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Biomedical subjects

K Breddin

Publications and source records attributed to K Breddin.

At least 37 records · Page 2Linked to original sources
PubMed1983

[Prevention of postoperative thrombotic complications with heparin and dihydroergotamine. A randomized double-blind study].

In a randomized double-blind study of 660 patients with predominantly abdominal-surgical procedures the thrombosis-preventing effect of the following was compared: heparin 5000 (low-dose heparin), heparin 2500, a combination of heparin 2500 and 0.5 mg dihydroergotamine (HDHE 2500), 0.5 mg dihydroergotamine (DHE), and placebo. All preparations were administered three times daily. Radiofibrinogen test gave the following thrombosis incidence: heparin 5000-15.4%; heparin 2500-24%; HDHE 2500-13.2%; DHE-24.6%; placebo-28.9%. Bleeding complications, included postoperative blood loss (more than 500 ml), unusually marked bleeding from drains, seroma, wound haematoma, and re-operation. The rate of these complications was 18.5% with heparin 5000, 7.8% with placebo, 5.6% with DHE, 4% with heparin 2500 and 3.1% with HDHE 2500. The non-specific tolerance to the various preparations was good, especially in that there was no increased risk of coronary complications with HDHE or DHE, and there was no pointer to peripheral vasospasms. This study confirms the synergistic thrombosis-preventing effect of combined heparin-dihydroergotamine.

Abdomen↗
PubMed1980

Optical density variations and microscopic observations in the evaluation of platelet shape change and microaggregate formation.

Addition of Ristocetin to formalin-fixed platelets suspended in diluted PPP induces a marked increase in turbidity which is not caused by platelet shape change but by the formation of microaggregates. If diluted PPP of patients with severe von Willebrand's disease is used, only an initial increase in turbidity and no further decrease is observed without any form variation of the platelets but again with formation of many microaggregates. In normal PRP diluted with buffered EDTA, ADP induces an increase in turbidity without further changes in optical density. Simultaneously platelets immediately change their shape with formation of pseudopodia and sphering but at the same time also microaggregates appear. Shape change and microaggregate formation can also be observed after the addition of Collagen to undiluted PRP which is followed by the formation of large aggregates and a decrease in optical density. Increase in optical density in undiluted PRP is not a specific indicator of platelet shape changes. Microaggregates can alone or partially be responsible for these changes. For the evaluation of platelet shape changes but also for the estimation of microaggregate formation microscopic methods are preferred.

Adenosine Diphosphate↗
PubMed1980

The German-Austrian aspirin trial: a comparison of acetylsalicylic acid, placebo and phenprocoumon in secondary prevention of myocardial infarction. On behalf of the German-Austrian Study Group.

In a multicenter clinical trial on the prevention of recurrent myocardial infarction, 946 patients who had survived a myocardial infarction for 30-42 days were randomly allocated to acetylsalicylic acid (ASA, 1.5 g/day) (317 patients), placebo (309 patients) or phenprocoumon treatment (320 patients) and were followed to determine the incidence of total mortality, coronary death and nonfatal recurrent myocardial infarction. The ASA and placebo groups were treated in double-blind fashion. The observation period for each patient was 2 years. Total mortality was lower in the ASA group (27 patients) than in the placebo (32 patients) and phenprocoumon groups (39 patients). There were 13 coronary deaths (fatal myocardial infarction and sudden death) in the ASA group, 22 in the placebo group and 26 in the phenprocoumon group. This represents a reduction rate of 42.3% in the ASA group compared with placebo (p less than 0.1) and of 46.3% in the ASA group with phenprocoumon (p approximately 0.07). Considering male patients alone, the difference regarding coronary death is significant between ASA vs placebo (p less than 0.05, reduction rate 56.4%) and ASA vs phenprocoumon (p less than 0.05, reduction rate 55.6%). Coronary events (coronary death and nonfatal recurrent myocardial infarctions) were lower in the ASA group (24 events) than in the placebo (37 events) (p less than 0.07) or phenprocoumon group (32 events).

