A number of studies have reported that oxidant stress reduces the activity
of isolated Na+ - K+ ATPase and Ca2+ ATPase which are known to affect the c
ell membrane integrity. The aim of the study is to determine whether the ad
ministration of lisinopril is able to protect the membrane-bound enzyme lev
els in isolated guinea pig hearts and also ascertain whether or not a relat
ionship exists between oxygen free radicals and membrane bound Na+ - K+ ATP
ase and Ca2+ ATPase. Forty guinea pig hearts were studied in an isolated Kr
ebs-Henseleit solution-perfused Langendorff cardiac model. In all groups ca
rdioplegic: arrest was achieved by administering St. Thomas' Hospital cardi
oplegic solution (STHCS). Group 1 (control, n = 10) received only STHCS. Gr
oup 2 (n = 10) were arrested with lisinopril (1 mu mol 1(-1)) added STHCS,
Group 3 (n = 10) were pretreated with oral lisinopril (0.2 mg kg(-1) twice
a day) for 10 days and then arrested with STHCS. Group 4 were also pretreat
ed with oral lisinopril (0.2 mg kg(-1) twice a day for 10 days), arrested w
ith STHCS and reperfused with lisinopril added to Krebs-Henseleit solution
(1 mu mol 1(-1)). Hearts were subjected to normothermic global ischaemia fo
r 90 min and then reperfused at 37 degrees C. Pretreatment and addition of
lisinopril in the reperfusion buffer improved the levels of membrane-bound
enzymes. When the treated groups were compared with control hearts, the bes
t results were achieved in group 4. The Na+ - K+ and Ca2+ ATPase levels inc
reased from 466.38+/-5.99 to 560.12+/-18.02 and 884.69+/-9.13 to 1287.71+/-
13.01 nmolPi mg(-1) protein h(-1) respectively (p < 0.05). These results su
ggest that lisinopril protects the cell membrane integrity and lessens free
radical-induced oxidant stress. Copyright (C) 2000 John Wiley & Sons, Ltd.