RESUMEN
The anti-arrhythmic effects of intravenous magnesium sulfate, on bouts of supraventricular tachycardia (SVT) secondary to reentry phenomenon, are evaluated in twelve patients undergoing an electrophysiological testing, because of paroxysmal SVT, the pathway of which is an intranodal reentry (eight patients) or includes an atrio-ventricular accessory route (orthodromic SVT: four patients). At the completion of the basic testing, a stable SVT is induced and an intravenous bolus of 3 grams of magnesium sulfate is administered in three minutes. The length of the SVT cycle is significantly increased from 349 +/- 71 ms to 394 +/- 70 ms (p 0.001). The injection of magnesium relieves the SVT in less than five minutes in three patients (intranodal reentry: two cases; accessory pathway: one case), or an efficacy of 25 p. cent. No incident is reported following administration of the product; but the functional tolerance may be considered as poor, mainly consisting of flushing sensations of brief duration. This study demonstrates the antiarrhythmic properties of intravenous magnesium sulfate during bouts of SVT; however, its efficacy appears moderate at the dose mentioned.
Asunto(s)
Sulfato de Magnesio/uso terapéutico , Taquicardia Supraventricular/tratamiento farmacológico , Adulto , Anciano , Femenino , Humanos , Inyecciones Intravenosas , Sulfato de Magnesio/administración & dosificación , Masculino , Persona de Mediana EdadRESUMEN
Complement activation was evaluated in plasma and synovial fluid from patients with rheumatoid arthritis. The activation fragment C3dg and the fluid-phase terminal complement complex were used as indicators of initial and terminal activation, respectively. Considerable activation of the whole complement cascade was demonstrated in most synovial fluid samples and in one-third of the plasma samples. No correlation was found between the level of activation products in synovial fluid and the level in plasma. Therefore, both compartments must be examined in order to evaluate local and systemic complement activation in rheumatoid arthritis.