Platelet life-span in normal pregnancy and pre-eclampsia as determined by a non-radioisotope technique

Rákóczi, I; Tallián, F; Bagdány, S; Gáti, I

doi:10.1016/0049-3848(79)90161-0

Cited by 115 publications

(24 citation statements)

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“…This condition correlates with their mean arterial pressure, plasma lactate dehydrogenase, and the degree of thrombocytopenia (39). Several small studies, which suggest that pretreatment with aspirin may reduce the incidence of PIH in women at risk of developing the disease (40)(41)(42)(43), also support the possibility that thromboxane formation is of functional importance, perhaps contributing to reduced placental blood flow (22,24).…”

Section: Resultsmentioning

confidence: 89%

“…A representative spectrum of the 14,15-diol is depicted in Fig 1. Urinary excretion of 14,15-DHET (Fig. 2 Top) in nonpregnant women ranged from below limits ofdetection (==3 pg/mg of creatinine) to 24 pg/mg of creatinine. In healthy pregnant women, there was a trend toward an increase in 14,15-DHET (range, <10-118) with a median of 85 pg/mg of creatinine; however, the difference was not statistically significant.…”

Section: Resultsmentioning

confidence: 99%

“…To study whether disordered EET formation might contribute to the pathophysiology of human disease, we assessed the in vivo synthesis of EETs in a setting where their properties might be of pathophysiological relevance, that of pregnancy-induced hypertension (PIH) (21)(22)(23)(24) in a 1.0-ml reaction vial and concentrated to dryness under a nitrogen stream. The arachidonic acid was then dissolved in 31 ,ul of dry methylene chloride and the vial was cooled at 0°C in an ice-water slurry.…”

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confidence: 99%

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Endogenous biosynthesis of arachidonic acid epoxides in humans: increased formation in pregnancy-induced hypertension.

Catella

Lawson

Fitzgerald

et al. 1990

Proc. Natl. Acad. Sci. U.S.A.

156

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Arachidonic acid is metabolized by means of P450 isoenzyme(s) to form epoxyeicosatrienoic acids (EETs) and their corresponding dihydroxy derivatives (DHETs). In the present study, we established the presence in human urine of 8,9-, 11,12-, and 14,15-EETs and their corresponding DHETs by developing quantitative assays and using negative ion, chemical ionization GC/MS and octadeuterated internal standards. Urinary excretion of 8,9-and 11,12-DHET increased in healthy pregnant women compared with nonpregnant female volunteers. By contrast, excretion of 11,12-DHET and 14,15-DHET, but not the 8,9-DHET regioisomer, increased even further in patients with pregnancy-induced hypertension. Intravenous administration of [3H]14,15-EET to three dogs markedly increased its DHET in plasma. The terminal half-life ranged from 7.9-12.3 min and the volume of distribution (3.5-5.3 liters) suggested limited distribution outside the plasma compartment. Negligible radioactivity was detected in urine; this fact infers that under physiological circumstances, urinary DHETs largely derive from the kidney. That P450 metabolites of arachidonic acid are formed in humans supports the hypothesis that these metabolites contribute to the physiological response to normal pregnancy and the pathophysiology of pregnancy-induced hypertension.Studies in vitro have demonstrated that arachidonic acid is metabolized by P450 monooxygenases (1-3). Indeed, a P450 isoenzyme with substrate specificity for arachidonate acid has recently been purified from human liver (4). The products of this reaction include hydroxyeicosatetraenoic acids, to and w-1 alcohols, and epoxyeicosatrienoic acids (EETs) and their corresponding diols (5).Among the biological properties of cytochrome P450-dependent arachidonic acid metabolites in vitro are the modulation of vascular tone (6-8) and the regulation of ion transport (9, 10) and water handling (11) in the renal tubule and toad bladder (12). These metabolites inhibit Na+/K+-transporting ATPase in the cornea (13), depress glomerular filtration (14) and inhibit platelet function (15). In addition, the vascular capacity to form these compounds has recently been shown (16,17) to be exaggerated in several animal models of hypertension.Despite these observations and the regionally selective formation of endogenous EETs in rat liver (18), skepticism has persisted about the role of EETs in human disease in vivo. This uncertainty stems from a paucity of information on the actual synthesis of these compounds in vivo (19) and caution in extrapolating tissue capacity for forming EETs in the in vivo situation. For example, for other arachidonic acid metabolites, tissue capacity exceeds in vivo formation rates by orders of magnitude and has been a misleading guide to alterations in prostaglandin biosynthesis (20).To study whether disordered EET formation might contribute to the pathophysiology of human disease, we assessed the in vivo synthesis of EETs in a setting where their properties might be of pathophysiological relevance, th...

