par Henning, R J;Becker, Hans Werner;Vincent, Jean Louis 
;Thijs, L.;Kalter, E;Weil, Max Harry
Référence Chest, 79, 2, page (186-194)
Publication Publié, 1981-02
;Thijs, L.;Kalter, E;Weil, Max HarryRéférence Chest, 79, 2, page (186-194)
Publication Publié, 1981-02
Article révisé par les pairs
| Résumé : | Hemodynamic and metabolic effects of methylprednisolone were investigated in a double-blind study of 28 patients with acute myocardial infarction (AMI), confirmed by unequivocal electrocardiographic and enzyme changes. Measurements were performed prior to and at 1.5, 3, 4, 4.5, 12 and 24 hours following infusion of methylprednisolone (13 patients) or placebo (15 patients). Although systemic vascular resistance decreased from 1,750 to 1,420 dynes . sec . cm-5 (p less than .001) and cardiac index increased from 2.77 to 3.10 L/min/m2 (p less than .02) between 0 and 4.5 hours, an abnormal increase in blood lactate was observed in 10 of the 13 patients following administration of methylprednisolone (3.0 vs 1.2 mM/L, p less than .001). Lactate elevation appeared one hour after infusion of methylprednisolone, was maximal at 12 hours, and persisted for more than 24 hours. There was no significant change in blood lactate in placebo treated patients. A transient but significant decrease in plasma volume was also observed following infusions of methylprednisolone. The elevation of blood lactate could not be explained by the reduction in plasma volume since the most striking increases in lactate were observed 12 hours following the initial infusion of methylprednisolone when the plasma volume was returning to the control value. No significant differences in other hemodynamic or metabolic parameters, infarct size or patient survival were observed between the two groups. We conclude that the hemodynamic benefits of glucocorticoids characterized by increased cardiac output and lowered systemic vascular resistance are counterbalanced by the potentially unfavorable conditions of lactate elevation and volume depletion. |
