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G V Born

Publications and source records attributed to G V Born.

At least 55 records · Page 3Linked to original sources
PubMed1988

Concomitant release of sialic acids and calcium by neuraminidase from rat aorta in situ.

Male Wistar rats were heparinized and killed with pentobarbital. The upper and lower ends of the aortae were cannulated and the blood was washed out with saline until the washings contained calcium and sialic-acid-reacting material at minimal concentrations. The aortae were perfused with neuraminidase for 15 min. This caused the appearance of calcium as well as of sialic acids in the perfusate in total amounts of about 5.3 nmol and about 3.6 nmol per aorta respectively. The molar ratio of about 1.5 is sufficiently close to that determined for the association of calcium with sialic acids in vitro to suggest that their association is similar in vivo.

Animals↗
PubMed1988

Evidence for the dependence of arterial haemostasis on ADP.

The possible involvement of adenosine diphosphate (ADP) in haemostatic platelet aggregation was investigated by determining the duration of primary haemorrhage as standardized bleeding times from punctures of small mesenteric arteries in anaesthetized rats. The bleeding times were highly significantly increased by infusing into the mesenteric arterial blood flowing towards the punctures either the nucleotide-dephosphorylating enzyme apyrase or the ADP-receptor antagonists ATP, adenosine 5'-(beta,gamma-methylene)triphosphonate (AMP-PCP) or 2-methylthioadenosine 5'-(beta,gamma-methylene)triphosphonate (2-MeS-AMP-PCP). The increases in bleeding times could not be accounted for by local vasodilator effects of the agents. It is concluded that the presence of ADP through local release and/or formation at sites of vascular injury contributes significantly to haemostasis, presumably by accelerating platelet aggregation.

Adenine Nucleotides↗
PubMed1987

Comparison of uptake and degradation of low density lipoproteins by arteries and veins of rabbits.

The uptake and degradation of low density lipoproteins were compared in arteries and veins of rabbits in vivo. Rabbits were injected with low density lipoproteins labelled singly with 125I (125I-LDL) or doubly with 131I and with [125I]tyramine cellobiose (TC-LDL) which remains trapped intracellularly. After increasing times up to 24 h the largest vessels were perfused to remove blood, fixed in situ and excised. When the uptake of 125I-LDL by arteries and veins was compared on the basis of luminal surface area, there were no significant differences up to 3.5 h. When degradation rates of double labelled LDL were compared after 24 h on the same basis, the arteries contained significantly more TC label than the veins, but when the comparison was based on dry weights there were no significant differences. These results show that veins, like arteries, take up LDL from the circulating blood; and they suggest that the preferential accumulation of LDL in arteries susceptible to atherosclerosis may be accounted for, at least in part, by more degradation of LDL in arteries than in veins.

Animals↗
PubMed1987

In vitro effect of a microfibrillar collagen hemostat on platelets.

Microscopic particles of microfibrillar collagen hemostat (MCH) have been shown to pass through a 40-micron blood transfusion filter. This study indicates that MCH passing through the filter retains a significant portion of its ability to aggregate platelets in vitro and the aggregating ability is dose related. The extent of platelet aggregation in the presence of the MCH filtrate or an ADP standard was measured photometrically and log dose-response curves constructed from the data. An ED50 of 3.6 micrograms protein/ml platelet-rich plasma (PRP) was calculated at a protein concentration of 7.6 mg/ml in the MCH filtrate and an ED50 of 5.9 micrograms protein/ml PRP at 12 mg/ml protein in the MCH filtrate. The platelet aggregating ability of the MCH filtrates corresponded to 18.8 and 39.6% of the maximum response produced by adenosine-5'-diphosphate. These findings support the view that blood contaminated with MCH should not be returned to a patient's circulation.

Adenosine Diphosphate↗
PubMed1986

Haemorheological influences on platelet thrombogenesis.

This lecture is concerned mainly with questions about how haemodynamic conditions in atherosclerotic arteries affect arriving platelets that aggregate there and about the chemical agents responsible for making the platelets reactive. The effects of haemodynamic conditions and the agents are known mainly from in vitro experiments in which aggregation can be quantitatively correlated with blood flow and biochemical effects by simple and reproducible methods; the relevance to the more complicated situations in haemostatis and thrombosis is uncertain. It is difficult to devise quantitative in vivo methods, mainly because of the rapidity with which platelets adhere and aggregate in diseased or damaged blood vessels. Hypotheses for explaining in vivo platelet aggregation in biochemical and terms must take the haemodynamic situation into account.

