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Biomedical subjects

G V Born

Publications and source records attributed to G V Born.

At least 109 records · Page 6Linked to original sources
PubMed1980

Long-term effect of lithium on the uptake of 5-hydroxytryptamine by human platelets.

1 The content, uptake and storage of 5-hydroxytryptamine (5-HT) in platelets were determined in eight manic-depressive patients not on lithium (Li); in ten manic-depressive patients on Li; and in ten apparently normal persons as controls. 2 Platelets from the patients, whether or not on Li, contained less 5-HT than platelets from normal people. 3 5-HT uptake and storage by platelets from untreated patients were significantly lower than those of control subjects. 4 When patients had been on Li for 3 months or longer the diminished uptake and storage of 5-HT by their platelets were more than fully reversed. 5 Li added to platelet-rich plasma in vitro had no effect on the uptake of 5-HT by platelets.

Adult↗
PubMed1980

Increases in aggregation by and uptake of 5-hydroxytryptamine with platelets from rabbits treated with chlorpromazine.

1 Citrated platelet-rich plasma was prepared from New Zealand white rabbits before, during and after administration of chlorpromazine (2 mg/kg) intramuscularly once daily for 3 to 4 weeks. 2 In these plasmas, the velocity of platelet aggregation by 5-hydroxytryptamine (5-HT) added at 1, 3 and 10 microM increased greatly, beginning 3 to 4 days after the start of chlorpromazine injections and lasting for a similar period after they were terminated. The increase had two maxima, the first after 6 to 10 days and the second after 17 to 24 days. Chlorpromazine treatment did not affect aggregation by adenosine diphosphate (ADP). 3 The uptake of 5-HT by rabbit platelets was very fast and linear for less than 10 s. In platelets from untreated rabbits the uptake had a Km of 0.35 +/- 0.08 microM and a Vmax of 39.8 +/- 6.1 pmol 10(-8) platelets 10(-1) (n = 5). 4 In platelets from rabbits injected with chlorpromazine (see (2) above) both kinetic constants increased significantly, the Km to 0.88 +/- 0.08 microM and the Vmax to 67.8 +/- 5.5 pmol. 10(-8) platelets. 10(-1) s (n = 9).

Animals↗
PubMed1980

Suppression of the intravascular adherence of granulocytes by N-acetyl neuraminic (sialic) acid.

Adherence of granulocytes to the endothelium of small veins in different microvascular beds was quantified by visual counting of the adherent cells. Increased adherence of granulocytes induced by the stress of preparation or by ultraviolet light irradiation of the microvasculature was greatly reduced by i.v. administration of sialic acid. In the rabbit ear chamber laser irradiation induced increased granulocyte stickiness which was similarly prevented by intra-arterial infusion of sialic acid. In normal rats, sialic acid treatment induced granulocytosis and the effect was more striking on Busulphan-induced leucopenia in rats. Glucuronic acid applied under identical conditions had no effect on granulocyte adhesiveness in vivo or on the peripheral blood granulocyte count. According to these findings exogenous sialic acid greatly reduces the effect different pathogenic stimuli have of inducing adherence of granulocytes to blood vessel walls and induces granulocytosis by mobilizing cells from the "marginating" and reserve pools.

Animals↗
PubMed1979

Effects of D- and L- enantiomers of adenosine, AMP and ADP and their 2-chloro- and 2-azido- analogues on human platelets.

Aggregation of human platelets by ADP and the inhibition of this effect by adenosine are apparently mediated by different receptors. One of the criteria for receptors is that they show stereospecificity for their ligands. We have synthesized L-enantiomers of D-adenosine, AMP and ADP, together with their corresponding photolysable 2-azido analogues so that platelet receptors could be tested for stereospecificity. All of the L-enantiomers were completely inactive as aggregators or inhibitors of platelet function. None of the L-enantiomers changed levels of platelet cAMP. 2-Azido-L-adenosine, AMP and ADP are proposed as useful controls in photoaffinity experiments for non-specific labelling.

Adenosine↗
PubMed1979

Inhibition of platelet thrombus formation by chlorpromazine acting to diminish haemolysis.

