Nitric oxide and prostacyclin inhibit fetal platelet aggregation: A response similar to that observed in adults

Varela, Angelique F.; Runge, Alice; Ignarro, Louis J.; Chaudhuri, Gautam

doi:10.1016/0002-9378(92)91748-y

Cited by 21 publications

(6 citation statements)

References 20 publications

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“…It is known that platelet activation occurs in healthy pregnancy and is more pronounced in preeclampsia. This may represent compensation or adaptation whereby the platelets are more sensitive to NO in preeclampsia [17], and furthermore that fetal platelets are more sensitive to NO as compared with maternal platelets [18]. These mechanisms can prevent thrombosis in preeclamptic mother and in the fetus despite high viscosity and hematocrit.…”

Section: Discussionmentioning

confidence: 99%

Clinical Experience of Long-Term Transdermal Treatment with Nitric Oxide Donor for Women with Preeclampsia

Nakatsuka

Tada

Kimura

et al. 1999

Gynecol Obstet Invest

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Isosorbide dinitrate (ISDN), a nitric oxide donor, was applied transdermally for 4–16 days to 4 preeclamptic women with oligohydramnios, intrauterine fetal growth retardation (IUGR), and elevated resistance of blood flow in the uterine arteries. Pulsed Doppler ultrasonography revealed immediate and drastic improvement of pulsatility index (PI) of uterine arteries following treatment with ISDN. The average PI in uterine arteries of the 4 patients was reduced to approximately 67% of that of the untreated state. In 2 patients the amniotic fluid gradually increased over a few days which suggested improvement of fetoplacental circulation during administration of ISDN. This study suggests that long-term transdermal ISDN is an effective therapy, at least in a portion of preeclamptic women, to avoid maternal hypertension, fetal distress, oligohydramnios, and IUGR, and consequentially to prolong the gestational period.

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Section: Discussionmentioning

confidence: 99%

Clinical Experience of Long-Term Transdermal Treatment with Nitric Oxide Donor for Women with Preeclampsia

Nakatsuka

Tada

Kimura

et al. 1999

Gynecol Obstet Invest

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“…George et al found a doubling of bleeding time in neonates after 30 min of inhalation of 40 ppm NO [12], whereas no effect on platelet aggregation responses to agonists in vitro was seen. This large increase in bleeding time might be related to an increased susceptibility of immature platelets to NO [31], but it is more likely that clinical improvement caused by the NO inhalation might have indirectly influenced the bleeding time. Table 2 Platelet P-selectin expression (% positive cells), and time to count 5000 platelets (seconds) on each experimental occasion: before and during inhalation of NO or control gas, and before and after aspirin.…”

Section: Discussionmentioning

confidence: 99%

Inhaled nitric oxide does not influence bleeding time or platelet function in healthy volunteers

Albert

Norman

Wallén

et al. 1999

Eur J Clin Investigation

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“…97 Ex vivo aggregation studies are complicated by the very short half-life of NO and, as a result, there are contradictory reports of its effects on neonatal platelet aggregation, with the discrepancies probably due to differences in experimental methodology. [98][99][100] Keh and colleagues, 101 using SIN-1 as an in vitro NO donor, demonstrated inhibition of GPIIb/IIIa activation (measured as PAC-1 binding) in platelets from newborns, their mothers, and nonpregnant controls. The relative inhibition was similar in all three groups (70 ± 5%), but the neonatal platelets showed the typical hyporeactive profile in baseline studies, making the inhibition potentially more significant.…”

Section: Nitric Oxidementioning

confidence: 99%

Neonatal Platelet Function

Israels

Rand²,

Michelson³

2003

Semin Thromb Hemost

102

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Healthy newborns maintain normal circulating platelet counts, with a platelet ultrastructure that does not differ from adults. In vitro assessments of intrinsic platelet function, however, have demonstrated transient hyporesponsiveness that is most marked in platelets from preterm infants. Decreased responses were originally considered to be the result of platelet activation and degranulation during labor and delivery, but more recent studies of platelet activation markers have not supported this theory. Decreased activation responses are due to relative deficiencies of phospholipid metabolism, calcium mobilization, granule secretion, and aggregation. These result in turn from differences in intrinsic signal transduction in the neonatal platelet compared with the adult. In contrast, there is enhanced platelet adhesion due to the presence in neonatal plasma of larger, more functionally potent von Willebrand factor multimers. These ultralarge multimers may result from decreased activity of von Willebrand factor-cleaving protease in neonatal plasma and are associated with shorter bleeding times and Platelet Function Analyser-100 closure times in neonates. In the immediate newborn period, this enhanced platelet adhesion may compensate for the decreased intrinsic platelet activation in healthy neonates, but may leave sick neonates at increased risk of bleeding.

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Nitric oxide and prostacyclin inhibit fetal platelet aggregation: A response similar to that observed in adults

Cited by 21 publications

References 20 publications

Clinical Experience of Long-Term Transdermal Treatment with Nitric Oxide Donor for Women with Preeclampsia

Clinical Experience of Long-Term Transdermal Treatment with Nitric Oxide Donor for Women with Preeclampsia

Inhaled nitric oxide does not influence bleeding time or platelet function in healthy volunteers

Neonatal Platelet Function

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