The protective effect of lisinopril on membrane-bound enzymes in myocardial preservation

Abstract

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 cell membrane integrity. The aim of the study is to determine whether the administration of lisinopril is able to protect the membrane-bound enzyme levels in isolated guinea pig hearts and also ascertain whether or not a relationship exists between oxygen free radicals and membrane bound Na+ - K+ ATPase and Ca2+ ATPase. Forty guinea pig hearts were studied in an isolated Krebs-Henseleit solution-perfused Langendorff cardiac model. In all groups cardioplegic arrest was achieved by administering St. Thomas' Hospital cardioplegic solution (STHCS). Group 1 (control, n = 10) received only STHCS. Group 2 (n = 10) were arrested with lisinopril (1 μmol l-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 pretreated with oral lisinopril (0.2 mg kg-1 twice a day for 10 days), arrested with STHCS and reperfused with lisinopril added to Krebs-Henseleit solution (1 μmol l-1). Hearts were subjected to normothermic global ischaemia for 90 min and then reperfused at 37°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 best results were achieved in group 4. The Na+ - K+ and Ca2+ ATPase levels increased 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 suggest that lisinopril protects the cell membrane integrity and lessens free radical-induced oxidant stress. Copyright (C) 2000 John Wiley and Sons, Ltd.