Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Animal experimental studies conducted at the turn of the century resulted in the use of magnesium sulphate as an anticonvulsant in humans. In U.S. clinics, parenteral administration of magnesium sulphate became a routine procedure in the treatment of eclampsia and pre-eclampsia. This treatment has proved very effective in treating convulsions in pregnancy provided an adequate dosage was given amounting to up to 60 g daily. Mother and infant mortality were largely eliminated. Numerous clinical studies showed a negligible side effect rate. Side effects in the foetus: These are due to penetration of magnesium into the foetal blood circulation. Reports on an inhibition of cardiac rate fluctuation and changes in calcium levels have been contradictory, and hence not generally accepted. It is claimed that the parathormone level may drop slightly. Isolated reports on foetal magnesium intoxications associated with depression of breathing, slackness and hyporeflexia often prompt the conclusion that this disease pattern had been due to immaturity and asphyxia. Generally, foetal magnesium blood levels do not correlate well with signs of magnesium intoxication. Urine excretion is greatly slowed down in foetal immaturity. Side effects in the mother: Short-term relaxing action on the uterus has been described frequently. High dosages have been successfully used in arresting labour if there is a tendency to premature birth. Increase in uterine blood flow was seen after administration of magnesium sulphate in animal experiments. Magnesium is said to reduce blood coagulation by influencing fibrinolysis and thrombocyte resistance. However, a somewhat enhanced loss of blood during birth is said to be more likely due to relaxation of the uterus than to a disturbance of blood coagulation. Rapid intravenous injection causes short-term flushing, nausea and vomiting. Short-acting drops in blood pressure are possible. The cardiac output is said to increase at the conventional dosage level whereas the peripheral resistance drops due to vasodilation. Increases and decreases in heart rate have been reported, but in most cases no changes were seen. Changes in ventricular action time occur with toxic doses only, which can lead to cardiac arrest in the diastole. Other toxic signs are hyporeflexia, depressed breathing and CNS depressions which may result in coma. Hyporeflexia always occurs before the other toxic signs appear, so that it can be used as a clinical control criterion. Calcium gluconate, given via the IV route, is a good and rapid-acting antidote.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Use of magnesium sulfate as an anticonvulsant in severe pregnancy toxemia and eclampsia]. 655 75

The effects of cold and restraint and of some of the antiulcer drugs on adenosine nucleotide content in the gastric glandular mucosa were examined. A bioluminescence technique was used to measure the amount of ATP and its metabolites in gastric mucosal tissue. Cold-restraint produced gastric lesions and increased the gastric mucosal ATP. Verapamil pretreatment attenuated these lesions and further intensified the ATP increase in a dose-related manner. The ATP/ADP ratio and the Atkinson index were also elevated. Calcium gluconate produced similar effects. Atropine or EGTA pretreatment protected or worsened the gastric lesion, respectively, but did not have any influence on the changes in mucosal energy metabolism. Ranitidine pretreatment lessened the lesion formation but had no influence on the nucleotide content. These findings indicate that the metabolic rate of the gastric mucosa is suppressed during cold-restraint conditions; this depression is probably due to hypothermia and reduction of mucosal metabolism. The lesion-protecting mechanisms of the drugs do not seem to be mediated through their effects on mucosal energy metabolism. The oxygen- and ATP-sparing effects of verapamil may contribute partly to its gastro-protective effect.
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PMID:Role of gastric glandular mucosal energy metabolism in cold-restraint gastric lesion formation. 818 16