The results reported here indicate that under appropriate conditions glucocorticoids may induce a reproducible protective effect in experimental AMI and stroke in the rat and provide the first evidence that the DXM-induced protection may be mediated via the formation and release of lipocortins, thus being able to prevent AA release and generation of injurious mediators. Large scale production of lipocortins is required for further studies on their antiischemic and antiarrhythmic effect in various models and different species as well as for the elucidation of their mode of action. It seems likely that lipocortin release is an underlying mechanism in the organism against various damaging factors. The glucocorticoid controversy in prevention of ischemic disorders may at least in part be due to the fact that little attention has been paid to stress conditions in animal experiments. It is premature to predict whether lipocortins would be appropriate for human therapy. Some undesirable effects of steroid treatment, e.g. teratogenicity , might also be mediated via lipocortin release. Intracisternal administration of human lipocortin might be useful in cases of severe acute cerebral edema when the traumatized cells may be incapable of responding to glucocorticoid treatment.
ASJC Scopus subject areas
- Pharmacology (medical)