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F A Belamarich

Publications and source records attributed to F A Belamarich.

At least 19 recordsLinked to original sources
PubMed1976

Similarities between platelet contraction and cellular motility during mitosis: role of platelet microtubules in clot retraction.

The effects of inhibitors of mitosis, energy metabolism and protein synthesis on clot retraction were investigated. The results show that (1) Incubation of colchicine (0-01-0-1 mM) with platelet-rich plasma (PRP) inhibits the subsequent retraction of clots derived from diluted PRP. (2) Inhibition of clot retraction by high concentrations of colchicine (up to 40 mM) can be overcome by increasing the platelet concentration in the system. (3) Incubation of clots in colchicine or 80% D2O solutions inhibits their retraction. Exposure of partially retracted clots to these agents is without effect. (4) Hydrostatic pressure retards clot retraction. (5) Incubation of PRP with either 2-deoxy-D-glucose or antimycin alone does not affect clot retraction, but a combination of these agents is inhibitory. (6) Clot retraction is not inhibited by puromycin or cycloheximide. (7) Platelets in retracting clots have constricted regions containing microfilaments and pseudopods containing microtubules. Fibrin strands are progressively condensed around the constricted regions as retraction advances. (8) The development of platelet constriction, platelet pseudopods and the intracellular microfilaments are delayed in colchicinized clots, corresponding to the retardation of retraction. Following the initial delay of retraction colchicinized clots, like controls, show condensation of fibrin strands adjacent to these constricted areas of platelets containing microfilaments. The formation of pseudopods is impaired and no microtubules are found in platelets in the presence of colchicine. The above results suggest that the thrombin-induced platelet contraction during clot retraction is a coordinated movement, which, under optimal conditions involves both microtubules and microfilaments. The contraction of microfilaments produces the constriction of platelets and brings about clot retraction by reducing the angle between fibrin strands. Platelet microtubules are related to the development of pseudopods and play a supplementary role in facilitating microfilament-mediated cellular constriction. The similarities between platelet contraction and cellular motility in mitosis is discussed.

Antimycin A↗
PubMed1975

Aggregation and release in thrombocytes of the duck.

Avian thromboyctes are aggregated by a number of substances that cause platelet aggregation, and evidence suggests that this response is related to the release of serotonin (5-hydroxytryptamine, 5-HT) from intracellular granules. In this study duck thrombocytes released 5-HT during collagen-induced aggregation, but thrombocytes incubated with 14C-labeled adenine did not release radioactive adenine nucleotides. These results indicate the existence of a metabolic pool of adenine nucleotides that is separate from released constituents of the cell. No unlabeled adenine compounds were detected in the supernatants of aggregated thrombocytes indicating either the rapid alteration of released nucleotides or the absence of a specific release pool of adenine nucleotides. Finally there is no release of the intracellular enzyme markers, lactate dehydrogenase, beta-glucuronidase, and acid phosphatase, during collagen-induced aggregation. These findings suggest that avian thrombocytes exhibit a specific release reaction and that serotonin acts as the functional counterpart of ADP in platelet aggregation.

Adenine↗
PubMed1975

Serotonin transport by cultured bovine aortic endothelium.

Endothelial cells isolated from bovine aortas without prior treatment with enzymes were cultured in RPMI 1640 medium containing 17% fetal calf serum and antibiotics. The endothelial cells at confluency (7 days) were similar to endothelium in situ or to freshly isolated endothelial cells from blood vessels as seen by light, scanning, and electron microscopy. Cultured and freshly isolated indothelial cells exposed to labeled serotonin, even in the presence of iproniazid (5 x 10-4M), took up approximately 125 and 250 pmoles 14C-serotonin/mg protein, respectively, in 3 hours. Imipramine (10-4M) reduced uptake for both cell groups. Cold (4 degrees C) and metabolic inhibitors sharply reduced serotonin uptake by both freshly isolated and cultured endothelial cells. Ouabain (10-5M) almost completely blocked serotonin transport. Six analogues of serotonin at concentrations ten times above experimental serotonin concentrations did not affect serotonin transport in the cultured endothelial cells but did reduce it in the freshly isolated endothelial cells by 50%. The data on transport suggest that serotonin uptake is not unique to pulmonary endothelium, as has been suggested previously. In addition, using cultured indothelial cells to study serotonin transport is compatible with using other serotonin model systems such as platelets, lung, or brain. Lastly, serotonin uptake by endothelial cells may involve an active transport mechanism similar to that described for the pulmonary circulation, platelets, and insect salivary glands.

Animals↗
PubMed1973

Calcium uptake and associated adenosine triphosphatase activity of isolated platelet membranes.

A platelet subcellular fraction, sedimenting between 14,000 and 40,000 g and consisting primarily of membrane vesicles, accumulates up to 200-400 nmoles calcium/mg protein in the presence of ATP and oxalate. Steady-state levels of calcium accumulation are attained in 40-60 min. Calcium uptake requires adenosine triphosphate (ATP), is enhanced by oxalate, and is accompanied by the release of inorganic phosphate. Calcium accumulation and phosphate release require magnesium and are inhibited by Salyrgan (10 microM) and adenosine diphosphate (ADP) (1 mM), but not by ouabain (0.1 mM). The ATPase activity is stimulated by low concentrations of calcium (5-10 microM) and is inhibited by 2 mM EGTA. Electron microscopic histochemistry using lead nitrate to precipitate released phosphate results in lead precipitates localized primarily at the inner surface of membrane vesicles. These results provide evidence for a membrane ATPase that is stimulated by low concentrations of calcium and may be involved in the transport of calcium across the membrane. It is postulated that the observed calcium uptake activity is an in vitro manifestation of a calcium extrusion pump in the intact platelet.

Adenosine Diphosphate↗