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Biomedical subjects

W Buczko

Publications and source records attributed to W Buczko.

At least 19 recordsLinked to original sources
PubMed1992

Effect of aspirin on the fibrinolytic response in perfused rat hindquarters.

The role of aspirin on tissue plasminogen activator (t-PA) release was studied in rats after experimental venous occlusion. For this purpose, we developed a new experimental model which combines a vascular perfusion system (isolated rat hindquarters) with vascular stimulation, namely the application of venous stasis. Application of venous stasis for 30 min induced the release of t-PA from the vascular endothelium into the perfusate (from 0.19 +/- 0.05 to 0.39 +/- 0.05 UI/ml), reaching a peak 90 s after reperfusion. Aspirin administered to rats 60 min before the experiments (100 mg/kg i.v.), or dissolved in Tyrode solution (100 microM), suppressed 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) synthesis (0.38 +/- 0.09 in control and < 0.01 and 0.15 +/- 0.09 ng/ml, respectively, in aspirin-treated groups) but did not prevent the increase in fibrinolytic activity after venous occlusion (from 0.20 +/- 0.04 to 0.38 +/- 0.06 and from 0.07 +/- 0.03 to 0.27 +/- 0.03 IU/ml, respectively, in the aspirin-treated group). Our results suggest that the increase in fibrinolytic activity after experimental venous occlusion in isolated rat hindlegs is modulated by mechanism(s) other than the cyclooxygenase pathway in the vascular wall.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Cardiovascular effects of acetaldehyde in pithed rats.

The influence of acetaldehyde (30 mg/kg i.v.) on blood pressure and heart rate in anesthetized and pithed rats was studied. In anesthetized rats we observed a small increase, and a subsequent considerable decrease in mean blood pressure. The latter did not occur in pithed rats. Stimulation of the circulatory system in anesthetized and in pithed rats was completely abolished by administration of phentolamine or reserpine. Both in anesthetized and in pithed rats acetaldehyde caused an increase in heart rate which was inhibited in animals treated earlier with propranolol or reserpine. Our results demonstrated that besides its peripheral action, acetaldehyde exerts central effects which cause severe hypotension.

Acetaldehyde↗
PubMed1992

Influence of acetaldehyde on the vasopressor effect of serotonin in pithed rats.

In pithed rats, the intravenous (i.v.) administration of serotonin (3, 10, 30, 100, 300 and 1000 micrograms/kg) produced a dose-dependent increase in blood pressure. The pressor response to serotonin was reduced by acute acetaldehyde administration in a dose of 30 mg/kg i.v. and by 5-HT2 antagonist ketanserin (0.03 mg/kg i.v.). However, the lowest doses of acetaldehyde (10 and 20 mg/kg) were ineffective. In in vitro studies we also demonstrated that acetaldehyde (0.43 mM/l) and ketanserin (0.1 microM/l) inhibited the serotonin-induced vasoconstriction of isolated rat tail artery. In both experimental models the combination of acetaldehyde with ketanserin decreased the action of serotonin to the same extent as did ketanserin alone. In pithed rats pretreated with a high dose of ketanserin (3 mg/kg i.v.) serotonin produced hypotension by stimulation of 5-HT1 receptors. This effect was not enhanced by acetaldehyde (30 mg/kg) injection. Our data suggested that the action of acetaldehyde on the effects of serotonin in pithed rats was non-specific and independent of its interaction with serotonergic 5-HT1 and 5-HT2 receptors in blood vessels.

Acetaldehyde↗
PubMed1992

[Platelet aggregation during the recombinant human erythropoietin (rHuEPO) treatment of patients with uremia].

Patients with uraemia have a defect haemostasis caused by severe anaemia and disturbances of platelet/vessel wall interactions. Recombinant human erythropoietin (rHuEPO) treatment not only corrects anaemia, but also shortens the bleeding time. There are few reports dealing with changes of haemostasis during the first month of rHuEPO treatment. We studied platelet function after 1, 2, 4, 8, and 12 weeks of rHuEPO treatment. Erythropoietin was given to 19 dialysed patients with chronic uraemia in a dose of 2000 u subcutaneously 3 times a week. Bleeding time showed a significant fall as early as after the first week of rHuEPO treatment (p < 0.05). After the first month the bleeding time became normal in most of the patients. A significant rise in ristocetin-induced platelet aggregation was observed from the first week of therapy. It showed a strong correlation with the shortening of the bleeding time. Collagen-induced aggregation followed the same pattern but the changes were not striking. There was not significant difference in platelet adhesion, platelet aggregation in the whole blood and those induced by ADP and arachidonic acid. Platelet serotonin concentration was also showed to increase during rHuEPO therapy. We conclude that rHuEPO improves haemostasis by influencing platelet aggregation possibly involving a serotoninergic mechanism but on the other hand may increase a tendency to thrombosis.

Adult↗
PubMed1992

Factors affecting interstate use of inpatient care by Medicare beneficiaries.

This article examines the extent to which interstate inflow and outflow of patients affects their observed use of Medicare Part A inpatient care. Interstate patient flow can bias utilization rates and may be due to seasonal migration, interstate inpatient care market areas, or purposive seeking of specialized/high-quality care. Examination of state level patient flow data drawn from 1987 Medicare discharge indicate that most interstate patient flow occurs between adjacent states probably as an outgrowth of interstate markets. Regression analyses of patient flow data suggest that while seasonal migration is an important determinant of patient flow, its importance is secondary to that of indicators of the availability of specialized services. These findings suggest research questions that may be best answered in detailed analyses of inpatient utilization in interstate market areas and seasonal migration.

