sábado, 20 de marzo de 2010

Inflammatory ascites formation induced by macromolecules in mice and rats

Different macromolecules were administered i.p. to stimulate formation
of protein-rich ascitic fluid in rodents. Stimulatory effect of plant
lectins depended on the attachment to cell surface carbohydrates, ConA
was used in the majority of experiments. The time course of
ConA-induced ascites was divided into an early (up to 4h) and a late
phase (from 6h on), with a transitional period between the two. Water
and protein accumulation showed parallel time courses: volume of the
ascitic fluid peaked at around 3h, and fibrin threads appeared after
6h. Viscosity of the ascitic fluid and its supernatant increased with
time, reaching maximal fibrinogen concentration at around 16h.
Peritoneal permeability, followed by pleural and pericardial
effusions, was elicited only by lectins which form soluble complexes
with serum glycoproteins, whereas the effect of serum-precipitating
lectins was restricted to the peritoneum. Macromolecules with serial
positive charges (e.g. polylysine or polyethyleneimine) enhanced
peritoneal permeability by ionic interactions with cell surface
molecules. Viscosity of the polycation-induced ascitic fluid did not
tend to increase with time and corresponded to the early-phase of the
ConA-induced ascites. Polyglutamate, a polyanionic macromolecule,
inhibited the effect of polycations, but not that of ConA. The most
efficient stimulatory macromolecules appear to induce ascites by
non-covalent cross-linking of cell surface glycoproteins or
glycosaminoglycans or both. A similar mechanism may operate in the
maintenance of basal secretion to prevent eventual desiccation.
Non-covalent cross-linking appears to be a common denominator of both
basal and enhanced permeability.

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