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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seizure prophylaxis is standard intrapartum therapy for patients with pregnancy-induced hypertension. Magnesium sulfate is used in the United States in spite of limited literature comparing its efficacy with other anticonvulsants. Fifty patients with pregnancy-induced hypertension were prospectively randomized to receive magnesium sulfate or phenytoin for seizure prophylaxis. Patients were observed for toxicity, side effects, and labor outcomes, and the neonates were evaluated for side effects of the therapy. Three patients were excluded with adverse reactions to medications (one in magnesium sulfate group, two in phenytoin group). No differences were found in patient tolerance, adverse reactions, or neonatal outcomes between groups. Maternal free phenytoin levels were 13.0% +/- 0.4% of total phenytoin (serum albumin, 2.5 to 3.5 gm/dl), significantly higher than in nonpregnant patients. Neither free phenytoin levels nor percentage of total phenytoin that was free correlated significantly with maternal albumin levels. The pharmacokinetics of phenytoin loading in the massively obese pregnant patient may differ and require further evaluation. Phenytoin is a well-tolerated alternative to magnesium sulfate for seizure prophylaxis in the patient with mild pregnancy-induced hypertension.
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PMID:Magnesium sulfate versus phenytoin for seizure prophylaxis in pregnancy-induced hypertension. 195 52

The effect of magnesium sulfate on ventricular refractoriness and its efficacy for torsade de pointes (TdP) were studied in nineteen dogs. After the administration of quinidine sulfate (30 mg/kg), TdP was induced by ventricular pacing in ten of 19 dogs (52.6%), polymorphic ventricular tachycardia in seven (36.8%), ventricular fibrillation in two (10.5%). Quinidine sulfate caused significant increases in QTc interval, ventricular effective refractory period (ERP) and dispersion of ERP(dERP), and decrease in ERP/QT. Magnesium sulfate significantly increased ERP (p less than 0.01), but it did not change QT interval, resulting in significant increasing of ERP/QT (0.41 +/- 0.05 to 0.61 +/- 0.05, p less than 0.01). It decreased dERP but not significantly. Magnesium sulfate prevented the induction of TdP in eight of 10 dogs (80.0%) (30 mg/kg in four and 60 mg/kg in four). In conclusion, magnesium sulfate has value as first aid therapy for drug-induced TdP. If patients have ischemic heart disease or hypertension, we recommend infusion of magnesium for the initial therapy of TdP.
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PMID:Effect of magnesium sulfate on ventricular refractoriness and its efficacy for torsade de pointes. 209 63

Eclampsia is the most serious manifestation of a toxaemic encephalopathy which may also have nonconvulsive manifestations, such as headache, visual disorders or retinal or cortical origin, confusion or disturbances of consciousness. Some authors consider eclampsia as being only one particular aspect of hypertensive encephalopathy. However, recent studies have drawn attention to the importance of angiospasm which might not be a pure reaction to hypertension but might result from a relative deficiency in vascular prostacyclin. These physiopathological factors, to which must sometimes be added disseminated intravascular coagulation, account for computerized tomographic and neuropathological findings showing cerebral oedema and, in complicated cases, ischaemic or haemorrhagic lesions. Medical treatment must rapidly control the convulsive attacks as well as the arterial hypertension. Magnesium sulfate is not much used outside the United States where it is now strongly controverted. The obstetrical management depends on the time when eclampsia occurs and on the efficacy of the medical treatment.
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PMID:[Eclampsia]. 214 84

Evidence in vitro and in humans suggest that Mg2+ can alter systemic and renal vascular tone. However, the mechanism of these effects is not known. The role of vasodilator prostaglandin release and Ca2+ flux in Mg2+-induced changes in blood pressure and renal blood flow was studied in 10 normal subjects maintained on a fixed 80-mEq Na+ and K+ diet. Magnesium sulfate infused at 200 mg/hr for 3 hours reduced systolic and diastolic blood pressure within 1 hour (from 119 +/- 2 [SEM] to 109 +/- 4 mm Hg systolic; from 74 +/- 3 to 64 +/- 4 mm Hg diastolic; p less than 0.02). This hypotensive response was seen in all subjects and persisted for 3 hours. The pulse rate did not change, but renal blood flow (p-aminohippurate clearance) increased (from 902 +/- 78 to 1108 +/- 130 ml/min/1.73 m2; p less than 0.05). The Mg2+ infusion produced a significant increase in the excretion of the stable prostaglandin I2 (PGI2) metabolite 6-keto-PGF1 alpha (from 96 +/- 12 to 154 +/- 16 ng/g creatinine; p less than 0.01). In contrast, urinary PGE2 was not altered (328 +/- 75 vs 399 +/- 145 ng/g creatinine; p greater than 0.6). To evaluate the functional role of PGI2 release, the cyclooxygenase inhibitors indomethacin (75 mg) or ibuprofen (600 mg) were given before the Mg2+ infusion. Both cyclooxygenase blockers, given in doses that inhibited immunoreactive 6-keto-PGF1 alpha release, completely prevented the Mg2+-induced decline in blood pressure and increased renal blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1987 Apr
PMID:Evidence that prostacyclin mediates the vascular action of magnesium in humans. 243 56

