Correlations between age-dependent protein and lipid concentrations in plasma and platelet functions in children.

The correlations between the levels of various plasma proteins and lipids and platelet function on glass and platelet factor 3 (PF 3)-availability in children of different age-groups were investigated. Several statistically significant positive and some significant negative correlations were found. Although conclusions based solely on such correlations should be considered with reservation, in our opinion the following factors should stimulate platelet function: prealbumin (adhesion and PF 3-availability in all age-groups, aggregation--specifically for children in puberty); alpha 1-antitrypsin (PF 3-availability); alpha 2-macroglobulin (platelet spreading capacity, PF 3-availability); plasminogen (platelet adhesion and aggregation--specifically for boys in puberty); caeruloplasmin (number of "free adhering platelets" spreading capacity); lysolecithin and lecithin (time-dependent increase of spontaneous platelet adhesion and aggregation, PF 3-availability); and free fatty acids (FFA) (PF 3-availability). Plasminogen and complement component C'3 show a negative relationship to the time-dependent increase of spontaneous platelet adhesiveness and aggregability in platelet-rich plasma.

Thrombocyte functions, thrombelastograms and fibrinogen of healthy children in different age groups.

Platelet counts, adhesiveness, aggregation and spreading capacity, as well as the thrombopoiesis index, thrombelastogram and fibrinogen were examined in 74 healthy children aged from 2 to 14 years. Sex-linked differences were only found in the thrombopoiesis index. Age-linked differences showed in practically all the parameters, especially in the platelet counts, fibrinogen and thrombelastograms.

[Changes on platelet adhesion, aggregation and production in course of mumps and mumps meningitis (author's transl)]. / Veränderungen von Thrombozytenadhäsion, -aggregation und -neubildung im Verlauf des Mumps und der Mumps-Meningitis.

In 20 children with mumps and mumps meningitis thrombocyte functions, the thrombopoiesis and the platelet count were examinated over a four week period. The spontaneous, standardized platelet adhesion and aggregation on silikonized glass surface showed a statistically significant increase from the 5th to the 15th day of the illness. Within the first four days a decrease of the megathrombocyte portion respectively of the youngest platelet forms was noted as revealed by the platelet spreading preparations. Then the thrombopoiesis index as well as the platelet count arised from the 5th day of the illness parallel to the other platelet functions. The enhanced thrombopoiesis diminished at the end of the 3rd week of the illness but the platelet adhesion and aggregation continued to be further increased. A distinct correlation could be established between the development of the specific antibodies and increased platelet adhesion, aggregation and thrombopoiesis in epidemic parotitis. The influence of the immune complexes and of the virus itself, furthermore the occurrence of the regenerating phase as well as the effects of the possible thromboplastic activity following a tissue damage or an inflammatory reaction were discussed.

Effects of thrombin, chymotrypsin and aggregated gamma-globulins on the proteins of the human platelet membrane.

Analysis of platelet membrane proteins and glycoproteins by SDS polyacrylamide gel electrophoresis was carried out before and after treatment with thrombin. Extended incubation with thrombin (in the presence of EDTA or adenosine, which inhibit aggregation) produced extensive changes in the bands observed. With incubation times of a few minutes however, the changes were restricted to a glycopeptide, GP IV (approx. 90,000 Daltons) and one or two polypeptides of low molecular weight, in particular polypeptide 16 (approx. 23,000 Daltons). At 0--3 degrees C only polypeptide 16 was still hydrolyzed. Chymotrypsin, which does not activate platelets, attacked glycopeptides I, II, III but no changes were apparent in GP IV and polypeptide 16. When chymotrypsin-treated platelets were further incubated with thrombin, only GP IV and one to two low molecular weight polypeptides, especially polypeptide 16, were affected. As polypeptide 16 appears to be an integral membrane component it is possible that it, either by itself or in combination with GP IV, represents the primary thrombin substrate involved in platelet activation. Aggregated IgG, which also activates platelets, does not modify the membrane glycoproteins but does change the low molecular weight region in particular band 16.

[Failure of platelet spreading in thrombasthenia due to changes of high molecular weight membrane glycopeptides (author's transl)]. / Veränderungen der hochmolekularen Membranglykoptoreine bei Thrombasthenie als Ursache der fehlenden Plättchenausbreitung

Rabbit and thrombastheinic platelet membranes were examined by SDS polyacrylamide gel electrophoresis. Both rabbit and thrombasthenic platelets failed to spread on siliconized glass surfaces and revealed platelet membrane glycoprotein patterns quite different from those of normal human platelet membranes. Typical for normal platelet membranes are four high molecular weight glycoprotein bands. The platelet membranes from rabbits and from one thrombasthenic patient showed only the first major glycopolypeptide with an apparent molecular weight of 135000 and 120000 D respectively. Other platelet membrane glycopeptides (both the carbohydrate and polypeptide moiety) were completely absent in thrombasthenia. The rabbit platelet membrane yet contains two strong polypeptides in this high molecular weight region, however, without corresponding carbohydrate moieties. Therefore, we support the view that the carbohydrate chains from two high molecular weight glycoproteins are of importance for platelet spreading on glass surfaces.