摘要

There is substantial evidence of increased platelet reactivity in vivo and in vitro during pregnancy. Platelet activation occurs in pregnancy with a risk of the development of preeclampsia. In this study, platelet behavior was studied during 28-40 weeks of gestation in a group of women who remained normotensive and a group of nonpregnant female controls. Platelet aggregation and ATP release stimulated by agonists (i.e. collagen and adenosine 5′-diphosphate) were markedly enhanced in washed platelets from pregnant subjects. Furthermore, the collagen-evoked increase in intracellular Ca2+([Ca2+]i) mobilization in fura-2-AM-loaded platelets was also enhanced in pregnant subjects. Moreover, the binding activity of fluorescein isothiocyanate-triflavin toward the platelet glycoprotein IIb/IIIa complex did not significantly differ between the nonpregnant and pregnant groups. In addition, the amount of thromboxane A2 (TxA2) formation from pregnant subjects was significantly greater than that from nonpregnant subjects in both resting and collagen-activated platelets. On the other hand, prostaglandin E2 formation in the presence of imidazole in either resting or arachidonic acid (100 μM)-treated platelets did not significantly differ between these two groups. The levels of cyclic AMP formation in both resting and prostaglandin E1 (10 μM)-treated platelets from pregnant subjects were significantly lower than those in nonpregnant subjects. Nitric oxide production was measured by a chemiluminescence detection method in this study. The extent of nitrate production in either resting or collagen-stimulated platelets from pregnant subjects did not significantly differ from that of platelets from the nonpregnant group. We conclude that the agonist-induced hyperaggregability of platelets from normal pregnancy may be due, at least partly, to an increase in TxA2 formation and a lowering of the level of cyclic AMP formation, which leads to increased [Ca2+]i mobilization and finally to enhanced platelet aggregation and ATP release.
原文英語
頁(從 - 到)17-25
頁數9
期刊Journal of Biomedical Science
9
發行號1
DOIs
出版狀態已發佈 - 2002

指紋

Platelets
Blood Platelets
Pregnancy
Collagen
Thromboxane A2
Platelet Aggregation
Cyclic AMP
Adenosine Triphosphate
Integrin beta3
Platelet Glycoprotein GPIIb-IIIa Complex
Agglomeration
Fura-2
Alprostadil
Platelet Activation
Platelet Membrane Glycoproteins
Luminescence
Pre-Eclampsia
Fluorescein
Dinoprostone
Arachidonic Acid

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

引用此文

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title = "Mechanisms involved in agonist-induced hyperaggregability of platelets from normal pregnancy",
abstract = "There is substantial evidence of increased platelet reactivity in vivo and in vitro during pregnancy. Platelet activation occurs in pregnancy with a risk of the development of preeclampsia. In this study, platelet behavior was studied during 28-40 weeks of gestation in a group of women who remained normotensive and a group of nonpregnant female controls. Platelet aggregation and ATP release stimulated by agonists (i.e. collagen and adenosine 5′-diphosphate) were markedly enhanced in washed platelets from pregnant subjects. Furthermore, the collagen-evoked increase in intracellular Ca2+([Ca2+]i) mobilization in fura-2-AM-loaded platelets was also enhanced in pregnant subjects. Moreover, the binding activity of fluorescein isothiocyanate-triflavin toward the platelet glycoprotein IIb/IIIa complex did not significantly differ between the nonpregnant and pregnant groups. In addition, the amount of thromboxane A2 (TxA2) formation from pregnant subjects was significantly greater than that from nonpregnant subjects in both resting and collagen-activated platelets. On the other hand, prostaglandin E2 formation in the presence of imidazole in either resting or arachidonic acid (100 μM)-treated platelets did not significantly differ between these two groups. The levels of cyclic AMP formation in both resting and prostaglandin E1 (10 μM)-treated platelets from pregnant subjects were significantly lower than those in nonpregnant subjects. Nitric oxide production was measured by a chemiluminescence detection method in this study. The extent of nitrate production in either resting or collagen-stimulated platelets from pregnant subjects did not significantly differ from that of platelets from the nonpregnant group. We conclude that the agonist-induced hyperaggregability of platelets from normal pregnancy may be due, at least partly, to an increase in TxA2 formation and a lowering of the level of cyclic AMP formation, which leads to increased [Ca2+]i mobilization and finally to enhanced platelet aggregation and ATP release.",
keywords = "Cyclic AMP, Hyperaggregability, Normal pregnancy, Platelets, Thromboxane A",
author = "Sheu, {Joen Rong} and George Hsiao and Lin, {Wen Yi} and Tzeng-Fu Chen and Chien, {Yi Yi} and Lin, {Chien Huang} and Tzeng, {Chiu Ruey}",
year = "2002",
doi = "10.1159/000048195",
language = "English",
volume = "9",
pages = "17--25",
journal = "Journal of Biomedical Science",
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TY - JOUR