Preeclampsia, a major cause of fetal and maternal morbidity and mortality, may be difficult to distinguish clinically from other hypertensive disorders of pregnancy. Signs helpful in its diagnosis include presentation during late gestation in a nullipara with edema and proteinuria, and one or more of the following: hemoconcentration, hypoalbuminemia, liver function and/or coagulation abnormalities, and increased urate levels. Measures that may prove useful in differentiating preeclampsia from less dangerous forms of hypertension are decreased antithrombin III levels, increments in serum iron and carboxyhemoglobin, and decreases in urinary calcium. Major pathophysiological features of preeclampsia are decreased cardiac output, pulmonary capillary wedge pressure, and plasma volume; and marked increases in peripheral vascular resistance, as well as exaggerated pressor responses to endogenous angiotensin II and catecholamines. Renal hemodynamics decrease, in part as a result of a characteristic morphological lesion in glomeruli ("endotheliosis"), and there may be increased vascular permeability leading to albumin loss from the intravascular space. When gestation is advanced, termination is the treatment of choice; when temporization is required, several antihypertensive medications whose safety and efficacy have been tested in pregnant women are available. Magnesium sulfate remains the drug of choice for impending convulsions (the eclamptic phase of the disease). Finally, the etiology of preeclampsia remains unknown, but a popular theory suggests that alterations in prostaglandin metabolism may be responsible for the hypertension and coagulopathy in this disorder. In this respect, prophylactic treatment with low doses of aspirin, which decrease platelet thromboxane production but spare endothelial prostacyclin release, may decrease the incidence of preeclampsia in "high-risk" populations.
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PMID:Preeclampsia: pathophysiology, diagnosis, and management. 265 50

From the pre-natal follow-up it was remarkable that cases have been admitted relatively late. Hints to a possible development of preeclampsia could be seen from patients history or the routine check up, for example the registration of edema, fetal growth retardation and oligohydramnios. For early diagnosis of preeclampsia we recommend: Calculation of mean arterial blood pressure or its non-invasive measurement; determination of hematocrit, uric acid and total plasma protein (in particular hemorheologic measurements). Hypomagnesemia in preeclampsia, as described by some authors, was also seen in our cases. The complex symptomatology of preeclampsia could be attributed to a generalised disturbance of microcirculation, which leads to definite reactions of the organs concerned. The microcirculatory failure is caused by vasoconstriction, hemoconcentration, hyperviscosity and hypercoagulation (up to DIC and consumption coagulopathy). The resulting symptoms and syndromes can be: EPH, HELLP, hemolytic-uremic Syndrome, hepato-renal Syndrome, thrombocyte and antithrombin III deficiency etc. The drug of choice for treatment of preeclampsia is magnesium sulfate. Its application is based on long-term clinical experience and new aspects on the physiologic and pharmacologic role of magnesium. The recommendations of the German High Blood Pressure League to use calcium antagonists as a basis in the treatment of high blood pressure can be fulfilled particularly in pregnancy by the physiologic calcium antagonist Mg++. Magnesium sulfate should be given in a dosage of 24-72 g daily. The dose should also be made dependent from urinary output. Further treatment patterns of preeclampsia should be adjusted according to each case. The present results also support our hypothesis that magnesium deficiency (besides predisposing factors) could be responsible for the development of preeclampsia (present model shown in detail). Consequently, the early and long-term substitution of magnesium in pregnancy could help reduce preeclampsia.
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PMID:[Pathophysiology and clinical aspects of pre-eclampsia]. 404 84

Magnesium sulfate is primarily used for its anticonvulsive effects in treating hypertensive disorders of pregnancy. However, we have frequently observed significant falls in blood pressure in patients suffering from severe pregnancy-induced hypertension in whom little or no additional hypotensive medication was necessary for maintenance of diastolic blood pressure at 90 to 100 mm Hg while using recommended doses of this drug. We compared resting mean arterial pressure and vascular response to infusions of 50 ng/kg/min of angiotensin II and 2500 ng/kg/min of Levophed (norepinephrine) before and during infusion of a loading dose of 200 mg of magnesium sulfate intravenously in 15 minutes, followed by continuous infusions of 50 and 100 mg/hr intravenously in chronically prepared virgin (n = 14) and primigravid (n = 12) rabbits at 24 to 28 days' gestation (term = 30 +/- 1 day). Resting mean arterial pressure and vascular response to angiotensin II and norepinephrine were significantly decreased in the primigravid and virgin animals. Magnesium sulfate may attenuate blood pressure by decreasing the vascular response to pressor substances.
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PMID:The effects of magnesium sulfate infusion on blood pressure and vascular responsiveness during pregnancy. 646 20

