Lipid peroxidation during myocardial reperfusion.
Reperfusion of heart muscle after prolonged ischaemia is associated with metabolic and functional abnormalities and eventual cell death. Free radical induced lipid peroxidation of cell membranes is thought to be a major mechanism in the evolution of reperfusion damage. The evidences in support for this kind of damage are based on tissue malondialdehyde quantitation by the thiobarbituric acid test (TBA-test). In an attempt to verify this topic we have subjected isolated and Langendorff perfused rabbit hearts to a period of 60 minutes of severe ischaemia plus 30 minutes of reperfusion. At appropriate time points malondialdehyde was determined in the tissue by means of TBA-test and directly by reversed phase, high pressure, liquid chromatography (HPLC). We have found no correlation between the two compared assays. During reperfusion, there was the formation of non-lipid related, malondialdehyde-like, TBA-reactive substance which leads to overestimations of the extent of lipid peroxidation. On the contrary, by direct HPLC quantitation, there was a decrease of tissue malondialdehyde during ischaemia and during the early phases of reperfusion. Our results demonstrate that TBA-test is not a reliable index of malondialdehyde accumulation in organ system.
Ceconi
C
C
Cattedra di Cardiologia, Università degli Studi di Brescia, Italy.
Cargnoni
A
A
Pasini
E
E
Condorelli
E
E
Currello
S
S
Ferrari
R
R
D000818:Animals; D002851:Chromatography, High Pressure Liquid; D003402:Creatine Kinase / Q000378:metabolism*; D066298:In Vitro Techniques; D007511:Ischemia / Q000378:metabolism; D015227:Lipid Peroxidation / Q000502:physiology*; D008297:Male; D008315:Malondialdehyde / Q000032:analysis*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism*; D011817:Rabbits
D008315:Malondialdehyde; D003402:Creatine Kinase