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Biomedical subjects

W Buczko

Publications and source records attributed to W Buczko.

At least 91 records · Page 5Linked to original sources
PubMed1995

A study of platelet functions, some hemostatic and fibrinolytic parameters in relation to serotonin in hemodialyzed patients under erythropoietin therapy.

Erythropoietin corrects anemia and improves hemostasis, but on the other hand bears a risk of thrombotic complications. Therefore in the present study an attempt has been made to evaluate bleeding time, platelet functions and some hemostatic and fibrinolytic parameters in relation to blood and platelet serotonin before and after 1, 2, 4, 8 and 12 weeks of treatment. 22 chronically hemodialyzed patients were administered with human recombinant erythropoietin (rHuEPO) in a dose of 2000 IU s.c. 3 times a week. Bleeding time was shortened significantly as early as after 1 week of the therapy, whereas hematocrit and hemoglobin increased after 2 weeks. These changes lasted throughout the study. Only a transient rise in platelet count, collagen-induced platelet aggregation, beta-thromboglobulin and VIII:C activity were observed during therapy relative to baseline values. ADP- and arachidonic acid-induced platelet aggregation seemed to be unaffected by rHuEPO treatment, whereas a gradual and progressive enhancement in platelet aggregation in response to ristocetin was found, starting from the 2nd week of the therapy. It lasted throughout the study and correlated inversely with the bleeding time and positively with a rise in both blood and platelet serotonin. rHuEPO did not alter plasminogen, fibrinogen, platelet factor 4, alpha 2 macroglobulin levels, protein C activity and euglobulin clot lysis time. A decline in protein C and S concentrations and antithrombin III activity observed during the therapy were counterbalanced by a fall in the activity of alpha 2 antiplasmin, C1 esterase inhibitor and plasminogen activator inhibitor. It is concluded that rHuEPO may improve platelet/vessel wall interactions possibly by means of serotonergic mechanisms. A lowered activity of inhibitors of fibrinolysis may be regarded as a protection against a general tendency to thrombosis during rHuEPO therapy.

Adenosine Diphosphate↗
PubMed1995

Enhanced vascular plasminogen activator (t-PA) release by epinephrine in aged rats.

Adrenergic stimulation induces an acute fibrinolytic response in the vascular wall and can play an important role in limiting thrombus growth. The incidence of thrombotic disease increases with age. As many adrenergic functions are affected by aging, the vascular response to adrenergic stimulation was studied in young (3 +/- 1 months) and aged (18 +/- 3 months) rats, using an experimental model of vascular perfusion. Five min epinephrine (EPI) infusion (0.15-25 microM) induced a dose-dependent increase in tissue-type plasminogen activator (t-PA) release and in perfusion pressure, in both young and aged rats. In the latter, however, the basal activity of t-PA was significantly higher than in young animals (0.22 +/- 0.02 vs 0.13 +/- 0.01 U/ml; means +/- SE; p < 0.01, n = 40) and EPI infusion induced a significantly higher increase in t-PA activity (0.78 +/- 0.06 vs 0.47 +/- 0.08 U/ml, p < 0.01, for 6.25 microM EPI). The response was characterized by a delayed onset. In contrast, the increase in the perfusion pressure by EPI was significantly lower in aged that in young rats, its basal levels being normal. To evaluate whether the increased vascular response of t-PA was peculiar for adrenergic stimulation, we infused platelet activating factor (PAF), an inducer of t-PA release, not related to catecholamines. PAF, during five-minute infusion induced a rapid and dose-dependent (100-1250 pM) increase in t-PA release, to the same extent in both young and aged rats. In conclusion, basal t-PA secretion was increased in aged rats probably as a response of vascular endothelium to chronic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1995

[Fibrinolytic and peripheral serotonergic system in patients with glomerulonephritis].

Some fibrinolytic parameters, whole blood and plasma serotonin were studied in normotensive and hypertensive patients with glomerulonephritis. Diminished activity of tissue plasminogen activator (tPA) and a significant prolongation of the euglobulin clot lysis time was observed in hypertensive and normotensive patients with glomerulonephritis when compared to healthy volunteers. Antigen and activity of inhibitor of tissue plasminogen activator (PAI) was found to be higher in hypertensive patients relative to control group. Whole blood serotonin was significantly lower, whereas plasma serotonin was higher in normotensive and hypertensive patients with glomerulonephritis when compared to healthy subjects. Impairment in fibrinolysis and elevated plasma serotonin levels may contribute to the increased risk of thromboembolic complications and accelerated atherosclerosis in these patients.

