Key result
Corticosteroids exert complex anti-inflammatory effects through granulocyte redistribution, lymphopenia, vasoconstriction, prostaglandin inhibition, and lysosomal membrane stabilization.
Corticosteroids exert complex anti-inflammatory effects through cellular redistribution, vascular changes, and inhibition of inflammatory mediators, though the in vivo significance of some mechanisms remains uncertain.
Informs corticosteroid use in inflammatory states; leaves open the in vivo dominance of specific pathways.
The anti-inflammatory action of corticosteroids is complex. At a cellular level, they cause redistribution of granulocytes, resulting in increased circulating granulocytes and reduced tissue pools. They also cause lymphopenia. The significance of these phenomena in relation to the anti-inflammatory activity of steroids is unknown. The most obvious pharmacological effects of corticosteroids are seen on blood vessels. They cause adrenergically mediated vasoconstriction and non-competitive antagonism of vasodilation due to prostaglanin E and bradykinin. Prostaglandin formation is inhibited by corticosteroids but whether this is due to an effect on enzymic synthesis or release is uncertain. Corticosteroids stabilize the lysosomal membrane preventing release of lysosomal enzymes in vitro but the significance of this in vivo is debatable.
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Malcolm W. Greaves (1976) conducted a review in Inflammation. Corticosteroids was evaluated. Corticosteroids exert complex anti-inflammatory effects through granulocyte redistribution, lymphopenia, vasoconstriction, prostaglandin inhibition, and lysosomal membrane stabilization.
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