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Oxygen free radicals in erythrocytes during open heart operation
1Department of Biochemistry, Medical School, Anadolu University, Eskişehir, Turkey.
Insights
Cardiopulmonary bypass (CPB) surgery causes myocardial ischemia, leading to increased harmful oxygen free radicals. The body's antioxidant defenses, like superoxide dismutase (SOD), are overwhelmed during this process.
Area of Science:
- Cardiology
- Biochemistry
- Physiology
Background:
- Myocardial ischemia during cardiopulmonary bypass (CPB) is a significant clinical concern.
- Understanding the biochemical response to ischemia-reperfusion injury is crucial for patient outcomes.
Purpose of the Study:
- To investigate the impact of myocardial ischemia during CPB on oxidative stress markers.
- To evaluate the activity of superoxide dismutase (SOD) and levels of reduced glutathione (GSH) and lipid peroxide (LP).
Main Methods:
- Blood samples were collected from the coronary sinus at four time points: before CPB, immediately after CPB, and at 15 and 30 minutes post-CPB.
- Assays were performed to measure SOD activity, GSH levels, and LP levels.
Main Results:
- SOD activity significantly decreased post-CPB and remained reduced.
- LP levels significantly increased throughout the post-CPB period, indicating lipid peroxidation.
- GSH levels showed a slight increase during ischemia and reperfusion.
Conclusions:
- CPB-induced myocardial ischemia generates significant oxygen free radicals.
- The rate of free radical generation appears to exceed the cell's antioxidant capacity, specifically intracellular SOD.
- These findings highlight the oxidative stress associated with CPB and suggest potential targets for therapeutic intervention.
Abstract:
This study was performed to observe the effect of myocardial ischemia on the patients undergoing cardiopulmonary bypass (CPB) operation. For this aim, superoxide dismutase (SOD) activities, reduced glutathione (GSH) and lipid peroxide (LP) levels were determined in blood samples which were obtained from the coronary sinus. Sampling times were as follows: (1) Before CPB. (2) Immediately after CPB. (3) Fifteen minutes after the second specimen. (4) Thirty minutes after the second specimen. SOD activities of these groups were 5135.10 +/- 278.51 U/g Hb, 3505.64 +/- 302.09 U/g Hb, 4206.55 +/- 272.25 U/g Hb, 4707.20 +/- 270.91 U/g Hb respectively. Also the LP levels were 1.90 +/- 0.29 nmol MDA/ml, 4.37 +/- 0.52 nmol MDA/ml, 4.09 +/- 0.39 nmol MDA/ml, 2.74 +/- 0.30 nmol MDA/ml respectively. GSH levels were slightly increased during ischemia and reperfusion; 103.27 +/- 5.18 mg/dl, 125.00 +/- 10.36 mg/dl, 125.00 +/- 6.61 mg/dl, 111.18 +/- 8.22 mg/dl respectively. SOD activities were reduced significantly in second group (p < 0.001), in third and fourth groups (p < 0.01) as compared with control group. Also LP levels were increased significantly in all groups (p < 0.001) as compared with controls. Our results confirm the generation of oxygen free radicals from ischemia and reperfusion of heart during CPB. Also it appears that oxygen free radical generation exceeds the capacity of intracellular SOD, which is the most important scavenger of free radical in the cell.