Adult↗
PubMed1994

EP3 receptor-mediated inhibition of the neurogenic vasopressor response in pithed rats.

In pithed rats, we studied the effects of prostaglandin E2 and of subtype-selective prostaglandin E receptor (EP receptor) ligands on the rise in blood pressure induced by electrical stimulation of the preganglionic sympathetic nerves. Prostaglandin E2, the EP1/EP3 receptor agonist sulprostone and the EP2/EP3 receptor agonist misoprostol inhibited the electrically induced increase in diastolic blood pressure (rank order of potencies sulprostone > or = misoprostol > or = prostaglandin E2); the rise in blood pressure induced by exogenously added noradrenaline was not affected by these compounds. The inhibitory effect of sulprostone on the electrically induced vasopressor response was not significantly changed by indomethacin. Iloprost (an agonist at EP1 and prostacyclin receptors (IP receptors)) failed to affect the electrically evoked increase in blood pressure. The present study suggests that prostaglandin E2 inhibits the release of catecholamines in pithed rats via prostanoid receptors of the EP3 subtype, probably located presynaptically on the postganglionic sympathetic nerve fibres.

Alprostadil↗
PubMed1994

Bypassing of local hospitals by rural Medicare beneficiaries.

Several previous studies of hospital utilization by nonelderly rural residents suggest that local rural hospitals have been increasingly bypassed, often for care in urban hospitals. This resulted in lost volume for rural hospitals, detracting from their financial viability. It is not clear to what extent elderly rural residents also bypass local hospitals and whether this reflects regionalization of treatment for some conditions or avoidance of local hospitals assumed to provide inadequate care. This study examines hospital use by aged rural Delaware Medicare beneficiaries living in a ZIP code area that has a local hospital during Fiscal Year (FY) 1987 (N = 670). Most of these Medicare beneficiaries were hospitalized locally. Those beneficiaries who bypassed local rural hospitals usually did so because cardiovascular surgical procedures were required and were often only performed in large urban teaching hospitals. Beneficiaries using nonlocal hospitals were similar to users of local hospitals with respect to age and sex and traveled an average of nearly 42 miles for treatment. "Bypassing" here appears to be due primarily to regional specialization of care rather than abandonment of local rural hospitals by rural residents.

Aged↗
PubMed1994

Prostacyclin is required for t-PA release after venous occlusion.

The role of vascular cyclooxygenase pathway on tissue-type plasminogen activator (t-PA) release after venous occlusion was studied in anesthetized rats. After the inferior vena cava was clamped for 30 min, fibrinolytic activity increased from 143.7 +/- 14.5 to 209.5 +/- 10.3 mm2 (mean +/- SE, P < 0.002). This increase was prevented by aspirin at high (100 mg/kg i.v.) but not at low doses (1 mg/kg i.v.). Dazoxiben (10 mg/kg i.v.), an inhibitor of thromboxane synthase, was ineffective on the fibrinolytic response. Both the basal levels of 6-ketoprostaglandin F1 alpha and its increase after venous occlusion were suppressed by 100 mg/kg aspirin administration (from 0.64 +/- 0.2 to 0.05 +/- 0.002 ng/ml before occlusion, P < 0.001; and from 1.08 +/- 0.2 to 0.06 +/- 0.002 ng/kg after occlusion, P < 0.001), whereas they were both unaffected by aspirin at low doses (from 0.53 +/- 0.06 before to 1.20 +/- 0.08 ng/ml after stasis). Moreover, iloprost, a stable analogue of prostacyclin, reversed the aspirin inhibitory effects on fibrinolytic activity by restoring t-PA vascular release after venous stasis. Our results provide experimental evidence that an intact cyclooxygenase pathway in vascular wall is required for the fibrinolytic activity increase after venous occlusion in rats.

6-Ketoprostaglandin F1 alpha↗
PubMed1994

Factors affecting charity care and bad debt charges in Washington hospitals.

Uncompensated care has become a major issue in hospital finance as the number of uninsured persons has increased and hospital revenues have declined. Uncompensated care charges have two components--charity care and bad debt--that are distinct conceptually but often are commingled in hospital accounting practice. Data on charges assigned to charity care and bad debt in 1987 for 82 short-stay hospitals in Washington were merged with data from the 1987 Medicare Cost Report and AHA Annual Survey. The regression analyses performed indicate that the determinants of the percent of charges for charity care, bad debt, and total uncompensated care differ and suggest that bad debt should be isolated from charity care when estimating a hospital's level of effort in providing care to indigent patients.

Accounts Payable and Receivable↗
PubMed1994

[Serotonin--blood platelets, vessels].