Magnesium sulfate has attracted interest as a potential neuroprotectant but passage of magnesium ion into the central nervous system has not been well documented. For this study, we quantified plasma and cerebrospinal fluid (CSF) ionized magnesium concentration after systemic magnesium sulfate infusion in patients with intracranial hypertension. Patients ( N = 9) received an intravenous infusion of 5 g/20 mmol magnesium sulfate (125 mL of a 4% wt/vol solution) over 30 minutes. Before and after dosing, CSF (from an indwelling ventricular catheter) and blood samples were collected at hourly intervals. Ionized magnesium concentration in all samples was determined using an electrolyte analyzer. Baseline plasma and CSF ionized magnesium concentrations were 0.58 +/- 0.05 and 0.82 +/- 0.06 mmol/L, respectively. Intravenous magnesium sulfate infusion significantly increased plasma ionized magnesium concentration (peak, 0.89 +/- 0.11 mmol/L), but CSF magnesium levels did not change during the 4-hour study. Systemic administration of magnesium sulfate failed to increase CSF ionized magnesium concentration in patients with intracranial hypertension despite increasing plasma magnesium levels by >50%.
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PMID:Intravenous magnesium sulfate does not increase ventricular CSF ionized magnesium concentration of patients with intracranial hypertension. 1180 9

Gestational hypertension and preeclampsia are common disorders during pregnancy, with the majority of cases developing at or near term. The development of mild hypertension or preeclampsia at or near term is associated with minimal maternal and neonatal morbidities. In contrast, the onset of severe gestational hypertension and/or severe preeclampsia before 35 weeks' gestation is associated with significant maternal and perinatal complications. Women with diagnosed gestational hypertension-preeclampsia require close evaluation of maternal and fetal conditions for the duration of pregnancy, and those with severe disease should be managed in-hospital. The decision between delivery and expectant management depends on fetal gestational age, fetal status, and severity of maternal condition at time of evaluation. Expectant management is possible in a select group of women with severe preeclampsia before 32 weeks' gestation. Steroids are effective in reducing neonatal mortality and morbidity when administered to those with severe disease between 24 and 34 weeks' gestation. Magnesium sulfate should be used during labor and for at least 24 hours postpartum to prevent seizures in all women with severe disease. There is an urgent need to conduct randomized trials to determine the efficacy and safety of antihypertensive drugs in women with mild hypertension-preeclampsia. There is also a need to conduct a randomized trial to determine the benefits and risks of magnesium sulfate during labor and postpartum in women with mild preeclampsia.
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PMID:Diagnosis and management of gestational hypertension and preeclampsia. 1285 Jun 27

Magnesium sulfate is widely used to prevent seizures in pregnant women with hypertension. The aim of this study was to examine the inhibitory mechanisms of magnesium sulfate in platelet aggregation in vitro. In this study, magnesium sulfate concentration-dependently (0.6-3.0 mM) inhibited platelet aggregation in human platelets stimulated by agonists. Magnesium sulfate (1.5 and 3.0 mM) also concentration-dependently inhibited phosphoinositide breakdown and intracellular Ca+2 mobilization in human platelets stimulated by thrombin. Rapid phosphorylation of a platelet protein of M(r) 47,000 (P47), a marker of protein kinase C activation, was triggered by phorbol-12-13-dibutyrate (PDBu, 50 nM). This phosphorylation was markedly inhibited by magnesium sulfate (3.0 mM). Magnesium sulfate (1.5 and 3.0 mM) further inhibited PDBu-stimulated platelet aggregation in human platelets. The thrombin-evoked increase in pHi was markedly inhibited in the presence of magnesium sulfate (3.0 mM). In conclusion, these results indicate that the antiplatelet activity of magnesium sulfate may be involved in the following two pathways: (1) Magnesium sulfate may inhibit the activation of protein kinase C, followed by inhibition of phosphoinositide breakdown and intracellular Ca+2 mobilization, thereby leading to inhibition of the phosphorylation of P47. (2) On the other hand, magnesium sulfate inhibits the Na+/H+ exchanger, leading to reduced intracellular Ca+2 mobilization, and ultimately to inhibition of platelet aggregation and the ATP-release reaction.
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PMID:Involvement of the antiplatelet activity of magnesium sulfate in suppression of protein kinase C and the Na+/H+ exchanger. 1473 Feb 6


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