The effect of captopril on membrane bound enzymes in ischemia–reperfusion injury

Abstract

There is substantial evidence that Na +K +/Mg 2+ ATPase and Ca 2+/Mg 2+ ATPase enzymes would effect the membrane integrity. Forty guinea pig ( n=10 in each group) hearts were studied in an isolated Krebs–Henseleit solution perfused Langendorff cardiac model. The first group was utilized as the control group. Group 2 hearts were arrested with captopril (200 μmol/l) added St Thomas Hospital Cardioplegic Solution (STHCS). Group 3 animals were pretreated with oral captopril (0.3 mg/kg/twice a day) for 10 days and then arrested with STHCS. Group 4 hearts were again pretreated with oral captopril (0.3 mg/kg/twice a day for 10 days) arrested with STHCS and reperfused with captopril added Krebs–Henseleit solution (200 μmol/l). Hearts were subjected to normothermic global ischemia for 90 min and than were reperfused at 37°C. When the treated groups were compared with control, best results were achived by group 4. The Na +K + and Ca 2+/Mg 2+ ATPase levels increased from 466.38±5.99 to 564.13±7.77 and 884.69±9.13 to 1254.29±5.75 nmol Pi/mg/prot/h respectively ( P<0.05). These results suggest that captopril protects the membrane integrity and thus played a role at the recovery of depressed membrane bound Na +K +/Mg 2+ ATPase and Ca 2+/Mg 2+ ATPase activity and also in ischemia–reperfusion injury.