The synthesis and metabolism of serotonin (5-HT), and different populations of 5-HT receptor is described in this paper. Since the platelets are the main source of serotonin in the blood, the interactions of this amine with platelets and vessels wall one also discussed. In this context, the author indicate the role of serotonin in the pathophysiology of cardiovascular system.

Animals↗
PubMed1993

Serotonergic mechanisms are involved in the hemostatic action of erythropoietin in uremic patients.

Recombinant human erythropoietin was administered to 12 patients with end-stage renal failure on long-term hemodialysis. They responded to the therapy with a shortening of the prolonged bleeding time, starting from the 1st week of therapy, before a significant increase in hemoglobin concentration was achieved. We also observed an increase in the activity of tissue plasminogen activator and a decrease in the activity of its inhibitor. There were no changes in platelet count but a significant increase in blood and platelet serotonin concentration was found. The shortening of the prolonged bleeding time before the correction of the anemia correlated with the rise in blood and platelet serotonin concentration during erythropoietin therapy. We suggest the possible involvement of an serotonergic mechanism in the hemostatic action of recombinant human erythropoietin.

Adult↗
PubMed1993

Inpatient transfer episodes among aged Medicare beneficiaries.

Examination of data derived from Medicare provider analysis and review (MEDPAR) discharge records for 152,337 transfer episodes of aged Medicare beneficiaries indicates that aged Medicare transfer patients have initial stays comparable to non-transfers in terms of length of stay, case-mix intensity, and total charges. During the final part of the transfer episode, however, transfers are clearly more intense cases than non-transfers. Patients treated for stroke or cardiovascular conditions are more likely to be transferred than other Medicare aged inpatients. The transfer episodes examined appear to reflect clinical considerations based primarily on patient need for specialized care.

Aged↗
PubMed1993

Influence of Tołpa Peat Preparation on haemostasis in rats.

The influence of Tołpa Peat Preparation (TPP) on certain parameters of haemostasis was studied. The present results indicate that TPP (100, 200 and 300 mg/kg p.o.) had no influence on the bleeding time, clotting time, thrombin time, prothrombin time, kaolin-kephalin time, euglobulin lysis time, the concentration of fibrinogen, the platelet count and ADP-induced platelet aggregation. No changes in animals after long-term treatment with TPP (100 mg/kg for two weeks) were found either. In in vitro studies TPP given in concentrations 10(-5), 10(-4), 10(-3) and 10(-2) g/cm3 was used and certain changes of the studied parameters, probably caused by the presence of high salt content in this substance, were observed.

Amino Acids↗
PubMed1993

[Possible role of serotonin in hemostatic the mechanism of action of desmopressin (DDAVP) in patients with uremia].

Haemorrhagic diathesis is a serious complication of uraemia. Desmopressin is known to shorten prolonged bleeding time in uraemia but mechanism of the haemostatic action of this drug remains still unknown. The aim of the work was to study the effect of desmopressin on some haemostatic parameters in relation to plasma and platelet serotonin. Desmopressin was administered i.v. to 33 haemodialysed patients (age range 27-66 years) in a dose of 0.4 microgram/kg b.w., 90 minutes after desmopressin infusion bleeding time became significantly shorter (p < 0.001) and correlated with the shortening of the euglobulin clot lysis time (r = -0.43, p < 0.05). Tissue plasminogen activator activity increased (p < 0.01) and its inhibitor (PAI) activity decreased (p < 0.001) after desmopressin infusion. A correlation between the fall in platelet serotonin content and changes in tissue plasminogen activator and PAI activities was found (r = 0.55, p < 0.01 respectively). A rise in plasma serotonin concentration was observed. In vitro desmopressin inhibited 14C serotonin uptake in a dose-dependent manner. After 2 hours of platelet incubation with desmopressin in a concentration of 4 ng/ml 16% of 14C serotonin was released. A possibility of serotoninergic mechanism in the haemostatic action of desmopressin is suggested.

Adult↗
PubMed1993

Lack of effect of acetaldehyde on the cardiovascular system in rats.

The present study was designed to evaluate the kinetics of acetaldehyde (ACT) and and its action on the cardiovascular system in rats. ACT (3, 6, 12 mg/kg i.p.) causes accumulation of this metabolite in the blood, at a concentration corresponding to that obtained from ethanol metabolism after its administration in doses of 1, 2, 4 g/kg p.o., respectively. After intraperitoneal injection of ACT there were no significant changes in blood pressure and heart rate in comparison to the control group. It appears that, in rats, ACT has no influence on the function of the cardiovascular system after the ingestion of ethanol.

Acetaldehyde↗
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↗