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Section: Resultsmentioning

confidence: 89%

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Endogenous biosynthesis of arachidonic acid epoxides in humans: increased formation in pregnancy-induced hypertension.

Catella

Lawson

Fitzgerald

et al. 1990

Proc. Natl. Acad. Sci. U.S.A.

156

View full text Add to dashboard Cite

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“…Platelet number declines to a degree greater than that which occurs during normal pregnancy prior to the onset of clinical disease in women who ultimately develop preeclampsia [44]. Platelet life span is decreased [45] and beta-thromboglobulin concentration is increased [46], confirming that the decline in platelet number results from consumption rather than reduced production of platelets. In at least some patients, beta thromboglobulin rises prior to the appearance of clinically evident disease [47].…”

Section: Mechanism Of Deliverymentioning

confidence: 49%

The role of serotonin in the preeclampsia-eclampsia syndrome

Weiner

1990

Cardiovasc Drug Ther

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The cause of preeclampsia, a syndrome unique to human pregnancy, is unknown. There is presently no effective pharmacologic therapy once the symptoms have appeared. Only delivery is curative. Preeclampsia likely has multiple etiologies, each of which activates a common pathway, culminating in diffuse endothelial damage, vasospasm, and hypertension. Current investigation suggests that serotonin has a pivotal role in the genesis of preeclamptic hypertension. The evidence, as obtained from human and animal study, is reviewed in this article, and areas in need of further study are highlighted. A modified series of Koch's postulates is employed for a framework. Serotonin is the agent but does not directly cause the hypertension. Rather, it is suggested that in a milieu characterized by a reduction in endothelial-derived relaxing factor and prostacyclin, serotonin augments the smooth muscle response to normally occurring concentrations of endogenous vasopressors. It is delivered to the site of action (the microvasculature) by the platelet, whose aggregation is encouraged by dysfunctional endothelium. Either inhibition of the delivery mechanism by a low, daily dose of aspirin, or inhibition of the peripheral serotonin type 2 (5HT2) receptor, effectively controls the hypertension.

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“…The reticular endothelial system found in the liver and spleen also has fenestrated capillaries; loss of endothelial filtration there leads to inflammatory injury, and later parenchymal necrosis. In response to the anti-angiogenic environment, the spleen sequesters platelet leading to relative thrombocytopenia, which is found in about half of patients with severe preeclampsia [37]. HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) is one of the most severe forms of preeclampsia, with increased morbidity and mortality for both mother and baby; [38] however, liver enzyme abnormalities do not indicate severity of disease.…”

Section: Organ Pathologymentioning

confidence: 99%

Updates in Preeclampsia

Sanders

Hess

2015

Curr Anesthesiol Rep

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Hypertensive disorders of pregnancy, specifically preeclampsia, cause significant morbidity and mortality in both the mother and fetus. Changes in the diagnostic criteria have attempted to improve the ability to identify and initiate treatment. Recently, it has been discovered that a placenta-derived anti-angiogenic environment directly contributes to the pathological cause of preeclampsia. The early identification of these anti-angiogenic markers may enhance diagnosis of the disease in the future. Patients with preeclampsia need to be treated with caution in regard to airway and coagulation; however, neuraxial anesthesia, when appropriate, is preferred. During labor, the increase in placental blood flow secondary to epidural analgesia can improve fetal perfusion. Spinal and epidural anesthesia are safe for cesarean delivery in mothers with preeclampsia, and may be preferred over general anesthesia. Preeclampsia is a complex disorder that impacts day to day decisions of anesthesia care provider.

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Platelet life-span in normal pregnancy and pre-eclampsia as determined by a non-radioisotope technique

Cited by 115 publications

References 5 publications

Endogenous biosynthesis of arachidonic acid epoxides in humans: increased formation in pregnancy-induced hypertension.

Endogenous biosynthesis of arachidonic acid epoxides in humans: increased formation in pregnancy-induced hypertension.

The role of serotonin in the preeclampsia-eclampsia syndrome

Updates in Preeclampsia

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