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Biomedical subjects

K Breddin

Publications and source records attributed to K Breddin.

At least 55 records · Page 3Linked to original sources
PubMed1977

Use of platelet inhibitor drugs in peripheral and cerebral vascular disorders.

A review is given on the clinical studies performed with aspirin in patients with chronic vascular occlusions of the limbs and on studies in cerebral ischemia using aspirin and sulfinpyrazone. Aspirin reduces the risk of reocclusions in patients after vascular surgery and also reduces the risk of peripheral vascular occlusions in diabetic patients. In doses of 1.2-1.5 g/day it also reduces the frequency of transient ischemic attacks. Conclusive results of similar studies with sulfinpyrazone and dipyridamole can be expected of the ongoing studies. Aspirin has no effect on the course of glomerulonephritis in children. Warfarin plus dipyridamole seem to have some effect in patients renal allografts. Sulfinpyrazone and ASA reduced the incidence of shunt thromboses in hemodialyzed patients. Several case reports in patients with thrombocytemia or Raynaud's syndrome made it likely that treatment with antiplatelet drug reduces the incidence of vascular occlusions.

Arterial Occlusive Diseases↗
PubMed1977

Photometric platelet aggregation test III: a new tool for the detection of enhancet platelet aggregation.

In clinical investigation on ehnanced platelet aggregation the changes of the various tests with time after blood sampling must be considered. The photometric PAT III for the evaluation of spontaneous aggregation showed enhanced aggregation in a high percentage of patients with vascular disease, and prospective data obtained so far make it likely that enhanced aggregation is a risk factor for thrombosis. More prospective studies are necessary to prove whether continuously enhanced spontaneous platelet aggregation is indicating progressive atherosclerosis.

Coronary Disease↗
PubMed1976

On the measurement of spontaneous platelet aggregation. The platelet aggregation test III. Methods and first clinical results.

A new measuring device was developed for the study of "spontaneous" aggregating activity of thrombocytes. In the photometric platelet aggregation test (PAT III) 0.6 ml of platelet-rich plasma (PRP) are rotated in a disc-shaped cuvette at 20 rpm and 37 degrees C. Changes in optical density of PRP which are induced by the formation of platelet aggregates are continuously registered using a chart recorder. PAT III was developed for the detection of enhanced platelet aggregation, indicating a risk of thrombosis and thromboembolic complications. In 146 healthy individuals a certain percentage showed slight primary aggregation (alpha1) which in some cases was followed by marked aggregation (alpha2) at a certain time (Tr) after the beginning of rotation. The percentage of individuals showing alpha2 increased with age. An increase of plasma pH in the rotating sample, which was caused by diffusion of CO2, was an important conditioning factor for aggregation. The test results depended on the platelet count in PRP. Aggregation curves were suppressed by admixture of erythrocytes and lipid turbidity. The tendency of platelets to aggregate increased within 60-90 min following blood sampling. During this period the interval to the onset of aggregation (Tr) became shorter and the maximum aggregation speed (alpha 2) increased with time. PAT III yielded reproducible results when it was carried out more than 60 min after blood drawing. In a group of 327 diabetic patients "spontaneous" aggregation occurred more frequently in all age groups as compared with the controls. Additional equipment was available for the registration of ADP-, collagen-, or epinephrine-induced aggregation similar to Born's and O'Brien's method. The device can easily be mounted on an Eppendorf photometer without further alterations.

Age Factors↗
PubMed1975

[Measurement of spontaneous platelet aggregation. Platelet aggregation test III (author's transl)].

A new measuring device for the estimation of the "spontaneous" aggregating activity of thrombocytes has been developed. In this photometric platelet aggregation test (PAT III) a small amount (0.6 ml) of platelet-rich plasma (PRP) is being rotated in a disc-shaped cuvette at 20 rpm, at 37% C. Changes in optical density of PRP which are induced by the formation of platelet aggregates are continuously registered using a chart recorder. The decisive trigger mechanism for aggregation is an increase of plasma pH in the rotating sample which is caused by evaporation of CO2. The results of the test depend on the platelet count in PRP. Aggregation curves are misrepresented by admixture of erythrocytes and lipid turbidity. The tendency of platelets to aggregate increases within 60-90 min following blood sampling. During this period the time interval to the onset of aggregation(Tr) is shortening, and the maximum aggregation speed (alpha2) is increasing. The spontaneously enhanced aggregation tendency of thrombocytes may be reliably measured from 60 min after drawing the blood. The reason for these time-dependent changes which are also demonstrable in ADP-collagen-or epinephrine-induced aggregation is probably the primary shape change of platelets, which occurs after blood drawing and makes them "stickly" and aggregable. PAT III was developed for the detection of enhanced platelet aggregation, indicating a risk of thrombosis and thromboembolic omplications. The new measuring device has been designed as "universal" aggregometer. Additional equipment is available for the registration of ADP-collagen-or epinephrine-induced aggregation similar to Born's and O'Brien's methods. The device may be mounted easily on an Eppendorf photometer without further modifications.

Adenosine Diphosphate↗
PubMed1975

[Frequently recurring cyclic megakaryocytopenic-thrombopenic purpura].

An unusual case of acquired frequently remitting megakaryocytopenic-thrombocytopenic purpura in a 54 years old man is reported. The patient could be followed up anamnestically for 11 years. Regularly megakaryocytopenic-thrombocytopenic periods were followed by complete remissions. Platelet survival was normal in thrombocytopenic and in remission phases. No immune mechanism could be detected. The exceptional position of this disorder within the inhomogenous group of intermittent thrombocytopenic purpuras is discussed, and the common criteria with three other published cases are pointed out.

Adult↗