![]() ![]() ( +info)Īssessment of the effects of endothelin-1 and magnesium sulphate on regional blood flows in conscious rats, by the coloured microsphere reference technique. The decreased arrhythmicity is related to enhancement of homogeneity in repolarization, but not to attenuation of prevailing ischaemia, improvement of autonomic nervous derangements or myocardial salvage. CONCLUSIONS: Magnesium suppresses early ventricular arrhythmias in acute myocardial infarction. ![]() QT dispersion corrected for heart rate correlated with hourly ventricular premature beats (rs = 0.48 P < 0.001) and ventricular tachycardias (rs = 0.27 P < 0.05). In testing the pathophysiological mechanisms, serum magnesium levels after infusion correlated with hourly ventricular premature beats (rs = -0.47 P < 0.01), ventricular tachycardias (rs = -0.26 P < 0.05), and QT dispersion corrected for heart rate (rs = -0.75 P < 0.001), but not with SDANN, LF/HF ratio or peak creatine kinase MB. ![]() The number of ischaemic episodes on vectorcardiography were equal, and peak creatine kinase MB release did not differ between the groups. QT dispersion corrected for heart rate was decreased in both measurements at 24 h and 1 week (P < 0.001). Magnesium decreased the number of hourly ventricular premature beats (P < 0.001) and the number of ventricular tachycardias (P < 0.05). QT dispersion corrected for heart rate was measured from the 12-lead ECG. ![]() Occurrence of ventricular arrhythmias and heart rate variability (SD of 5-min mean sinus beat intervals over a 24 h period, SDANN low frequency/high frequency amplitude ratio, LF/HF ratio), and the number of ischaemic episodes on vectorcardiography were measured from the first day of treatment. METHODS AND RESULTS: Fifty-nine consecutive patients with acute myocardial infarction were randomized to receive 70 mmol of magnesium (n = 31) infused over 24 h or placebo (n = 26). We tested whether the effect of magnesium could be attributed to an influence on the autonomic control of the heart, changes in disturbed repolarization, relief of ischaemia or limitation of myocardial injury. (2/407)AIMS: Magnesium treatment suppresses ventricular arrhythmias in acute myocardial infarction and possibly mortality after infarction, but the underlying mechanisms are inadequately understood. ( +info)ĭecreases by magnesium of QT dispersion and ventricular arrhythmias in patients with acute myocardial infarction. Both of these metabolic parameters positively correlated with resultant neurologic outcome measured daily in the same animals immediately before the magnetic resonance determinations. Magnesium carbonate nist webook free#Subsequent magnetic resonance studies demonstrated that the administered magnesium penetrated the blood-brain barrier after injury and resulted in an increased brain intracellular free magnesium concentration and associated bioenergetic state as reflected in the cytosolic phosphorylation potential. The identical concentrations required for improved neurologic outcome suggest that improvement in outcome was dependent on the magnesium cation and not the associated anion. optima of each salt was 250 micromol/kg and 750 micromol/kg, respectively. Both magnesium salts improved neurologic outcome in rats when administered as a bolus at 30 min after injury. The present study has therefore characterized the dose-response characteristics of the most commonly used sulfate and chloride salts of magnesium in a severe model of diffuse traumatic axonal injury in rats. However, given that these earlier studies have used a number of different salts, dosages, and routes of administration, follow-up studies of the neuroprotective properties of magnesium are complicated, with comparisons to the earlier literature virtually impossible. (1/407)A number of studies have demonstrated that magnesium salts given after traumatic brain injury improve subsequent neurologic outcome. Optimization of magnesium therapy after severe diffuse axonal brain injury in rats. ![]()
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