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A platelet release defect induced by aspirin or penicillin G does not increase gastrointestinal blood loss in thrombocytopenic rabbits
Author(s) -
Giles Alan R.,
And Penny Greenwood,
Tinlin Shawn
Publication year - 1984
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1984.tb02861.x
Subject(s) - platelet , aspirin , medicine , saline , sodium salicylate , gastrointestinal tract , bleeding time , pharmacology , platelet aggregation
S ummary. Gastrointestinal blood loss was compared in groups of normal and thrombocytopenic animals treated with medications known to induce qualitative platelet dysfunction. Thrombocytopenia was induced in rabbits by the intraperi‐toneal injection of busulphan dissolved in polyethylene glycol (PEG) at a dose of 60 mg/kg. Control animals received PEG alone; each group subsequently received daily intravenous injections of penicillin G, aspirin, sodium salicylate or isotonic saline. Mean daily gastrointestinal blood loss was determined by monitoring the appearance of 51Cr radioactivity in the faeces following the administration of 51Cr‐labelled erythrocytes prior to the administration of the test and control therapies. The administration of penicillin G was not associated with increased gastrointestinal blood loss in the thrombocytopenic animals as compared with the saline treated thrombocytopenic controls. Platelet aggregation studies confirmed the presence of a mild but significant defect in platelet aggregation. Aspirin produced a more pronounced defect in platelet aggregation but did not induce increased bleeding in the normal animals as compared with the controls, nor did it exacerbate the bleeding in thrombocytopenic animals. Sodium salicylate did not produce an aggregation defect and did not significantly modify gastrointestinal blood loss. It was concluded that drug‐induced qualitative platelet dysfunction does not necessarily increase bleeding through intact vessels despite previous evidence of a significant effect on platelet plug formation as monitored by the bleeding time.