TY - JOUR
T1 - Platelet arachidonic acid metabolism in patients with cardiovascular disorders
AU - Ghigo, D.
AU - Treves, S.
AU - Bussolino, F.
AU - Libero, L.
AU - Orzan, F.
AU - Bazzan, M.
AU - Pannocchia, A.
AU - Tamponi, G.
AU - Bosia, A.
PY - 1988
Y1 - 1988
N2 - There is increasing evidence that prostaglandins (PG) and thromboxane (Tx) play a major role in the pathogenesis of coronary artery disease. The regulation of arachidonic acid (AA) metabolism through cyclooxygenase (COx) pathway and the AA-dependent Ca2+ influx were investigated in platelets from 10 patients with unstable angina and 10 controls. The activation of the hexose monophosphate shunt (HMS), a sensitive index of the flux through the PGG2 to PGH2 step of the COx pathway, in response to AA was significantly enhanced in platelets from patients. AA-induced malonyldialdehyde (MDA) production as well as AA-evoked Ca2+ flux and glutathione-dependent peroxidase activity resulted significantly increased. Moreover, platelet sensitivity to prostacyclin (PGI2), measured as inhibition of Ca2+ flux, was highly decreased. Thus far, evidence is presented for intrinsic platelet hyperactivity (at the PG-peroxidase reaction of the COx pathway) in patients with unstable angina: the resulting increase in PGH2 and TxA2 synthesis, alone or in combination with decreased PGI2 sensitivity, may account for a facilitated thrombus formation.
AB - There is increasing evidence that prostaglandins (PG) and thromboxane (Tx) play a major role in the pathogenesis of coronary artery disease. The regulation of arachidonic acid (AA) metabolism through cyclooxygenase (COx) pathway and the AA-dependent Ca2+ influx were investigated in platelets from 10 patients with unstable angina and 10 controls. The activation of the hexose monophosphate shunt (HMS), a sensitive index of the flux through the PGG2 to PGH2 step of the COx pathway, in response to AA was significantly enhanced in platelets from patients. AA-induced malonyldialdehyde (MDA) production as well as AA-evoked Ca2+ flux and glutathione-dependent peroxidase activity resulted significantly increased. Moreover, platelet sensitivity to prostacyclin (PGI2), measured as inhibition of Ca2+ flux, was highly decreased. Thus far, evidence is presented for intrinsic platelet hyperactivity (at the PG-peroxidase reaction of the COx pathway) in patients with unstable angina: the resulting increase in PGH2 and TxA2 synthesis, alone or in combination with decreased PGI2 sensitivity, may account for a facilitated thrombus formation.
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M3 - Article
C2 - 3248116
AN - SCOPUS:0024267251
VL - 47
JO - Biomedica Biochimica Acta
JF - Biomedica Biochimica Acta
SN - 0232-766X
IS - 10-11
ER -