Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This is the first report of the successful use of magnesium sulfate (MgSO4) in 3 consecutive patients with torsades de pointes (TdP). In 1 patient, TdP was induced by a combination of quinidine and amiodarone, in the second by procainamide, and in the third by an overdose of imipramine. The QT intervals before TdP were 0.70, 0.64 and 0.56 second, respectively. A bolus of 1.0 to 2.0 g MgSO4 25% abolished the TdP in all 3 patients; but in the third patient, because of recurrent TdP, a second bolus of 1.0 g and a continuous 24-hour infusion of 1.0 mg/min were administered, preventing TdP. There was no immediate shortening in the QT interval in any patient after MgSO4. Magnesium can be given safely even in patients with acute myocardial infarction, angina pectoris or systemic hypertension, conditions in which isoproterenol is contraindicated; it can be applied faster than temporary cardiac pacing; and its use for TdP appears worthy of additional trials.
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PMID:Magnesium therapy for torsades de pointes. 669 82

Although the recognition and treatment of preeclampsia theoretically should eliminate eclampsia, it has not disappeared and remains a substantial threat to maternal and fetal well-being. The therapy of choice for treatment and prevention of convulsions is magnesium sulfate (MgSO4 . 7H2O USP) and that for severe hypertension is intravenous hydralazine. Delivery of the fetus and placenta is recommended after the mother is stabilized from the effects of the convulsion(s). If the mother is to be transported before delivery, it is important that she receive an adequate dose of MgSO4.
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PMID:Eclampsia: treatment and referral. 706 97

The objective of this study was to determine the serum levels of magnesium associated with various intravenous infusion rates of magnesium sulfate (MgSO4) in high-order multiple gestations. A retrospective review of 12 triplet and 4 quadruplet pregnancies cared for in Phoenix from August 1988 to January 1992 was performed. The mothers received MgSO4 for tocolysis of preterm labor. Serum magnesium levels were drawn to help manage patients with symptoms of an excessive magnesium level or an inadequate tocolytic effect. The results are presented for triplets and quadruplets with and without pregnancy-induced hypertension (PIH). The serum levels of Mg++ in triplets and quadruplets were similar to those in singleton pregnancies described in the literature. Higher serum levels of Mg++(7.0-7.5 mg/dL) seemed to be necessary for successful tocolysis. Serum levels of Mg++ in patients with underlying PIH were significantly higher at the same intravenous infusion rate. MgSO4 may need to be administered at infusion rates of 4-5 g/h to achieve therapeutic levels in women with triplets and quadruplets. PIH should require lower infusion rates to achieve therapeutic serum levels of Mg++.
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PMID:Serum magnesium levels during magnesium sulfate tocolysis in high-order multiple gestations. 765 Jun 59

1. We assessed regional haemodynamic responses to the vasodilator, MgSO4, in the absence and presence of the nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), in conscious chronically instrumented Long Evans rats (n = 9). 2. MgSO4 (loading dose 220 mumol kg-1 min-1 for 7 min, maintenance dose 56 mumol kg-1 min-1 for 7 min), alone, caused slight bradycardia and hypotension accompanied by reductions in renal and mesenteric flows, but a marked hyperaemic vasodilatation in the hindquarters (flow, delta 54 +/- 6%, vascular conductance, delta 77 +/- 5%). 3. L-NAME (183 nmol kg-1 min-1) caused hypertension (29 +/- 2 mmHg) accompanied by bradycardia (-51 +/- 6 beats min-1) and reductions in flow and vascular conductance in the renal (-18 +/- 4% and -35 +/- 3%, respectively), mesenteric (-35 +/- 3% and -49 +/- 3%, respectively), and hindquarters (-26 +/- 3% and -42 +/- 3%, respectively) vascular beds. In the presence of L-NAME, the hypotensive and bradycardic effects of MgSO4 were still apparent, but its hindquarters hyperaemic vasodilator effect was significantly attenuated. 4. In order to determine if the inhibitory action of L-NAME on the hindquarters hyperaemic vasodilator action of MgSO4 was a non-specific effect, due to the change in baseline conditions caused by L-NAME, we also examined responses to MgSO4 in the presence of endothelin-1 (12.5 pmol kg-1 min-1) or angiotensin II (50 pmol kg-1 min-1). In the presence of either peptide, the overall effects of MgSO4 on hindquarters flow and vascular conductance were unchanged. 5. In a separate experiment (n = 8) we determined that the inhibitory effect of L-NAME on the hyperaemic vasodilator response to MgSO4 was prevented by L-arginine, and also demonstrated that the Beta2-adrenoceptor antagonist, ICI 118551, caused significant inhibition of the hindquarters haemodynamic effects of MgSO4.6. We conclude that the hindquarters haemodynamic effects of MgSO4 in conscious rats involve a substantial L-NAME-sensitive component which depends on activation of Beta2-adrenoceptors, probably asa consequence of adrenal medullary adrenaline release.
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PMID:Effects of NG-nitro-L-arginine methyl ester on regional haemodynamic responses to MgSO4 in conscious rats. 801 14

