Search PubMed⌕ Search

Biomedical subjects

A Stadnicki

Publications and source records attributed to A Stadnicki.

13 recordsLinked to original sources
PubMed1995

Inhibition of plasma kallikrein prevents peptidoglycan-induced arthritis in the Lewis rat.

We investigate whether the previously shown contact system activation plays a pathogenetic role in a rat model of acute inflammation induced by peptidoglycan-polysaccharide (PG-APS) using a new specific plasma kallikrein inhibitor, Bz-Pro-Phe-boroArg-OH (P8720). Group I (control) received neither PG-APS nor inhibitor. Group II (disease-treated) received PG-APS intraperitoneally (IP) and P8720 orally. Group III (disease-untreated) received PG-APS IP. Anemia was evident at 49 h in group III but was not present (P < 0.01) in groups I and II. Spleen weight was significantly decreased in group II compared to group III. Acute arthritis progressively developed in group III from 27 to 49 h, but P8720 decreased the joint swelling in group II by 61% (P < 0.0005). We observed a significant fall in prekallikrein and factor XI (P < 0.01) in groups II and III but not in group I. The decrease in the functional levels of high molecular weight kininogen (P < 0.05) observed in group III were prevented by P8720 in group II. The changes in T-kininogen and alpha 1-inhibitor 3 acute-phase proteins were partially prevented by P8720. We conclude that the inflammatory reactions leading to arthritis and anemia, as well as the acute-phase reaction, are due in part to contact activation, and that specific kallikrein inhibitors may have therapeutic potential.

Acute-Phase Proteins↗
PubMed1991

Factor XIII subunits in relation to some other hemostatic parameters in ulcerative colitis.

The hemostatic parameters, particularly with respect to F.XIII subunits, were examined in 48 untreated UC patients (22 at active and 26 at quiescent stage). UC active patients showed a significant decrease of F.XIII subunit "a," compared with healthy subjects, as well as in UC patients in remission. In contrast, the level of F.XIII subunit "b" in each group was similar. Compared with normal subjects, UC active patients revealed a significant decrease in AT III concentration, prolonged ELT, and elevated fibrinogen level. In addition, the elevated titer of SDPS test for SFMC appeared in approximately 40% of those patients. However, no strict relationship was found between the presence of positive SDPS and diminution of AT III, as well as of F.XIIII subunit "a" in active UC state. In patients in remission, AT III level and ELT were similar to those as in the control group, but fibrinogen concentration was elevated. Such constellation of hemostatic parameters may indicate a tendency to blood hypercoagulability in UC active patients, whereas, in general, these changes are not associated with the stage of remission. The present data may also suggest that F.XIII behavior pattern should be taken into account in the clinical management of UC.

Adolescent↗
PubMed1987

Modulatory effect of the gastrointestinal tract (gut) on fibrinolysis and fibrinogen derivatives.

We have investigated some components of the fibrinolytic system and fibrinogen derivatives in blood samples taken simultaneously from the human portal and cubital veins. In the first series the blood was drawn during laparotomy from 12 cholecystectomized, otherwise healthy patients. The mean value of euglobulin lysis time was significantly lower in the portal than in the cubital vein. The values of the fibrinogen, plasminogen, serial dilution protamine sulfate, and ethanol gelation tests in both samples were quite similar. In the second series blood was taken from eight patients with cancer of the gut and from six cholecystectomized patients. The staphylococcal clumping test (SCT) in serum was performed for fibrin degradation products (FDP) in samples from both veins. In patients with cancer the mean FDP level was significantly higher in the portal than in the cubital vein. In cholecystectomized patients the SCT was negative in samples from both veins. We conclude that fibrinogen pathway metabolism does not differ in the portal and cubital veins under normal conditions, whereas in neoplastic disease fibrinogen degradation is greater in the portal vein. We also suggest that the gut probably modulates fibrinolytic activity in normal conditions.

Arm↗
PubMed1985

The effect of histamine (H2) receptor antagonists on the fibrinolytic activity in vitro.

The effect of cimetidine and ranitidine on the fibrinolytic activity in vitro was tested. The inhibition rate of spontaneous lysis rose proportionally to the increasing drug doses. However, a similar effect was obtained with two other drugs of different chemical structures and pharmacological properties. Streptokinase activated fibrinolyse was not affected by either of the drugs at any concentration. Nor was clot formation affected in these experiment conditions. The results of the tests in vitro indicate that inhibition of euglobulin fibrinolysis by H2-receptor antagonists is not specific for these drugs and not connected with their pharmacological properties. It is possible to assume that, during therapeutic use, cimetidine and ranitidine have no antifibrinolytic effect. Possible explanation and relevance of these observations are discussed.

Blood Coagulation↗
PubMed1985

Modulatory effect of the gut on. Polymorphonuclear leukocytes motility. Preliminary report.

We have compared the spontaneous and stimulated motility of PMN from blood samples taken simultaneously from human portal and cubital vein. Blood was taken during laparotomy from 10 cholecystectomized patients and from 6 patients in whom carcinoma of pancrease was confirmed. In all subjects both spontaneous and stimulated migration rates of PMN from the portal vein were lower than that of PMN isolated from the cubital vein; the differences were significant. We conclude that the gut probably modulates the motility of PMN.

Adult↗
PubMed1984

Ranitidine and haemostasis in man.

The effect of ranitidine on the fibrinolytic activity and clotting factors was examined in 36 patients treated with ranitidine for gastric and duodenal ulcer in a randomized double-blind trial. Twenty patients were treated with ranitidine, and 16 received a placebo. The following determinations were made: euglobulin lysis time, coagulation time, prothrombin time, thrombin time, fibrinogen level and platelet count. It was found that therapeutic doses of ranitidine in patients with gastric and duodenal ulcer did not affect the relevant coagulation parameters.

Adult↗