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Biomedical subjects

G V Born

Publications and source records attributed to G V Born.

At least 127 records · Page 7Linked to original sources
PubMed1977

Inhibition by a stable analogue of adenosine triphosphate of platelet aggregation by adenosine diphosphate.

1 In citrated platelet-rich plasma, freshly prepared from rabbit blood, the velocity of platelet aggregation was within limits proportional to the log of the concentration of added adenosine diphosphate (ADP). 2 Addition of either adenosine triphosphate (ATP) or its beta,y-methylene analogue inhibited aggregation similarly except that the analogue was about half as potent as ATP. beta,y-Methylene ATP also reversed the optical effects associated with the shape change of platelets very similarly to ATP itself. 3 As beta,y-methylene ATP is not a substrate for nucleoside diphosphokinase, these observations do not support the proposition that inhibition of aggregation by added ATP is due to its utilization by the nucleoside diphosphokinase of platelets.

Adenosine Diphosphate↗
PubMed1977

Changes in the concentration of leucocytes and platelets in the peripheral blood during sterile inflammation in rabbits.

Glycogen in isotonic saline was infused into the peritoneal cavities of rabbits to produce sterile inflammation. This caused a small increase in the haematocrit value and larger decreases in the concentrations of circulation leucocytes and platelets. Circulating granulocytes decreased by about 40% in 2 h and increased in the next 2 h to about 4 times their initial concentration. Acetyl salicyclic acid (ASA) (10 mg/kg) infused with the glycogen did not affect the decrease significantly but accelerated the subsequent increase. Circulating mononuclear leucocytes, mostly lymphocytes, decreased progressively by about 75% after 4-5 h. This decrease was not affected by ASA. Circulating platelets decreased by about 30% in the first hour; this decrease was accelerated and augmented by ASA. Subsequently the platelet concentrations remained constant for at least 4-5 h. Glycogen so infused is known to activate complement, and ASA to inhibit prostaglandin synthetase. Therefore the results suggest that (i) the initial decrease in circulating granulocytes is mediated by activated complement; (ii) the emigration of granulocytes from blood into the inflammatory exudate is increased by prostaglandins; (iii) the initial decrease in circulating platelets is mediated by activated complement and antagonized by prostaglandins; and (iv) the decrease in circulating lymphocytes is mediated by activated complement and uninfluenced by prostaglandins.

Animals↗
PubMed1976

Increase in sialic acids removable by neuraminidase during the shape change of platelets.

Human or rabbit platelets were activated by ADP or 5-hydroxytrypatamine and rapidly fixed with glutaraldehyde. The shape change associated with activation gave rise to an increase in sialic acids removable by neuraminidase. This increase, like the shape change, was prevented by adenosine or methysergide added before ADP or 5-hydroxytryptamine respectively. The results indicate the exposure of additional glycoprotein(s) on the platelet surface.

Adenosine Diphosphate↗
PubMed1976

Relation between the inhibition of aggregation and the concentration of cAMP in human and rat platelets.

Adenosine inhibits the aggregation of human but not of rat platelets whereas both are inhibited by prostaglandin E1 or by the pyrimido-pyrimidine compound RA233. In human platelets all three agents increase adenosine-3'-5'-cyclic monophosphate (cAMP). If the inhibition of aggregation depended on this increase, adenosine might be expected not to increase cAMP in rat platelets. Under conditions in which adenosine inhibited aggregation and increased cAMP in human platelets, adenosine caused a similar increase in cAMP in rat platelets without inhibiting their aggregation. The aggregation of rat platelets was inhibited as effectively as that of human platelets by PGE1 or RA233 at concentrations which caused greater increases in cAMP than did the highest concentrations (2.8 X 10(-4) M) of adenosine it was possible to use. When the increase of cAMP in rat platelets by PGE1 was limited to that produced by adenosine, PGE1 like adenosine failed to inhibit aggregation. Therefore, the difference in the inhibitory effectiveness of adenosine on rat and human platelets was quantitative rather than qualitative and apparently depended on the inability of adenosine to increase cAMP sufficiently in rat platelets. When cAMP had been increased by adenosine, PGE1 or RA233, the addition of ADP caused cAMP to decrease rapidly in both human and rat platelets to between +22 and -18% of control values, except that the decrease in rat platelets was to +40% after RA233 had been present for 0.5 min before ADP. The increase in cAMP produced in rat platelets by adenosine at 5 X 10(-6) to 2.8 X 10(-4) M for 3 min was associated with a small increase in aggregation velocity. It is suggested that the comparative ineffectiveness of adenosine as an inhibitor of platelet aggregation, particularly with rat but less so also with human platelets, is because, unlike PGE1 or RA233, adenosine has two opposing actions on aggregation; one being inhibition by activating adenylate cyclase and increasing cAMP, and the other being potentiation by uptake. This hypothesis accounts for the present results as well as for the earlier observation that dipyridamole which prevents the uptake of adenosine potentiates its inhibitory effect on the aggregation of human platelets.

