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Irreversible platelet aggregation does not depend on lipoxygenase metabolites.

Abstract：

:Previous investigations in our laboratory demonstrated the existence of an intrinsic mechanism, termed membrane modulation, capable of restoring sensitivity to aspirin treated platelets, resulting in irreversible aggregation in response to arachidonic acid (AA). The mechanism underlying correction of aspirin induced inhibition of platelet function, however, was not clear. In the present study we have evaluated the role of lipoxygenase (LO) metabolites of AA in securing irreversible aggregation of drug induced cyclooxygenase (CO) deficient platelets. Platelets treated with aspirin or Ibuprofen did not convert radiolabeled AA to thromboxane, but generated significant quantities of hydroxy acids via the LO pathway. However, drug exposed platelets, when stirred with epinephrine first and then challenged with AA, aggregated irreversibly. Eicosatetraynoic acid (ETYA 1, U53119) inhibited AA conversion by the LO pathway, whereas 5,8,11,14-eicosatetraynoic acid (ETYA 2) inhibited AA conversion by both CO and LO enzymes. Yet, at the inhibitory concentration these fatty acids failed to prevent AA induced irreversible aggregation of CO deficient, alpha adrenergic receptor stimulated platelets. Results of four studies show that the generation of LO metabolites of AA are not essential for securing irreversible aggregation of platelets.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Rao GH,Radha E,White JG

doi

10.1016/0006-291x(85)91768-1

subject

Has Abstract

pub_date

1985-08-30 00:00:00

pages

50-7

issue

1

eissn

0006-291X

issn

1090-2104

pii

0006-291X(85)91768-1

journal_volume

131

pub_type

杂志文章

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