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1

Influence of fibrinogen degradation products (FDP) on the ATPase activity in the rat heart

100%
Buczko W.
Acta Physiologica Polonica
|
1978
|
tom 29
|
nr 2
2

Effect of fibrinogen degradation product (FDP) on heart rate some metabolic parameters in the rat

100%
Buczko W.
Acta Physiologica Polonica
|
1978
|
tom 29
|
nr 3
3

Effect of fibrinogen degradation products on the rat blood vessels

100%
Buczko W.
Acta Physiologica Polonica
|
1977
|
tom 28
|
nr 2
4

The effect of bovine fibrinopeptides on the central action of chlorpromazine and amphetamine in rats

100%
Buczko W.
Acta Neurobiologiae Experimentalis
|
1976
|
tom 36
|
nr 4
5

Influence of trypsin on cytostatic effects of cyclophosphamide in rats with Guerin tumours

63%
Buczko W., Popow J.
Acta Physiologica Polonica
|
1976
|
tom 27
|
nr 4
6

Zastosowanie perfuzji wątroby szczura do oceny metabolizmu i transportu leków

63%
Wisniewski K., Buczko W.
Acta Physiologica Polonica
|
1970
|
tom 21
|
nr 1
7

The effects of trypsin-degradation products of albumin on the activity of the central nervous system

51%
Sobaniec W., Buczko W., Moniuszko-Jakoniuk J.
Acta Neurobiologiae Experimentalis
|
1975
|
tom 35
|
nr 1
8

Badanina nad udziałem angiotenzyny w transporcie i metabolizmie hydrazydu kwasu izonikotynowego ( INH)

51%
Danysz A., Buczko W., Wisniewski K.
Acta Physiologica Polonica
|
1970
|
tom 21
|
nr 6
9
Content available remote

Tissue plasminogen activator in the amygdala: a new role for an old protease

51%
Skrzypiec A. E., Buczko W., Pawlak R.
Journal of Physiology and Pharmacology. Supplement
|
2008
|
tom 59
|
nr 8
10

The effect of products of fibrinogen digestion by plasmin (P-FDP) on the central nervous system

51%
Wisniewski K., Buczko W., Moniuszko-Jakoniuk J.
Acta Neurobiologiae Experimentalis
|
1975
|
tom 35
|
nr 3
11

Enzymy szlaku kinureninowego

51%
Tankiewicz A., Pawlak D., Buczko W.
Postępy Higieny i Medycyny Doświadczalnej
|
2001
|
tom 55
|
nr 5
715-731
12

Kallikrein effect on the acquisition and extinction of conditioned reflexes in rats

51%
Moniuszko-Jakoniuk J., Buczko W., Wisniewski K.
Acta Physiologica Polonica
|
1986
|
tom 37
|
nr 1
13
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Content available

The influence of propranolol on the hypotensive action of ketanserin in normotensive rats

51%
Malinowska B., Pietraszek M., Chabielska E., Buczko W.
Acta Physiologica Polonica
|
1989
|
tom 40
|
nr 4
Malinowska, В., Pietraszek, M., Chabielska, E. and Buczko W.: The influence of propranolol on the hypotensive action of ketanserin in normotensive rats. Acta physiol, pol., 1989 40 (4): 356-362. In normotensive rats the effect of different doses of propranolol (1.0, 5.0 and 10.0 mg/kg i.p.) and ketanserin (10.0 mg/kg p.o.) on mean blood pressure and heart rate and on cardiovascular response to noradrenaline (0.1, 0.3, 0.5, 0,7 and 1.0 µg/kg i.v.) was examined. The drugs were given separately or together. Propranolol slightly reduced the hypotensive effect of ketanserin. On the other hand a decrease in heart rate caused by propranolol was not affected by ketanserin. Our results show that propranolol given with ketanserin did not change the effect of the latter on the cardiovascular system.
14
Content available remote

Angiotensin-[1-9], the product of angiotensin I conversion in platelets, enhances arterial thrombosis in rats

51%
Kramkowski K., Mogielnicki A., Leszczynska A., Buczko W.
Journal of Physiology and Pharmacology
|
2010
|
tom 61
|
nr 3
317-324
Angiotensin (Ang) (1-9) is the renin-angiotensin-system peptide found in the plasma of healthy volunteers and after angiotensin-converting-enzyme inhibitors therapy. In vitro experiments proved that Ang-(1-9) may be produced from Ang I. In our study, we tried to expand the poor data about the in vivo properties of Ang-(1-9). We revealed that Ang-(1-9) enhanced electrically stimulated arterial thrombosis in the carotid artery of Wistar rats. Losartan, a selective blocker of AT1 receptor for Ang II, abolished the prothrombotic activity of Ang-(1-9). This peptide increased plasma level of fibrinogen, augments fibrin generation, and similarly to Ang II, potentiated collagen induced platelet aggregation. Using HPLC, we found that after incubation of Ang-(1-9) with platelet homogenates or after intravenous administration this peptide is converted to Ang II. We concluded that Ang-(1-9) exerts an Ang II-like prothrombotic effect due to the conversion to Ang II in the circulatory system of rats and that platelets are involved in this process.
15
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Content available

The antithrombotic effect of captopril and losartan on experimental arterial thrombosis in rats

51%
Chabielska E., Pawlak R., Golatowski J., Buczko W.
Journal of Physiology and Pharmacology
|
1998
|
tom 49
|
nr 2
16
Content available remote

Peripheral distribution of kynurenine metabolites and activity of kynurenine pathway enzymes in renal failure