There is increasing evidence that the sudden, unpredicatable event initiating myocardial infarction is fissuring of an atherosclerotic plaque. The resulting haemorrhage into the arterial wall produces obstructive platelet thrombi, just as arterial haemorrhages elsewhere produce haemostatic platelet plugs. It has been suggested that such platelet aggregation depends on ADP originating in red cells which are subjected to excessive haemodynamic stress at the site of haemorrhage. The release of ADP from red cells has been demonstrated in vitro in equivalent condtions of shear stress; and other mechansims, such as activation by collagen, cannot account for the rapidity with which the platelets react. One of us (G.V.R.B.) has suggested that drugs capable of counteracting haemolysis might diminish the activating effect of erythrocytes on platelets and so inhibit their aggregation as thrombi. Thus, chlorpromazine, added to human blood at concentrations which diminish haemoylsis but do not directly affect platelet aggregation, prolonged the 'bleeding time' from small holes in artificial vessels where extravasation is terminated, as in living arterioles, by aggregated platelets. The bleeding time was also prolonged by apyrase, consistent with the conclusion that the chlorpromazine acted through decreasing plasma ADP. We show here that this occurs through the anti-haemolytic action of chlorpromazine.

Adenosine Diphosphate↗
PubMed1978

Inhibition by N-acetyl neuraminic acid of platelet thrombogenesis induced by laser injury to rat and hamster venules.

1 In rats and hamsters under barbiturate anaesthesia, laser radiation to venules about 50 micrometer in diameter in mesoappendix and cheek pouch respectively caused the formation of platelet thrombi which occluded the vessels in about 9 min. 2 This occlusion time was significantly prolonged by the intravenous injection of N-acetyl neuraminic acid (NANA) but not by D-glucuronic acid or beta-methoxyneuraminic acid, in doses which had no effect on blood pH or on the condition of the animals. 3 The results confirm the anti-thrombotic effect of NANA previously demonstrated with another technique.

Animals↗
PubMed1978

Quantification of the morphological reaction of platelets to aggregating agents and of its reversal by aggregation inhibitors.

1. In rabbit citrated platelet-rich plasma, the changes in shape of the platelets produced by adenosine diphosphate (ADP) or 5-hydroxytryptamine (5-HT) were observed by photometric and volumetric techniques and by measurements of platelet images on electron micrographs either directly or with an image analysing computer. This permitted the indirect manifestations of the shape changes to be correlated with the morphological features responsible for them, i.e. transformation of disks to more spherical forms and extrusion of blebs and spikes. 2. Following the addition of ADP, an initial brief peak in the light scattering records was associated with marked but transient irregularities in the surface of the platelets. These effects were absent when the other shape changes were produced by 5-HT. 3. When the optical manifestations of the shape changes induced by ADP were reversed by the addition of antagonists adenosine triphosphate, 2-chloroadenosine or prostaglandin E1, the morphological changes were reversed by a diminution in the number of spikes and the conversion of spherical platelet bodies to a more discoid form. 4. The volume of extracellular plasma trapped between platelets sedimented by centrifugation was proportional to the number of spikes which they extruded. Under all conditions, the volume of the platelets themselves remained remarkably constant at approximately 5 X 10(-9) microliter./platelet. 5. Addition of a calcium chelating agent alone produced a rapid persistent alteration in the optical properties of platelet-rich plasma. The magnitude of this alteration was proportional to chelator concentration but greater in some plasmas than in others. Similar optical effects were produced when the calcium concentration of platelet-rich plasma was increased by adding calcium. The optical effects produced by calcium or its chelators were unusual in that the changes in transmitted and horizontally scattered light were in opposite directions (transmitted light decreased, scattered light increased) whereas, in all other circumstances so far examined, these changes were in the same direction. The chelators caused the formation of spikes on the platelets without appreciably altering their disk shape, which may explain the unusual nature of the optical effects.

Adenosine↗
PubMed1977

Movement of sodium into human platelets induced by ADP.

1. In normal human platelets the concentrations of Na+ and K+ were 42.1 +/- 4.3 and 98.8 +/- 3.7 mequiv/l of platelet water respectively (mean +/- S.E. of 22 samples). 2. When platelet-rich plasma was incubated with 22Na+ at 37 degrees C for 2-3 h an increase in platelet Na+ concentration was found which was significant after 210 min. Platelet K+ concentration did not change significantly. The platelet 22Na+ radioactivity increased faster than did the total Na+ suggesting a Na+o-Na+ exchange process in unactivated platelets. 3. Addition of ADP to platelet-rich plasma resulted in platelet aggregation and a rapid rise (within seconds) in 22Na+-radioactivity within the platelets and after 300 s this increase diminished toward control levels. 4. Under the same experimental conditions, ADP did not bring about an increase of 36Cl- in the platelets. 5. Ouabain (10-(6) M) added to platelet-rich plasma induced an increase in Na+ concentration and 22Na+ radioactivity in the platelets, as well as a decrease in K+ concentration. ADP produced a further increase in 22Na+, which did not return toward control values, in the presence of ouabain. 6. The association of an increase in 22Na+ but not of 36Cl- accompanying aggregation by ADP suggests a selective mechanism for the movement of Na+ into platelets rather than a movement of NaCl together with water under an osmotic gradient.

Adenosine Diphosphate↗