Aged↗
PubMed1992

Influence of DAU 6215, a novel 5-HT3 receptor antagonist, on the cardiovascular system in anaesthetized and pithed rats.

The cardiovascular effects of DAU 6215, a novel 5-HT3 receptor antagonist were studied. DAU 6215 (20 micrograms/kg) inhibited the serotonin-induced Bezold-Jarisch reflex in anaesthetized rats, but did not affect the mean blood pressure and heart rate in anaesthetized rats, in anaesthetized animals after bilateral vagotomy and in pithed rats. This substance also did not affect the serotonin-induced rise in blood pressure in pithed rats and did not influence the response of the isolated rat tail artery to 5-HT. Moreover, DAU 6215 did not change the cardiovascular effects of noradrenaline- and angiotensin-II-stimulated constriction of rat tail artery. Our data suggest that DAU 6215 is rather a selective antagonist, without an affinity to 5-HT2, alpha-adrenoceptors, beta-adrenoceptors and angiotensin II receptors.

Anesthesia↗
PubMed1990

Influence of ethanol and serotonin on rat platelet aggregation.

We demonstrated that ethanol (1.0, 2.0 and 4.0 g/kg p.o.) significantly decreased blood platelet aggregation in a dose-dependent manner. The chronic administration of ethanol (6 g/kg daily for 4 weeks) also altered the sensitivity of rat platelets to ADP (4 mumol/l). We found that the acute and chronic administration of alcohol significantly increased the amplifying effect of 5-hydroxytryptamine (5-HT; 10(-6) mol/l) on ADP-induced aggregation. In all groups of rats, ketanserin (10(-5) mol/l) completely inhibited the amplification of aggregation induced by serotonin. In conclusion, the present results show that ethanol did not only produce inhibition of ADP-induced platelet aggregation but also affected the potentiating action of 5-HT on this process.

Administration, Oral↗
PubMed1990

Influence of acute and chronic ethanol administration on the vasopressor effect of serotonin in pithed rats.

In pithed rats, the intravenous administration of serotonin (3, 10, 30, 100, 300 and 1,000 micrograms/kg) produced a dose-dependent increase in blood pressure. This action of 5-HT was not changed by chronic ethanol intoxication (6.0 g/kg/day for 2 weeks). The pressor responses to serotonin were, in a dose-dependent manner, significantly reduced by acute ethanol administration (0.5, 1.0, 2.0 and 4.0 g/kg p.o.) and by ketanserin injection (0.03 mg/kg i.v.). However, ethanol (2.0 g/kg) did not amplify the dilator effect of serotonin in pithed rats pretreated with ketanserin (3.0 mg/kg i.v.). We also demonstrated that, in contrast to ketanserin (10(-7) mol/l), ethanol (0.05 mol/l) potentiated the serotonin-induced vasoconstriction of isolated rat tail arteries. These data suggest that the action of ethanol on the vasopressor effect of serotonin in pithed rats does not depend on its influence on serotonergic receptors in blood vessels.

Animals↗
PubMed1990

The serotonergic mechanisms are not involved in the inhibitory effect of captopril on rat platelet aggregation.

The influence of captopril on blood platelet aggregation and on serotonergic mechanisms in blood platelets were studied. In rats pretreated with captopril (10.0 mg/kg p.o.) platelet aggregation induced by ADP and collagen was significantly reduced. In vitro this drug had no inhibitory effect. Besides, captopril did not change the amplifying effect of serotonin on platelet aggregation. Captopril also had no influence on the uptake and storage of 5-hydroxytryptamine by rat blood platelets. These results show that serotonergic mechanisms are not involved in the suppressive effect of captopril on platelet aggregation.

Adenosine Diphosphate↗
PubMed1990

Study on mechanisms of a haemostatic effect of 1 deamino-8-D-arginine vasopressin (desmopressin) in uraemic patients.

The effect of 1 deamino-8-D-arginine vasopressin (DDAVP) on blood platelet serotonin and some parameters of haemostasis was investigated. DDAVP was administered intravenously in a dose of 0.4 micrograms/kg BW to 16 uraemic patients maintained on chronic haemodialysis in a double-blind crossover study compared with placebo. The bleeding time was significantly shortened after DDAVP administration from 21.3 +/- 8 minutes to 11.5 +/- 6 minutes (p less than 0.001). VIII: Ag increased from 239.1 +/- 94% to 473 +/- 293% (p less than 0.01). Euglobulin lysis time was shortened from 238 +/- 101 to 148 +/- 84 minutes (p less than 0.005). The platelet serotonin level was significantly reduced from 532 +/- 141 to 366 +/- 88 ng/10(9) platelets (p less than 0.02). There were no changes in haematocrit, platelet count, VIII: C levels and blood serotonin concentrations after DDAVP administration. In placebo group there were no changes in all investigated parameters. Our data indicate that DDAVP shortens prolonged bleeding time in uraemic probably by means of the serotonergic mechanism. Further studies are needed to confirm this suggestion.

Adult↗