British Journal of Anaesthesia, Vol 76, Issue 2 251-257, Copyright © 1996 by The Board of Management and Trustees of the British Journal of Anaesthesia
I. Tsuneyoshi, Y. Kanmura and N. Yoshimura
We have studied the effect of methylprednisolone on endotoxin-induced
depression of contractile function in human gastroepiploic arteries.
Endotoxin diminished the contractile response to noradrenaline in both the
presence and absence of endothelium. This attenuation began after 4 h and
reached a maximum after 10 h of endotoxin exposure. The cGMP content of
endotoxin-treated rings was approximately seven-fold higher than in control
rings. These endotoxin-mediated responses were blocked by L-NAME and
methylene blue. These data indicate that the main cause of vascular
hyposensitivity to noradrenaline was massive generation of nitric oxide.
Pretreatment with methyl-prednisolone at concentrations (2.0-20.0
micrograms ml-1) similar to those achieved in plasma after therapeutic
administration dose-dependently inhibited these endotoxin- mediated
responses. These data support the concept that pharmacological
administration of methylprednisolone has the potential to prevent
endotoxin-induced depression of the contractile response to noradrenaline
seen in endotoxaemic shock.
LABORATORY INVESTIGATIONS
Methylprednisolone inhibits endotoxin-induced depression of contractile function in human arteries in vitro
Department of Anesthesiology and Critical Care Medicine, Kagoshima University School of Medicine, 8-35-1 Sakuragaika, Kagoshima 890, Japan
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