4-Hydroxycoumarins↗
PubMed1980

[Platelet function and coagulation factors before and after the passage of microaggregate filters].

Citrated blood was investigated directly after blood sampling and 1 and 4 days after incubation at 4 degrees C before and after passage of a microaggregate filter (MF 10, Biotest). During the 4 days of incubation the platelet number was reduced from a mean of 200 000/microliter to a mean of 140 000/microliter. After the filter passage the platelet count was reduced in the freshly prepared blood samples by 10% and in the 4-days-old samples by 20%. Filter passage induced only a slight stimulation of platelets (sphering and pseudopode formation) in freshly prepared citrated blood. Aggregate formulation in the samples was small but increased continuously during the 4 days of incubation. In the 4-days-old samples the medium-sized aggregates consisting of 4-12 platelets were reduced while the number of small aggregates consisting of 2-3 single platelets increased after filter passage. Platelet aggregation was not changed by the filter passage but was continuously reduced during the storage time. The filter passage did not change the thromboplastin time, factor VIII values, fibrinogen, thrombin time and the thrombin coagulase time. The partial thromboplastin time values did not differ before and after filter passage in the freshly prepared and 1-day-old samples but were slightly shortened in the samples stored for 4 days with a large variation of the single values. The minimal platelet-stimulating effect, which could be demonstrated in freshly prepared blood samples only is reversible and corresponds to that observed if blood is drawn through a PVC catheter at blood sampling. In so far the microaggregate filter MF 10 had no thrombogenetic effect.

Blood Platelets↗
PubMed1978

[Primary shape change of platelets in vitro (author's transl)].

Studies with interference contrast microscopy reveal that platelets undergo a typical shape change within 30--60' after venepuncture, i.e. swelling, formation of large tentacles, tiny protrusions and vesicles at the platelet surface. This "shape change" can be observed in citrated blood and PRP, heparinized blood and EDTA-blood as well. It is enhanced by low incubation temperatures (4 degrees C, 10 degrees C) and delayed at 37 degrees C as compared with room temperature. An increased number of primarily shape changed platelets is found if platelets are strongly mechanically irritated at blood sampling. The shape change is partly reversible in vitro, it is completely or almost completely reversible in vivo. Some antiaggregating agents inhibit the in vitro shape change at varying degrees (Bencyclan, SH 869 greater than ASA greater than D-Propranolol). The shape change is partly inhibited after oral or i.v. administration of ASA. A typical transformation of platelets into "spheric" forms can be observed following the addition of Bencyclan, SH 869 and D-Propranolol to PRP in vitro. The spontaneous "primary shape change" which occurs in PRP or blood after blood sampling is probably different from the secondary ADP-induced shape change. The primary shape change may influence the results of different platelet function and aggregating tests. The shape change kinetics of "healthy" subjects and patients with Hodgkin's disease differ significantly. The described method may gain more clinical interest in the future.

Aspirin↗
PubMed1978

[The initial stage of thrombus formation in early stages of arteriosclerosis].

An arterial thrombosis develops via a lesion of the vascular wall. By the contact of the flowing blood with subendothelial collagen and basal membrane proportions the adhesion and aggregation of platelets develop which, depending on flowing conditions and local conditions, such as ADP-concentration, may lead to manifest thromboses. The prostaglandines have an essential influence on these processes. The relations of thrombosis to arteriosclerosis consist in the stimulation of the smooth muscle cells to proliferation by a factor of thrombocytes, in the organisation of experimental arterial thromboses with formation of an intima proliferation and in the complications of manifest arteriosclerosis by secondary thromboses. Methods for the proff of an increased inclination to thrombosis on the basis of an increased platelet function are critically discussed as to their clinical usability. A spontaneously increased aggregation of platelets is regarded as a reference to progressing arteriosclerosis. In these cases the significant increase of the spontaneous aggregation is of special importance in diabetics.

Adenosine Diphosphate↗