Is spontaneous platelet aggregation present in whole blood in vitro?
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Biomedical subjects
Publications and source records attributed to B Spławińska.
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Release of PGI2 by slices of muscularis and mucosa layers of rat corpus stomach was investigated. An anti-aggregatory substance that was released by slices of muscularis was identified as PGI2 in various bioassay systems including anti-serum against PGI2 as well as by stimulation of its generation with AA or PGH2 and by inhibition of this generation with indomethacin or tranylcypromine, respectively. PGI2 was the major PGs released from slices of muscularis. The release of PGI2 from muscularis surpasses a similar release of PGI2 from mucosa by a factor of 10. On the other hand, degradation of exogenous PGI2 was 4 times faster by mucosa than by muscularis slices. Our conclusion is that in the stomach corpus wall of rats, muscularis is the main source of PGI2, which may play a role in regulation of mucosal blood flow.
Patients with myocardial infarction, complicated by ventricular arrhythmias (Lown grade greater than or equal to 2), had higher (p less than 0.05) plasma beta-thromboglobulin level than that found in patients with uncomplicated infarction. This indicates higher platelet activation in the former group than in the latter. Such data provide rationale for clinical trial of antiplatelet drugs in cases of myocardial infarction complicated by severe arrhythmias.