T1 - Mechanisms involved in agonist-induced hyperaggregability of platelets from normal pregnancy

AU - Sheu, Joen Rong

AU - Hsiao, George

AU - Lin, Wen Yi

AU - Chen, Tzeng-Fu

AU - Chien, Yi Yi

AU - Lin, Chien Huang

AU - Tzeng, Chiu Ruey

PY - 2002

Y1 - 2002

N2 - There is substantial evidence of increased platelet reactivity in vivo and in vitro during pregnancy. Platelet activation occurs in pregnancy with a risk of the development of preeclampsia. In this study, platelet behavior was studied during 28-40 weeks of gestation in a group of women who remained normotensive and a group of nonpregnant female controls. Platelet aggregation and ATP release stimulated by agonists (i.e. collagen and adenosine 5′-diphosphate) were markedly enhanced in washed platelets from pregnant subjects. Furthermore, the collagen-evoked increase in intracellular Ca2+([Ca2+]i) mobilization in fura-2-AM-loaded platelets was also enhanced in pregnant subjects. Moreover, the binding activity of fluorescein isothiocyanate-triflavin toward the platelet glycoprotein IIb/IIIa complex did not significantly differ between the nonpregnant and pregnant groups. In addition, the amount of thromboxane A2 (TxA2) formation from pregnant subjects was significantly greater than that from nonpregnant subjects in both resting and collagen-activated platelets. On the other hand, prostaglandin E2 formation in the presence of imidazole in either resting or arachidonic acid (100 μM)-treated platelets did not significantly differ between these two groups. The levels of cyclic AMP formation in both resting and prostaglandin E1 (10 μM)-treated platelets from pregnant subjects were significantly lower than those in nonpregnant subjects. Nitric oxide production was measured by a chemiluminescence detection method in this study. The extent of nitrate production in either resting or collagen-stimulated platelets from pregnant subjects did not significantly differ from that of platelets from the nonpregnant group. We conclude that the agonist-induced hyperaggregability of platelets from normal pregnancy may be due, at least partly, to an increase in TxA2 formation and a lowering of the level of cyclic AMP formation, which leads to increased [Ca2+]i mobilization and finally to enhanced platelet aggregation and ATP release.

AB - There is substantial evidence of increased platelet reactivity in vivo and in vitro during pregnancy. Platelet activation occurs in pregnancy with a risk of the development of preeclampsia. In this study, platelet behavior was studied during 28-40 weeks of gestation in a group of women who remained normotensive and a group of nonpregnant female controls. Platelet aggregation and ATP release stimulated by agonists (i.e. collagen and adenosine 5′-diphosphate) were markedly enhanced in washed platelets from pregnant subjects. Furthermore, the collagen-evoked increase in intracellular Ca2+([Ca2+]i) mobilization in fura-2-AM-loaded platelets was also enhanced in pregnant subjects. Moreover, the binding activity of fluorescein isothiocyanate-triflavin toward the platelet glycoprotein IIb/IIIa complex did not significantly differ between the nonpregnant and pregnant groups. In addition, the amount of thromboxane A2 (TxA2) formation from pregnant subjects was significantly greater than that from nonpregnant subjects in both resting and collagen-activated platelets. On the other hand, prostaglandin E2 formation in the presence of imidazole in either resting or arachidonic acid (100 μM)-treated platelets did not significantly differ between these two groups. The levels of cyclic AMP formation in both resting and prostaglandin E1 (10 μM)-treated platelets from pregnant subjects were significantly lower than those in nonpregnant subjects. Nitric oxide production was measured by a chemiluminescence detection method in this study. The extent of nitrate production in either resting or collagen-stimulated platelets from pregnant subjects did not significantly differ from that of platelets from the nonpregnant group. We conclude that the agonist-induced hyperaggregability of platelets from normal pregnancy may be due, at least partly, to an increase in TxA2 formation and a lowering of the level of cyclic AMP formation, which leads to increased [Ca2+]i mobilization and finally to enhanced platelet aggregation and ATP release.

KW - Cyclic AMP

KW - Hyperaggregability

KW - Normal pregnancy

KW - Platelets

KW - Thromboxane A

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