title: 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 (200micromol/l) added St Thomas Hospital Cardioplegic Solution (STHCS). Group 3 animals were pretreated with oral captopril (0.3mg/kg/twice a day) for 10days and then arrested with STHCS. Group 4 hearts were again pretreated with oral captopril (0.3mg/kg/twice a day for 10days) arrested with STHCS and reperfused with captopril added Krebs-Henseleit solution (200micromol/l). Hearts were subjected to normothermic global ischemia for 90min and than were reperfused at 37 degrees 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.
authors.affiliation: Department of Cardiovascular Surgery, Marmara University School of Medicine, Istanbul, Turkey.
authors.forename: C S
authors.initials: CS
authors.lastname: Isbir
authors.forename: R
authors.initials: R
authors.lastname: Dogan
authors.forename: B
authors.initials: B
authors.lastname: Farsak
authors.forename: M
authors.initials: M
authors.lastname: Ayd1n
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000008:administration & dosage / Q000494:pharmacology*; D000818:Animals; D001639:Bicarbonates / Q000494:pharmacology; D002122:Calcium Chloride / Q000494:pharmacology; D002216:Captopril / Q000008:administration & dosage / Q000494:pharmacology*; D002314:Cardioplegic Solutions / Q000494:pharmacology; D002462:Cell Membrane / Q000187:drug effects* / Q000201:enzymology; D005069:Evaluation Studies as Topic; D005947:Glucose / Q000494:pharmacology; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008274:Magnesium / Q000494:pharmacology; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology* / Q000517:prevention & control; D011189:Potassium Chloride / Q000494:pharmacology; D011897:Random Allocation; D012965:Sodium Chloride / Q000494:pharmacology; D017392:Thiobarbituric Acid Reactive Substances; D014325:Tromethamine / Q000494:pharmacology
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D001639:Bicarbonates; D002314:Cardioplegic Solutions; C074097:Krebs-Henseleit solution; C041711:St. Thomas' Hospital cardioplegic solution; D017392:Thiobarbituric Acid Reactive Substances; D014325:Tromethamine; D012965:Sodium Chloride; D011189:Potassium Chloride; D002216:Captopril; D008274:Magnesium; D005947:Glucose; D002122:Calcium Chloride