title: An hypothesis on the consolidation and PGE1-induced deconsolidation of a platelet plug.
abstract: Consolidation is the final stage in haemostasis in which a platelet plug blocking a bleeding area of a vessel: (a) becomes impermeable to circulating plasma proteins and (b) contracts to resist blood pressure.
  
  
  OBJECTIVE
  The impermeabilization step of consolidation is accomplished through fluid uptake by the platelets from a hydrated intercellular glue formed during thrombin activation. Dehydration occurs through inhibition of the Na+,K+-ATPase of platelets with sodium and water uptake. However, and uniquely, due to the high cellular density of the platelet plug, access of peripheral plasma fluids to the plug is limited forcing the platelets to take up preferentially the fluid of interplatelet space. The increased adhesion properties of the dehydrated glue simultaneously furthers a decreased hydraulic permeability and an improved coupling of the contractile forces among platelets. In 'Deconsolidation', the fluid uptake process can be reversed and amplified by agents that increase cAMP, reactivating the Na+,K+-ATPase and expressing CFTR or equivalent Cl- secretory channels that force the extrusion of fluid from the platelets, with rehydration of the intercellular polymer and a large increase in the interplatelet space.
authors.affiliation: Department of Pharmacology, Temple University Medical School, Philadelphia, PA 19140, USA. ls23529@astro.temple.edu
authors.forename: Leon
authors.initials: L
authors.lastname: Salganicoff
authors.forename: Matteo A
authors.initials: MA
authors.lastname: Russo
mesh_terms: D000244:Adenosine Diphosphate / Q000502:physiology; D000527:Alprostadil / Q000502:physiology*; D000818:Animals; D001792:Blood Platelets / Q000502:physiology* / Q000648:ultrastructure; D002118:Calcium / Q000502:physiology; D002414:Cations, Monovalent / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000378:metabolism; D002712:Chlorides / Q000378:metabolism; D003018:Clot Retraction; D000242:Cyclic AMP / Q000502:physiology; D019005:Cystic Fibrosis Transmembrane Conductance Regulator / Q000502:physiology; D005110:Extracellular Space / Q000502:physiology; D005340:Fibrinogen / Q000502:physiology; D006801:Humans; D020100:Hydrogels; D008854:Microscopy, Electron; D008954:Models, Biological; D009995:Osmosis / Q000502:physiology; D010974:Platelet Aggregation / Q000502:physiology; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000502:physiology; D000254:Sodium-Potassium-Exchanging ATPase / Q000502:physiology; D013917:Thrombin / Q000502:physiology; D011503:Transglutaminases / Q000502:physiology; D014867:Water / Q000378:metabolism
chemical_list: C505032:CFTR protein, human; D002414:Cations, Monovalent; D015815:Cell Adhesion Molecules; D002712:Chlorides; D020100:Hydrogels; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D014867:Water; D019005:Cystic Fibrosis Transmembrane Conductance Regulator; D000244:Adenosine Diphosphate; D005340:Fibrinogen; D000242:Cyclic AMP; D011503:Transglutaminases; D013917:Thrombin; D000254:Sodium-Potassium-Exchanging ATPase; D000527:Alprostadil; D002118:Calcium