Article
Contemporary usage of obstetric magnesium sulfate: indication, contraindication, and relevance of dose.
Department of Obstetrics and Gynecology, Maternal Fetal Medicine, Bnai Zion Medical Center, Haifa, Israel.
Obstetrics and Gynecology (impact factor:
4.73).
01/2010;
115(1):186; author reply 186.
DOI:10.1097/AOG.0b013e3181c8893b
pp.186; author reply 186
Source: PubMed
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Citations (0)
- Cited In (3)
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Article: Placental leucine aminopeptidase- and aminopeptidase A- deficient mice offer insight concerning the mechanisms underlying preterm labor and preeclampsia.
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ABSTRACT: Preeclampsia and preterm delivery are important potential complications in pregnancy and represent the leading causes for maternal and perinatal morbidity and mortality. The mechanisms underlying both diseases remain unknown, thus available treatments (beta2-stimulants and magnesium sulfate) are essentially symptomatic. Both molecules have molecular weights less than 5-8 kDa, cross the placental barrier, and thus exert their effects on the fetus. The fetus produces peptides that are highly vasoactive and uterotonic and increase in response to maternal stress and with continued development. Fetal peptides are also small molecules that inevitably leak across into the maternal circulation. Aminopeptidases such as placental leucine aminopeptidase (P-LAP) and aminopeptidase A (APA) are large molecules that do not cross the placental barrier. We have shown that APA acts as an antihypertensive agent in the pregnant spontaneously hypertensive rat by degrading vasoactive peptides and as a result returns the animal to a normotensive state. P-LAP also acts as an antiuterotonic agent by degrading uterotonic peptides and thus prolongs gestation in the pregnant mouse. Given the ever increasing worldwide incidences of preeclampsia and preterm labor, it is imperative that new agents be developed to safely prolong gestation. We believe that the use of aminopeptidases hold promise in this regard.Journal of Biomedicine and Biotechnology 01/2011; 2011:286947. · 2.44 Impact Factor -
Article: Magnesium induces neuronal apoptosis by suppressing excitability.
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ABSTRACT: In clinical obstetrics, magnesium sulfate (MgSO(4)) use is widespread, but effects on brain development are unknown. Many agents that depress neuronal excitability increase developmental neuroapoptosis. In this study, we used dissociated cultures of rodent hippocampus to examine the effects of Mg(++) on excitability and survival. Mg(++)-induced caspase-3-associated cell loss at clinically relevant concentrations. Whole-cell patch-clamp techniques measured Mg(++) effects on action potential threshold, action potential peak amplitude, spike number and changes in resting membrane potential. Mg(++) depolarized action potential threshold, presumably from surface charge screening effects on voltage-gated sodium channels. Mg(++) also decreased the number of action potentials in response to fixed current injection without affecting action potential peak amplitude. Surprisingly, Mg(++) also depolarized neuronal resting potential in a concentration-dependent manner with a +5.2 mV shift at 10 mM. Voltage ramps suggested that Mg(++) blocked a potassium conductance contributing to the resting potential. In spite of this depolarizing effect of Mg(++), the net inhibitory effect of Mg(++) nearly completely silenced neuronal network activity measured with multielectrode array recordings. We conclude that although Mg(++) has complex effects on cellular excitability, the overall inhibitory influence of Mg(++) decreases neuronal survival. Taken together with recent in vivo evidence, our results suggest that caution may be warranted in the use of Mg(++) in clinical obstetrics and neonatology.Cell Death & Disease 08/2010; 1:e63. · 5.33 Impact Factor -
Article: Pre-eclampsia: pathophysiology, diagnosis, and management.
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ABSTRACT: The incidence of pre-eclampsia ranges from 3% to 7% for nulliparas and 1% to 3% for multiparas. Pre-eclampsia is a major cause of maternal mortality and morbidity, preterm birth, perinatal death, and intrauterine growth restriction. Unfortunately, the pathophysiology of this multisystem disorder, characterized by abnormal vascular response to placentation, is still unclear. Despite great polymorphism of the disease, the criteria for pre-eclampsia have not changed over the past decade (systolic blood pressure > 140 mmHg or diastolic blood pressure ≥ 90 mmHg and 24-hour proteinuria ≥ 0.3 g). Clinical features and laboratory abnormalities define and determine the severity of pre-eclampsia. Delivery is the only curative treatment for pre-eclampsia. Multidisciplinary management, involving an obstetrician, anesthetist, and pediatrician, is carried out with consideration of the maternal risks due to continued pregnancy and the fetal risks associated with induced preterm delivery. Screening women at high risk and preventing recurrences are key issues in the management of pre-eclampsia.Vascular Health and Risk Management 01/2011; 7:467-74.
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