology
|
2002
|
tom 53
|
nr 4,1
Human atherosclerotic plaque morphology at its various stages was extensively documented using light microscopy. However, much less is known of the ultrastructure of the human atherosclerotic plaque, in particular of ultrastructure of endothelial cells in atherosclerosis. Here, we analysed alterations of endothelial cells covering advanced atherosclerotic plaque in carotid artery using scanning electron microscope. Examination was performed on specimens from atherosclerotic lesions of the interior carotid artery, collected from 8 patients who had undergone endarterectomy. We found wide spectrum of pathological alterations of the luminal surface of atherosclerotic plaque. In dominant part of the vessel, endothelial layer was preserved but displayed pronounced irregularities in endothelial architecture including appearance of cuboidal cells. Some endothelial cells were covered by numerous microvilli and/or contained "craters" disrupting continuous surface of the endothelium. Platelets and leukocytes adhering to endothelium were frequently observed. There were also areas of the vessel lumen with endothelial denudation, in which the subendothelial surface containing fibrin proteins and collagen fibrils were visible. Interestingly, signs of proliferation of endothelial cells tending to cover the partially denuded vessel were observed. In summary, in scanning electron microscope, preserved endothelial cells of advanced atherosclerotic plaque displayed pronounced pathology; whether any of these changes represent the ultrastructural correlate of endothelial dysfunction remains to be established.
18
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Paradoxical augmentation of bradykinin-induced vasodilatation by xanthine-xanthine oxidase-derived free radicals in isolated guinea pig heart

51%
Olszanecki R., Kozlovski V. I., Chlopicki S., Gryglewski R. J.
Journal of Physiology and Pharmacology
|
2002
|
tom 53
|
nr 4,1
Increased generation of reactive oxygen species contribute to endothelial dysfunction in atherosclerosis, hypertension and heart failure. Recently, it was suggested that bursts of superoxide anions may inactivate endothelial surface-bound enzymes such as angiotensin converting enzyme (ACE). Here, we tested effects of xanthine/xanthine oxidase-derived superoxide anions on vascular responses and ACE activity in the isolated guinea pig heart. We analysed effects of intracoronary infusion of low concentration of xanthine oxidase (10 mU/ml) in the presence of xanthine (0,5 mM) (X/XO) on bradykinin, other endothelium-dependent and independent vasodilators (acetylcholine, ADP, SNAP), as well as vasoconstrictor responses to angiotensin I and angiotensin II. Surprisingly, X/XO significantly augmented coronary response to bradykinin without an effect on responses to ADP, acetylcholine, SNAP, angiotensin I and angiotensin II. In contrast, inhibition of ACE by perindoprilate (100 nM) resulted in augmentation of bradykinin-induced vasodilatation as well as diminution of angiotensin I-evoked vasoconstriction without an influence on other responses. In summary, in the isolated guinea pig heart, X/XO-derived free radicals selectively augmented coronary vasodilator response to bradykinin, which cannot be explained by X/XO- induced derangement of ACE. The mechanism of this paradoxical phenomenon, which might represent a defensive response of the coronary circulation to oxidative stress requires further investigations.
19
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Biphasic response to lipopolysaccharide from E.coli in the isolated ventilated blood-perfused rat lung

51%
Chlopicki S., Bartus J. B., Gryglewski R. J.
Journal of Physiology and Pharmacology
|
1999
|
tom 50
|
nr 4
20

Critical evaluation of normotensive rats as models for hypercholesterolaemia-induced atherosclerosis

45%
Pisulewski P. M., Kostogrys R. B., Lorkowska B., Bartus M., Chlopicki S.
Journal of Animal and Feed Sciences
|
2005
|
tom 14
|
nr 2
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