The total deliveries in Shanghai from 1981 to 1990 were 1,770,103 and there were 456 cases of maternal death. Among them, 42 cases were caused by pregnancy induced hypertension (PIH) which accounted for 9.21% and ranked fourth in the causes of maternal death in Shanghai. The maternal mortality of PIH was 2. 37/10(5). The cerebrovascular accident and heart failure were the leading causes which accounted for 66.67%. The study showed that strengthening prenatal care, supervising 3 main symptoms and signs of PIH, paying attention to mean arterial pressure (MAP), using antispasm drugs such as MgSO4 in proper way and timely termination of pregnancy are the key points of decreasing maternal death of PIH. The average MAP of 18 cases died of cerebrovascular accident was 17 kPa (1kPa = 7.5 mmHg). Among them, MAP > or = 18.7 kPa (140 mmHg) was found only in 4 cases which accounted for 22.22%. It suggested that the threshold value of cerebrovascular accident at the level of MAP > or = 18.7 kPa may be too high and need to be further studied.
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PMID:[Analysis on the causes of maternal death with pregnancy induced hypertension in Shanghai from 1981 to 1990]. 824 43

This case report describes a patient who ingested magnesium sulfate (MgSO4) for approximately four days as a treatment for pregnancy-induced hypertension. Stage II lactogenesis was delayed until the tenth postpartum day at which point the patient's breasts became fully engorged. No explanation for this delay was found, other than the possibility that magnesium sulfate treatment impeded lactogenesis. Implications for professionals who care for lactating women are discussed.
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PMID:Can magnesium sulfate therapy impact lactogenesis? 826 59

Magnesium sulphate has antiarrhythmic and antithrombotic properties, a coronary and systemic vasodilating action, a direct myocardial protective effect in experimental and clinical models of ischemia-reperfusion injury. Two meta-analyses have pooled the results of several small studies that had analyzed the effect of controlled hypermagnesiemia in acute myocardial infarction before the advent of thrombolytic and antithrombotic therapies. The results have shown a more than 50% mortality reduction, with a minimum estimated benefit of about 30%, and a reduction in ventricular arrhythmias of about 50%. In LIMIT-2, a double-blind trial of 2,316 patients where magnesium was administered as a 8 mMol bolus followed by a 24-hour infusion of 65 mMol, a 24% reduction in mortality was observed. However, these data have not been confirmed in the more than 58,000 patients of the ISIS-4 trial. In this study magnesium, at the same dose of the LIMIT trial, did not reduce 5-week mortality, neither in the general population (7.64% versus 7.24% in control patients, p = n.s.) nor in specific subgroups. The results of ISIS-4 have excluded the routine use of magnesium sulphate in acute myocardial infarction in the era of fibrinolysis and aspirin, beta-blockers and ACE-inhibitors. Nevertheless, magnesium administration could still be considered in certain clinical situations, such as 1) the presence of contraindications to fibrinolysis and aspirin, 2) the treatment of ventricular tachyarrhythmias unresponsive (or as an alternative) to lidocaine, 3) severe hypertension when beta-blockers are not indicated.
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PMID:[Magnesium sulfate in acute myocardial infarction]. 868 39