51%
Pawlak D., Tankiewicz A., Matys T., Buczko W.
Journal of Physiology and Pharmacology
|
2003
|
tom 54
|
nr 2
We investigated L-kynurenine distribution and metabolism in rats with experimental chronic renal failure of various severity, induced by unilateral nephrectomy and partial removal of contralateral kidney cortex. In animals with renal insufficiency the plasma concentration and the content of L-tryptophan in homogenates of kidney, liver, lung, intestine and spleen were significantly decreased. These changes were accompanied by increase activity of liver tryptophan 2,3-dioxygenase, the rate-limiting enzyme of kynurenine pathway in rats, while indoleamine 2,3-dioxygenase activity was unchanged. Conversely, the plasma concentration and tissue content of L-kynurenine, 3-hydroxykynurenine, and anthranilic, kynurenic, xanthurenic and quinolinic acids in the kidney, liver, lung, intestine, spleen and muscles were increased. The accumulation of L-kynurenine and the products of its degradation was proportional to the severity of renal failure and correlated with the concentration of renal insufficiency marker, creatinine. Kynurenine aminotransferase, kynureninase and 3-hydroxyanthranilate-3,4-dioxygenase activity was diminished or unchanged, while the activity of kynurenine 3-hydroxylase was significantly increased. We conclude that chronic renal failure is associated with the accumulation of L-kynurenine metabolites, which may be involved in the pathogenesis of certain uremic syndromes.
17
Content available remote

N-methylnicotinamide inhibits arterial thrombosis in hypertensive rats

51%
Mogielnicki A., Kramkowski K., Pietrzak L., Buczko W.
Journal of Physiology and Pharmacology
|
2007
|
tom 58
|
nr 3
There are few findings indicating that nicotinamide may potentially influence intravascular thrombosis. Interestingly, N-methylnicotinamide, one of the metabolites of nicotinamide - could be more potent than its parent compound. In the present study we have investigated the influence of N-methylnicotinamide on arterial thrombosis in normotensive and renovascular hypertensive rats. The contribution of platelets, coagulation and fibrinolytic systems in the mode of N-methylnicotinamide action was also determined. Furthermore, we examined the role of nitric oxide/prostacyclin in the mechanisms of N-methylnicotinamide action. N-methylnicotinamide, but not nicotinamide, administered intravenously into renovascular hypertensive rats developing electrically induced arterial thrombosis caused dose-dependent decrease of thrombus weight, collagen-induced platelet aggregation and plasma antigen/activity of plasminogen activator inhibitor - 1, without changing of occlusion time, routine coagulation parameters and plasma activity of tissue plasminogen activator. Indomethacin - an inhibitor of prostacyclin synthesis, completely abolished the antithrombotic and antiplatelet effect of N-methylnicotinamide, and the plasma level of 6-keto-PGF1alpha, prostacyclin metabolite, increased simultaneously with the inhibition of thrombus formation. Our study shows that N-methylnicotinamide via production/release of prostacyclin inhibits arterial thrombosis development. The antithrombotic effect of N-methylnicotinamide is accompanied by platelet inhibition and enhanced fibrinolysis, due to the decrease production of plasminogen activator inhibitor - 1.
18
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Content available

The role of endothelium in antithrombotic effect of the renin-angiotensin system blockade

51%
Buczko W., Matys T., Kucharewicz I., Chabielska E.
Journal of Physiology and Pharmacology
|
1999
|
tom 50
|
nr 4
19
Content available remote

Kynurenine and its metabolites in the rat with experimental renal insufficiency

51%
Pawlak D., Tankiewicz A., Buczko W.
Journal of Physiology and Pharmacology
|
2001
|
tom 52
|
nr 4,2
In uremia a great number of the endogenous metabolites that are ordinarily excreted in urine accumulate in the blood. Among these are the products of KYN degradation. In the present study we evaluated the peripheral KYN metabolism in the various stages of the rat experimental chronic renal insufficiency. Our results showed significant disturbances in peripheral kynurenic pathway, which resulted in the significant decrease of TRP plasma level and augmentation of concentration of its metabolites. The high concentrations of 3-hydroxykynurenine, xanthurenic acid, kynurenic acid, anthranilic acid and quinolinic acid positively correlated with degree of the renal insufficiency. Talking into account the biological properties of KYN metabolites, their accumulation in the blood, may be at least partially, responsible for severity of uremia as well as for uremic symptoms such as neuropathy, increased susceptibility to infections, hypertension, lipid disturbances and anemia.
20
Content available remote

The physiological significance of the alternative pathways of angiotensin II production

51%
Kramkowski K., Mogielnicki A., Buczko W.
Journal of Physiology and Pharmacology
|
2006
|
tom 57
|
nr 4
Although the use of angiotensin converting enzyme inhibitors (ACE-Is) in clinical practice brought the great chance to recognize the RAS role in the physiology and pathology, there are still many questions which we cannot answer. This article reviews actually known pathways of angiotensin II (Ang II) and other peptides of renin-angiotensin system (RAS) production and their physiological significance. The various carboxy- and aminopeptidases generate a range of peptides, like Ang II, Ang III, Ang IV, Ang-(1-7) and Ang-(1-9) possessing their own and known biological activity. In this issue especially the alternative pathways of Ang II synthesis involving enzymes other than angiotensin-converting enzyme (ACE) are discussed. We present many evidences for the significance of a new pathway of Ang II production. It has been clearly shown that Ang I may be converted to Ang-(1-9) by angiotensin-converting enzyme-related carboxypeptidase (ACE-2) and then into Ang II in some tissues, but the enzymes responsible for this process are unknown till now. Although there are many data proving the existence of alternative pathways of Ang II production, we can still block only ACE and angiotensin receptor 1 (AT1) in clinical practice. It seems that a lot needs to be done before we can wildly complexively control RAS and treat more effectively cardiovascular disorders such as hypertension or heart failure.
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