Adenosine↗
PubMed1976

The thrombocyte membrane in circulatory diseases.

There is no certain evidence for the proposition, often put forward, that thrombocytes, or platelets, are involved in atherogenesis. On the other hand, thrombotic deposits in arteries as well as in the blood channels of artificial organs consist at first mainly of platelets. This contribution reviews evidence indicating that the formation of such thrombi depends on alterations in the platelet membrane and that these in turn depend on an agent, apparently ADP, which is released from the erythrocytes.

Adenosine Diphosphate↗
PubMed1975

Accelerated uptake of 5-hydroxytryptamine by human blood platelets enriched in a sialic acid.

The enzymically catalysed incorporation of N-acetylneuraminic acid into human platelets, whether suspended in their own citrated plasma or in buffered saline containing 0.17 mM-sucrose, accelerated the uptake of 5-hydroxytryptamine. This acceleration decreased with time. The observations may be explained by assuming that N-acetylneuraminic acid is a component of a transport receptor for 5-hydroxytryptamine.

Biological Transport↗
PubMed1975

Binding of adenosine diphosphate to intact human platelets.

1. Human platelet-rich plasma was incubated at 37 degrees C with [8-14C]ADP and with human serum albumin labelled with 125I. The platelets were rapidly separated by centrifugation through silicone oil. From radioactivity determinations of plasma and platelet pellets the uptake of ADP, without or with break-down products, by the platelets was calculated on the assumption that the 125I radioactivity in the pellet represented trapped plasma. 2. ADP radioactivity was taken up by platelets within 10 sec and increased with time of incubation. The uptake of other nucleotide diphosphates was less initially and increased much more slowly. 3. Radioactivity added as ADP was recovered as ATP to the extent of 60%; as ADP of 30%; and as AMP of 10%. 4. Prostaglandin E1 which inhibited platelet aggregation had no effect on the initial or subsequent uptake or on this distribution of radioactivity. 5. The rate of rise in uptake was much slower when platelets were resuspended in plasma heated to 56 degrees C for 30 min. 6. Unlabelled adenosine inhibited the later, but not the initial, uptake while unlabelled ADP inhibited both. Dipyridamole, which blocks adenosine uptake, prevented the later but not the initial uptake. 7. [alpha-32P]ADP radioactivity was taken up at the earliest sampling time and the extent of uptake did not further increase. 8. Guinea-pig platelets, which do not take up adenosine, took up [8-14C]ADP radioactivity from purine-labelled ADP initially. 9. It was concluded that the initial uptake represented binding of ADP and that the later uptake represented labelled adenosine originating as a break-down product of ADP. 10. A Scatchard plot of ADP uptake indicated more than one type of binding site. There were approximately 88,000 high affinity sites per platelet which had an affinity constant of 5-41 X 10(5) M-1.

Adenosine↗
PubMed1973

Relationship between the velocity of rolling granulocytes and that of the blood flow in venules.

1. The mean velocities at which granulocytes roll along the walls of small venules have been related to their mean blood flow velocities in preparations of hamster cheek pouch and mouse mesentery. In animals anaesthetized with Nembutal, 30-200 mum venules were observed microscopically and the movement of rolling granulocytes quantitated on films. Apparent mean blood flow velocity was determined from films of embolizing platelet thrombi.2. In four venules the velocity distribution of about 100 rolling cells was almost symmetrical about the mode, with a small proportion moving at up to three times the mode velocity. Therefore, the mean and mode velocities were very similar.3. In two mesenteric and two cheek-pouch venules, blood flow velocity was temporarily altered during and after gentle compression with a fine glass fibre; this was associated with proportional changes in mean cell velocities.4. In four different venules of a hamster cheek pouch, the mean velocity of rolling granulocytes increased in proportion to the mean blood flow velocity (r = 0.963).5. In thirty-six venules of ten mouse mesenteries, the velocities were proportional (r = 0.915) between blood velocities of about 300 and 1000 mum/sec. Above this the velocity of the cells did not increase further.6. The rolling of granulocytes is presumably governed by two forces, the shear force of the flowing blood and an adhesive force between the surfaces of granulocytes and vascular endothelium. Our results suggest that, within limits, the proportionality between the velocities of blood flow and rolling cells is due to shear force, the adhesive force being similar for all the cells. The results suggest that this adhesion force per granulocyte is of the order of 10(-5) dynes.

Adhesiveness↗