Topic
Platelet
About: Platelet is a research topic. Over the lifetime, 36809 publications have been published within this topic receiving 1356298 citations. The topic is also known as: Blood Platelet & Blood Platelets.
Papers published on a yearly basis
Papers
More filters
TL;DR: It is demonstrated that NO can be synthesized from L-arginine by porcine aortic endothelial cells in culture and the strict substrate specificity of this reaction suggests that L- arginine is the precursor for NO synthesis in vascular endothelium cells.
Abstract: Nitric oxide (NO) released by vascular endothelial cells accounts for the relaxation of strips of vascular tissue1 and for the inhibition of platelet aggregation2 and platelet adhesion3 attributed to endothelium-derived relaxing factor4. We now demonstrate that NO can be synthesized from L-arginine by porcine aortic endothelial cells in culture. Nitric oxide was detected by bioassay5, chemiluminescence1 or by mass spectrometry. Release of NO from the endothelial cells induced by bradykinin and the calcium ionophore A23187 was reversibly enhanced by infusions of L-arginine and L-citrulline, but not D-arginine or other close structural analogues. Mass spectrometry studies using 15N-labelled L-arginine indicated that this enhancement was due to the formation of NO from the terminal guanidino nitrogen atom(s) of L-arginine. The strict substrate specificity of this reaction suggests that L-arginine is the precursor for NO synthesis in vascular endothelial cells.
4,803 citations
4,153 citations
TL;DR: A balance between formation of anti- and pro-aggregatory substances by enzymes could also contribute to the maintenance of the integrity of vascular endothelium and explain the mechanism of formation of intra-arterial thrombi in certain physiopathological conditions.
Abstract: Microsomes prepared from rabbit or pig aortas transformed endoperoxides (PGG2 or PGH2) to an unstable substance (PGX) that inhibited human platelet aggregation. PGX was 30 times more potent in this respect than prostaglandin E1. PGX contracted some gastrointestinal smooth muscle and relaxed certain isolated blood vessels. Prostaglandin endoperoxides cause platelet aggregation possibly through the generation by platelets of thromboxane A2. Generation of PGX by vessel walls could be the biochemical mechanism underlying their unique ability to resist platelet adhesion. A balance between formation of anti- and pro-aggregatory substances by enzymes could also contribute to the maintenance of the integrity of vascular endothelium and explain the mechanism of formation of intra-arterial thrombi in certain physiopathological conditions.
3,412 citations
TL;DR: Monoclonal antibody assessment of cancellous cellular marrow grafts demonstrated cells that were capable of responding to the growth factors by bearing cell membrane receptors and evidenced a radiographic maturation rate 1.62 to 2.16 times that of grafts without platelet-rich plasma.
Abstract: Platelet-rich plasma is an autologous source of platelet-derived growth factor and transforming growth factor beta that is obtained by sequestering and concentrating platelets by gradient density centrifugation. This technique produced a concentration of human platelets of 338% and identified platelet-derived growth factor and transforming growth factor beta within them. Monoclonal antibody assessment of cancellous cellular marrow grafts demonstrated cells that were capable of responding to the growth factors by bearing cell membrane receptors. The additional amounts of these growth factors obtained by adding platelet-rich plasma to grafts evidenced a radiographic maturation rate 1.62 to 2.16 times that of grafts without platelet-rich plasma. As assessed by histomorphometry, there was also a greater bone density in grafts in which platelet-rich plasma was added (74.0% +/- 11%) than in grafts in which platelet-rich plasma was not added (55.1% +/- 8%; p = 0.005).
2,587 citations
TL;DR: A method by which the aggregation of platelets may be followed quantitatively is described, and results obtained with the method are described.
Abstract: Inthe circulating bloodtheplatelets are normally carried along separately from each other and there is no evidence that they adhere to normal vascular endothelium. When the wall of a blood vessel is injured platelets adhere to it immediately (Hugues, 1953) and to each other to form aggregates on the damaged intima (Bizzozero, 1882). When the vessel wall is broken aggregates of platelets tend to seal the opening and so help to arrest bleeding (Fulton, Akers & Lutz, 1953); such aggregates have been called 'haemostatic plugs' (Roskam, 1954). When diseases, for example, atherosclerosis, damage the intima platelets again adhere to it and to each other. The aggregates so formed are called 'platelet or white thrombi', and they may increase in size until they block the flow of blood. The aggregation of platelets is, therefore, one of the immediate causes of thrombosis. Why damage to the intima should cause platelets to adhere and to aggregate is still unknown. This paper describes a method by which the aggregation of platelets may be followed quantitatively, and results obtained with the method are described; some of these have been briefly reported earlier (Born, 1962a, b; Born & Cross 1963).
2,094 citations