Lidocaine and MgSO4 are often coadministered to patients with pregnancy-induced hypertension. This study examined whether MgSO4 alters the lidocaine-seizure threshold in the rat and, if so, whether systemic MgSO4 administration is as effective as intracerebroventricular MgSO4 infusion. In Experiment 1, rats were administered 50% MgSO4 or 0.9% NaCl intravenously (IV) (20 microL/h) for 5 days. In Experiment 2, rats were administered 0.9% NaCl, 0.8% MgSO4, or 2.0% MgSO4 (10 microL/h) via intracerebroventricular infusion for 24 h. All rats then underwent continuous IV lidocaine infusion until onset of electroencephalographic seizures. In Experiment 1, plasma [Mg2+] was greater in the MgSO4 group (5.1 +/- 1.5 mg/dL vs 1.8 +/- 0.3 mg/dL) but neither the dose of lidocaine required to induce seizures (MgSO4 = 19 +/- 2 mg/kg; saline = 23 +/- 5 mg/kg) nor brain [Mg2+] (MgSO4 = 794 +/- 17 micrograms/g; saline = 788 +/- 33 micrograms/g) were changed. In Experiment 2, intracerebroventricular MgSO4 increased both brain [Mg2+] (2% MgSO4 = 923 +/- 79 micrograms/g; saline = 788 +/- 35 micrograms/g) and the lidocaine seizure dose (2% MgSO4 = 39 +/- 7 mg/kg; saline = 26 +/- 3 mg/kg). Although intracerebroventricular administration of MgSO4 produces an anticonvulsant effect, chronic hypermagnesemia does not alter whole brain [Mg2+] and therefore offers no protection from lidocaine-induced seizures in this model.
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PMID:The effects of plasma and brain magnesium concentrations on lidocaine-induced seizures in the rat. 894 90

We have studied the effects of magnesium on atrioventricular (AV) conduction times and surface electrocardiogram during both sinus rhythm and atrial pacing in seven dogs anaesthetized with 1 MAC of sevoflurane. A bolus dose of magnesium sulphate (MgSO4) 30, 60 and 90 mg kg-1 significantly increased plasma magnesium concentrations from 1.3 (SEM 0.1) to 15.3 (1.3) mg dl-1. MgSO4 significantly prolonged A-H (AV nodal conduction time during sinus rhythm), St-H (intra-atrial and AV nodal conduction time during atrial pacing) and H-S (total ventricular conduction time) intervals at doses > or = 30 mg kg-1 ; H-V interval (His-Purkinje conduction time) at doses > or = 60 mg kg-1; RR and PR intervals and QRS duration at doses > or = 30 mg kg-1 in a dose-related manner during both sinus rhythm and atrial pacing. QTc interval remained unchanged during sinus rhythm. The doses of MgSO4 used did not have deleterious effects on AV conduction times and surface electrocardiogram during 1 MAC of sevoflurane anaesthesia. This finding suggests that MgSO4 in high doses was safe and may be indicated for cardiac arrhythmia and hypertension during sevoflurane anaesthesia. However, further study is required to apply these findings to clinical anaesthesia.
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PMID:Effects of magnesium sulphate on atrioventricular conduction times and surface electrocardiogram in dogs anaesthetized with sevoflurane. 905 8

1. Based upon our previous work, we came to the conclusion that a decrease in placental blood volume was a possible factor behind intrauterine growth retardation (IUGR) in pregnancy-induced hypertension. 2. In a second study, we used an image analysis system to measure cross-sectional areas and wall thicknesses of central blood vessels of the spiral artery, the so-called 'central artery'. 3. It was thought that one of the more basic factors behind IUGR in pregnancy-induced hypertension might possibly be narrowings and spasms of the maternal placental blood vessels. 4. In this study, we found that the three drugs we used (MgSO4 center dot 7H2O, Solcoseryl and KCl) all resulted in an enlargement of the cross-sectional areas of the maternal blood vessels, and that MgSO4 center dot 7H2O, in particular, also relaxed maternal blood vessel spasms in SHRSP placenta.
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PMID:Studies on pregnancy hypertension and IUGR-SFD: effects of drugs on the blood vessels in the placenta of pregnant SHRSP. 907 94


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