O. Gribbe et al., Dexamethasone increases survival and attenuates induction of inducible nitric oxide synthase in experimental skin flaps, ANN PL SURG, 42(2), 1999, pp. 180-184
The molecule nitric oxide synthesized by the enzyme nitric oxide synthase (
NOS) has been shown to be of major physiological and pathophysiological imp
ortance in the body. During ischemia and reperfusion, induction of free ion
ic calcium (Ca2+)-independent inducible NOS (iNOS) is thought to result in
an overproduction of NO, leading to tissue damage, The glucocorticoid dexam
ethasone is known to inhibit the induction of iNOS, and the aim of the curr
ent study was to determine the effect of dexamethasone on viability and NOS
activity in an ischemic flap model on the dorsum of the rat. Vehicle (N =
20) or dexamethasone (N = 20) was administered 3 hours prior to operation,
The surviving area was measured and the flaps were removed after 24 hours f
or 10 rats in each group and after 48 hours for the remaining 10 rats in ea
ch group, Treatment with dexamethasone resulted in an improved flap viabili
ty at both 24 hours (p < 0.001) and 48 hours (p < 0.01), and a reduced indu
ction of Ca2+-independent NOS activity in the proximal part of the flaps at
24 hours (p < 0.001), In the current study the authors show that dexametha
sone attenuates the induction of Ca2+-independent NOS and increases surviva
l in experimental skin flaps.