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H Grun

Publications and source records attributed to H Grun.

8 recordsLinked to original sources
PubMed1992

Plasma clearance and net uptake of alpha-tocopherol and low-density lipoprotein by tissues in WHHL and control rabbits.

The mechanism(s) of uptake of vitamin E (alpha-tocopherol) by tissues is poorly understood. It has, however, been suggested from studies in vitro that the apolipoprotein B/E (apo B/E) receptor pathway for low-density lipoprotein (LDL) may be involved. To investigate the role of the apo B/E receptor pathway in vivo, we have studied the transport and uptake of alpha-tocopherol by tissues in Watanabe Heritable Hyperlipidaemic (WHHL) rabbits, which lack functional LDL (apo B/E) receptors, and controls. [3H]alpha-Tocopherol incorporated within LDL labelled with [14C]sucrose was used in these studies, as this enabled the uptake of both alpha-tocopherol and LDL to be studied independently. The principal findings were as follows. (1) Concentrations of the circulating lipids (including alpha-tocopherol) and LDL were increased and the plasma fractional disappearance rates of alpha-tocopherol and LDL decreased in the WHHL rabbits. (2) The WHHL rabbits clear more LDL and alpha-tocopherol from the circulation than controls do, because of their increased pool sizes of alpha-tocopherol and LDL. (3) The lipoprotein composition of the WHHL rabbits differed from that of the controls, and there was exchange of alpha-tocopherol between the lipoprotein fractions in vivo and in vitro. (4) High-affinity apo B/E receptors were not essential for the uptake of alpha-tocopherol by tissues. (5) Evidence from the plasma-clearance and tissue data suggest that alpha-tocopherol can be taken up by tissues in association with, and also independent of, LDL. We conclude that there are several different mechanisms for the uptake of alpha-tocopherol by tissues, which include receptor-dependent and receptor-independent pathways, independent transport and co-transport of alpha-tocopherol and LDL, and uptake from a number of different lipoproteins.

Animals↗
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↗
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↗