A longitudinal study of platelet behaviour and thromboxane production in whole blood in normal pregnancy and the puerperium

Louden, K. A.; Pipkin, Fiona Broughton; Heptinstall, S; Fox, Susan C.; Mitchell, J. R. A.; Symonds, E. M.

doi:10.1111/j.1471-0528.1990.tb02498.x

Cited by 49 publications

(51 citation statements)

References 18 publications

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“…3 During normal pregnancy platelet aggregation and secretion of ATP is increased compared with the non-pregnant individuals, reaching a prominent peak in the third trimester but returning to normal by 6-12 weeks post-partum. 4,5 Platelet binding to fibrinogen remained unchanged. 5,6 Fitzgerald et al indicated an elevated biosynthesis of thromboxane during pregnancy.…”

Section: Introductionmentioning

confidence: 82%

Ultrastructural analysis of platelets during three phases of pregnancy: A qualitative and quantitative investigation

Swanepoel

Pretorius

2014

Hematology

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Objectives: In the past, platelet morphology during normal pregnancy has not been given much attention. Methods: Electron microscopy analysis of platelets from 60 pregnant individuals (30 early pregnancy (weeks 8-14) participants and 30 late pregnancy (weeks 36-40) participants which were followed up 6-8 weeks post-partum) were compared to platelets from 30 non-pregnant individuals as well as each other to establish whether differences in platelet morphology exist during pregnancy. Results: Ultrastructural changes pertaining to the external and internal arrangements of platelets were visible. Fixated platelets showed pseudopodia formation and membrane blebbing. Increased and enlarged open canalicular system pores, pseudopodia formation, platelet spreading, and membrane blebbing were visible in vital platelets. Platelets from pregnancy were tightly packed and internal structures were different from the non-pregnant group. The internal granules showed modification in their occurrence within the cell. The α-and lysosomal granule counts were significantly increased during pregnancy while dense granule and mitochondrial numbers were significantly decreased. Discussion: This may point to a pregnancy-specific modification. The changes in platelet ultrastructure discerned in this study attribute to the hypercoagulable state associated with pregnancy. All ultrastructural alterations associated with pregnancy persist for at least 2 months after birth.

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Section: Introductionmentioning

confidence: 82%

Ultrastructural analysis of platelets during three phases of pregnancy: A qualitative and quantitative investigation

Swanepoel

Pretorius

2014

Hematology

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“…All of these data raise the question of whether there is an increase in the thromboxane biosynthetic pathway during pregnancy. Ylikorkala and Viinikka [27] found that platelet thromboxane formation is increased in vitro during pregnancy; however, another report suggested that there is no change in vitro during pregnancy [12]. These reports indicate that platelet thromboxane production in vitro during pregnancy remains unclear and controversial.…”

Section: Introductionmentioning

confidence: 69%

“…Increased platelet aggregation has been demonstrated in platelet-rich plasma (PRP) and in whole blood using various agonists such as adenosine 5)-diphosphate (ADP) and arachidonic acid (AA) [12,17,18]. The formation of thromboxane A 2 (TxA 2 ) in platelets is reported to increase in pregnancy [6,27].…”

Section: Introductionmentioning

confidence: 99%

Mechanisms Involved in Agonist-Induced Hyperaggregability of Platelets from Normal Pregnancy

et al. 2002

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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.

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“…Platelet hyperaggregation during third trimester was reported in a number of studies suggesting hyper functioning platelets near labor [38][39][40] . Recently reduced platelet aggregation was observed using a modified technology in light transmission aggregometry [41].…”

Section: Qualitative Changes In Platelets and Activation Markersmentioning

confidence: 99%

A Review of Hemostasis in Normal Pregnancy and Puerperium

Moiz¹

2017

Natl. j. health sci.

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Significant alterations are seen in hemostatic system during normal pregnancy and puerperium. Overall, it is a state of hypercoagulability and hypofibrinolysis mitigating the risk of severe bleeding during placental separation at delivery. On the flip side, it threatens a pregnant woman for thrombosis with the risk being four to six folds more in comparison to a non-pregnant woman. It is important to understand the hemostatic changes in normal pregnancy by all health care providers who manage pregnant women in obstetric wards, trauma, anesthesia and other circumstances. This review describes the changes in qualitative and quantitative changes in platelet, clotting factors, anticoagulants and fibrinolysis during normal pregnancy and puerperium.

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A longitudinal study of platelet behaviour and thromboxane production in whole blood in normal pregnancy and the puerperium

Cited by 49 publications

References 18 publications

Ultrastructural analysis of platelets during three phases of pregnancy: A qualitative and quantitative investigation

Ultrastructural analysis of platelets during three phases of pregnancy: A qualitative and quantitative investigation

Mechanisms Involved in Agonist-Induced Hyperaggregability of Platelets from Normal Pregnancy

A Review of Hemostasis in Normal Pregnancy and Puerperium

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