INCOMPLETE CEREBRAL-ISCHEMIA IN THE RAT PROVOKES INCREASE OF TISSUE AND PLASMA MALONDIALDEHYDE

Short-term incomplete cerebral ischemia was induced in the rat by bila terally clamping for 5 min the common carotid arteries; subsequent rep erfusion of 10 min was obtained by removing carotid occlusion. At the end of ischemia or reperfusion, animals were sacrificed by decapitatio n. A control group was represented by sham-operated rats. Peripheral v enous blood samples were withdrawn from the femoral vein from rats sub jected to cerebral reperfusion 5 min before ischemia, at the end of is chemia, and 10 min after reperfusion. A highly sensitive HPLC method f or the direct determination of malondialdehyde, oxypurines, and nucleo sides was used on 200 mu L of brain tissue and plasma extracts. Incomp lete cerebral ischemia induced the appearance of a significant amount of tissue malondialdehyde (undetectable in control animals) and a decr ease of ascorbic acid. A further 6.6-fold increase of malondialdehyde and a 18.5% decrease of ascorbic acid occurred after 10 min of reperfu sion. Plasma malondialdehyde, which was present in minimal amount befo re ischemia, significantly increased after 5 min of ischemia, being st rikingly augmented after 10 min of reperfusion. A similar trend was ob served for oxy-purines and nucleosides. From these data, it can be aff irmed that tissue concentrations of malondialdehyde and ascorbic acid, and plasma levels of malondialdehyde, oxypurines, and nucleosides, re flect both the oxygen radical-mediated tissue injury and the depressio n of energy metabolism, thus representing early biochemical markers of short-term incomplete brain ischemia and reperfusion in the rat.-