Many reports indicate that nitric oxide (NO) could be involved in migraine without aura (MWA), an extremely diffuse clinical event. Since monocyte may be a relevant source of NO, we analysed monocyte activation in MWA patients, in a period in which they were free of symptoms. NO basal production by MWA peripheral monocytes was significantly higher than in healthy subjects (91.25+/-8.6 mu M/10 degrees cells vs. 22.6+/-3.2 mu M /10(6) cells). Interestingly, even the release of prostaglandin E-2 (PGE(2)), was higher in MWA patients than in healthy subjects (3137+/-320 pg/10 degrees cells vs. 1531+/-220 pg/10(6) cells). The incubation of monocytes from healthy subjects and MWA patients with N-nitro-L-arginine methyl ester caused a marked decrease of both NO and PGE(2) release. We hypothesise that NOS and cyclooxygenase pathways in monocytes are linked and are, in MWA patients, up-regulated, even in a symptoms-free period. NO and PGE(2) hyperproduction could therefore be involved in the neurovascular modifications leading to migraine attacks.
Linked activation of nitric oxide synthase and cyclooxygenase in peripheral monocytes of asymptomatic migraine without aura patients / G., Stirparo; Zicari, Alessandra; M., Favilla; M., Lipari; Martelletti, Paolo. - In: CEPHALALGIA. - ISSN 0333-1024. - 20:2(2000), pp. 100-106. [10.1046/j.1468-2982.2000.00025.x]
Linked activation of nitric oxide synthase and cyclooxygenase in peripheral monocytes of asymptomatic migraine without aura patients
ZICARI, Alessandra;MARTELLETTI, Paolo
2000
Abstract
Many reports indicate that nitric oxide (NO) could be involved in migraine without aura (MWA), an extremely diffuse clinical event. Since monocyte may be a relevant source of NO, we analysed monocyte activation in MWA patients, in a period in which they were free of symptoms. NO basal production by MWA peripheral monocytes was significantly higher than in healthy subjects (91.25+/-8.6 mu M/10 degrees cells vs. 22.6+/-3.2 mu M /10(6) cells). Interestingly, even the release of prostaglandin E-2 (PGE(2)), was higher in MWA patients than in healthy subjects (3137+/-320 pg/10 degrees cells vs. 1531+/-220 pg/10(6) cells). The incubation of monocytes from healthy subjects and MWA patients with N-nitro-L-arginine methyl ester caused a marked decrease of both NO and PGE(2) release. We hypothesise that NOS and cyclooxygenase pathways in monocytes are linked and are, in MWA patients, up-regulated, even in a symptoms-free period. NO and PGE(2) hyperproduction could therefore be involved in the neurovascular modifications leading to migraine attacks.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.