Ce. Barandier et al., MANGANESE REDUCES MYOCARDIAL REPERFUSION INJURY ON ISOLATED RAT-HEART, Journal of Molecular and Cellular Cardiology, 30(4), 1998, pp. 837-847
It has been shown that reactive oxygen species produced during the ear
ly phase of myocardial post-ischemic reperfusion are one of the main c
auses of reperfusion injury. This observation has led to various antio
xidant strategies using many reactive oxygen species scavengers, inclu
ding manganese complexes. The aim of the present work was to provide a
reference study of the effects of manganese itself (MnCl2) on isolate
d rat hearts submitted to global total normothermic ischemia (30 min)
and reperfusion (60 min). McCl(2) was administered either during the f
irst 10 min reperfusion (10(-5)M and 10(-4)M) or throughout reperfusio
n (10(-4)M). After 10 min reperfusion, no functional difference was ev
idenced between control and manganese-treated groups, whereas high ene
rgy phosphate contents were significantly higher in treated groups. Mn
Cl2 10(-4)M enhanced the recovery of developed pressure between 40 and
55 min reperfusion. At the end of reperfusion. hearts treated during
the first 10 min reperfusion showed a better metabolic recovery. The g
roup treated throughout reperfusion showed a better metabolic recovery
, but a reduced coronary now and a weak recovery of developed pressure
. These results suggest that MnCl2, administered during the early phas
e of reperfusion, protects against myocardial reperfusion injury. This
effect might be mediated by manganese antioxidant properties. (C) 199
8 Academic Press Limited.