Key result
Methylprednisolone is linked to improved hemodynamics in shock, attenuating vasopressor-induced beta-receptor loss.
Why the study?
The effect of methylprednisolone on myocardial beta-adrenergic receptors and cardiovascular function after long-term catecholamine infusion in shock patients was unclear.
Does methylprednisolone improve hemodynamic parameters and preserve myocardial beta-adrenergic receptors in shock patients on long-term catecholamine infusion?
Observational (n=56)
Does methylprednisolone improve hemodynamic parameters and preserve myocardial beta-adrenergic receptors in shock patients on long-term catecholamine infusion?
Methylprednisolone may improve hemodynamics and preserve myocardial beta-adrenergic receptors in shock patients receiving long-term catecholamine infusions.
Methylprednisolone may improve hemodynamics in vasopressor shock; hypothesis-generating and requires randomized confirmation before practice change.
The effect of methylprednisolone on the myocardial beta-adrenergic receptors after long term ( > 72 h) catecholamine infusion was studied. In 56 patients with pulmonary arterial catheter, 10 mg/kg of methylprednisolone was given as an intravenous bolus. Significant increases could be seen in cardiac output and blood pressure in patients who were simultaneously treated with vasopressors like dopamine and/or dobutamine. In patients who were on dopamine infusion higher than 10 micrograms/kg/min methylprednisolone there was an increase in the systemic vascular resistance. Patients who were not on vasopressors but received methylprednisolone, had no similar changes in hemodynamic parameters. In an in vitro analysis of tissue from the myocardium in 12/56 patients who succumbed and in four additional patients who expired after multiple trauma, a beta-adrenergic receptor assay was performed. It was found that the long term infusion of catecholamines decreased the receptor number and the methylprednisolone abolished or caused the decrease to be less pronounced. In this study we could not control the selection of the patients; a randomized study needs to be conducted in the future.
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Saito et al. (1996) conducted an observational in Shock (n=56). Methylprednisolone vs. Patients not on vasopressors was evaluated on Hemodynamic parameters (cardiac output, blood pressure) and myocardial beta-adrenergic receptor number. Methylprednisolone administration in shock patients on vasopressors significantly increased cardiac output and blood pressure, and attenuated the catecholamine-induced decrease in beta-receptors.
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