Blood Platelets↗
PubMed1986

Comparison of the numbers of plasmalemmal vesicles in arterial and venous endothelia of rats.

The numbers of plasmalemmal vesicles in endothelial cells of rat blood vessels were determined on electron microscopic sections. In all vessels examined which included aorta and carotid and femoral arteries, vena cava and femoral vein, and lung and brain capillaries, the numbers were of the same order of magnitude. For arteries the numbers were about double those for the corresponding veins. About one-third of all vesicles could be stained with ruthenium red after its infusion into the vessels. The results make it improbable that differences in numbers of 'transport' vesicles in different types of blood vessel contribute significantly to the selective accumulation of atherogenic plasma proteins in arteries.

Animals↗
PubMed1986

Influence of dietary lipids on the effect of chlorpromazine on membrane properties of rabbit red cells.

The effect of diets containing different types of common natural oils on physical properties of red cells was investigated by using rabbits. The rabbits were fed for 18 months on a standard diet in which 8% of its energy content was provided by safflower oil and 32% energy by either more safflower oil or fish oil, linseed oil, olive oil or palm oil. Erythrocyte deformability was significantly decreased by the fish oil diet compared with each of the other diets. Osmotic fragility was significantly less (66 mM) for red cells from rabbits fed on the linseed oil diet, and significantly greater (71 mM) for red cells from rabbits on the fish oil diet, than for red cells from rabbits on the other three diets which did not differ significantly from each other (68 mM). With rabbits on the standard diet, the resistance of their erythrocytes to osmotic haemolysis was increased by chlorpromazine at concentrations below and decreased by concentrations above 30 microM. The dietary oils caused significant changes in the effects of chlorpromazine on osmotic fragility. The concentration at which the effect of chlorpromazine reversed from antihaemolytic to prohaemolytic was decreased by the safflower and linseed oil diets and increased by the fish oil diet, compared with the olive and palm oil diets. Analysis of the fatty acid compositions of the dietary oils on the one hand and of the red cell phospholipids on the other established, specifically, that in the presence of 30 microM chlorpromazine the percentage haemolysis was directly proportional to the linoleate content of the red cell phospholipids.

Animals↗
PubMed1986

Inherent dangers of simultaneous application of microfibrillar collagen hemostat and blood-saving devices.

Microfibrillar collagen hemostat is a topically applicable hemostatic agent that has been introduced relatively recently. Because of the possibility that this substance may pass through different blood-collecting circuits and cause organ damage if reintroduced into the patient's circulation, we performed a series of in vitro and in vivo experiments. The results of these experiments suggest that such a passage may indeed occur and could cause organ damage, either by direct or by induced embolization that cannot be completely prevented even with the application of commercially used filters. We therefore recommend that the substance should not be used if the shed blood is intended to be collected and returned into the patient's circulation.

Animals↗
PubMed1985

Edith Bülbring.

Explore the source record for details and available documents.

Germany↗
PubMed1985

Simulation of primary haemostasis in vitro.

Primary haemostasis was simulated in vitro under standardized geometrical, rheological and biochemical conditions. The system was based on the hypothesis that adenine nucleotides, especially adenosine 5'-diphosphate, released from injured vessel wall cells play an important role for the initial platelet aggregation following lesion of small vessels. The device allows the reproducible measurement of in vitro bleeding time and volume in small samples of whole blood.

Adenosine Diphosphate↗
PubMed1985

Unusually high concentrations of sialic acids on the surface of vascular endothelia.

Sialic acids present on luminal surfaces of vascular endothelium were determined by perfusing neuraminidase free of proteolytic activity through carotid arteries, iliac arteries and jugular veins of anaesthetized rabbits and guinea-pigs and through human umbilical veins. Total sialic acids released in I h from arteries and veins, determined fluorimetrically, were 24-51 X 10(6) molecules/micron 2 endothelial surface; this was more, by up to two orders of magnitude, than sialic acids releasable by neuraminidase from other types of cells, i.e. from 0.15 X 10(6) for human erythrocytes to 15 X 10(6) for human platelets. Sialic acids therefore provide extraordinarily high negative charge densities on vascular surfaces exposed to the flowing blood. As all circulating cells are also negatively charged, strong electrostatic repulsion must exist between them and normal vessel walls. These observations can therefore account for the general property of non-adherence of circulating cells in normal blood vessels of which the so-called 'non-thrombogenicity', meaning the non-adherence of platelets to normal vascular endothelium, is one example. It is suggested that a major biological function of these extraordinarily high negative charge concentrations is the mutual repulsion between endothelial surfaces and blood cells which promotes their unimpeded circulation.

Animals↗