Attempts at the improvement of cardiac blood supply.
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Biomedical subjects
G Temes
Publications and source records attributed to G Temes.
Is peripheral blood a reliable indicator of acute oxidative stress following heart ischemia and reperfusion?
BACKGROUND: Reactive oxygen species (ROS) play a crucial role in membrane damage in ischemic-reperfusion syndromes. The aim of our work was to determine whether blood samples taken from a peripheral vein are a reliable indicator to reflect the development of oxidative stress following acute heart ischemia and reperfusion. MATERIAL AND METHODS: In a dog model, the left descending coronary artery (LAD) was occluded for 60 min followed by 60 minutes of reperfusion. The lipid peroxidation marker malondialdehyde (MDA), endogenous antioxidants reduced glutathione (GSH), the activity of superoxide dismutase (SOD) enzyme and the stimulated radical production of isolated neutrophil granulocytes (PMN) were measured simultaneously from the peripheral vein and the coronary sinus before and at the end of the LAD occlusion, and again during reperfusion. RESULTS: MDA and SOD values increased during reperfusion. At the end of 1 hour the reperfusion changes in the coronary sinus were significant (p<0.05). GSH increased in the femoral vein, but decreased in the coronary sinus. The radical-producing capacity of PMNs decreased by the end of LAD occlusion, and a further significant decrease was measured during reperfusion in the coronary sinus (p<0.01). In the peripheral venous blood samples the decrease of PMN radical production became significant only at 30 minutes of reperfusion (p<0.02), and the earlier difference between the coronary sinus and the femoral vein tended to level out following 60 minutes of reperfusion. CONCLUSIONS: During early reperfusion following myocardial ischemia coronary sinus blood sampling gives an earlier indication of myocardial damage. At a later phase, peripheral blood samples may also be informative regarding the altered balance between ROS production and the antioxidant capacity.
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Effects of lidocaine on cerebral lipid peroxidation and neutrophil activation following complete compression ischemia.
The effect of lidocaine on brain lipid peroxidation, as reflected by jugular vein malondialdehyde concentrations, and of polymorphonuclear leukocyte activation in peripheral venous blood samples following transient global cerebral ischemia, were studied. In normothermic dogs subjected to a 10 min elevation of cerebrospinal fluid pressure and a subsequent 60 min reperfusion, the malondialdehyde concentration during the first 3 min of reperfusion increased significantly (p < 0.05) in the jugular vein. Lidocaine (10 mg/kg, i.v.), administered 10 min before ischemia, not only prevented the elevation of the malondialdehyde concentrations during ischemia, but also provoked a significant transient decrease 10 min after the start of reperfusion. A 10 min ischemia and a 60 min reperfusion caused no significant changes in the polymorphonuclear leukocyte radical production, neither following ischemia nor after addition of lidocaine. These results suggest that lidocaine exerts a scavenging action on free radical processes but that it has no direct effect on the polymorphonuclear leukocyte activation in the early phase of reperfusion following ischemia.
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