Related Experiment Videos
Effect of glutathion pretreatment on hypothermic ischemic cardioplegia
Insights
Glutathione (GSH) pretreatment protected the heart during cardiac surgery. GSH reduced cardiac enzyme release and lysosomal enzyme activity, indicating myocardial protection against ischemic injury from cardiopulmonary bypass.
Area of Science:
- Cardiology
- Biochemistry
- Pharmacology
Background:
- Glutathione (GSH) is vital for myocardial redox balance and membrane stabilization.
- Cardiac surgery often involves cardiopulmonary bypass (CPB) and ischemic cardioplegia, posing risks to myocardial tissue.
Purpose of the Study:
- To evaluate the protective effects of Glutathione (GSH) on myocardium during cardiac surgery involving CPB.
- To assess the impact of GSH on serum markers of myocardial injury.
Main Methods:
- Seventeen patients undergoing cardiac surgery were studied.
- Eight patients received intravenous GSH (200 mg/kg) before CPB.
- Serum levels of lysosomal enzymes (acid phosphatase, beta-glucuronidase), MB-CPK, and m-GOT were measured at various time points.
Main Results:
- GSH significantly suppressed acid phosphatase and beta-glucuronidase activity post-reperfusion.
- Serum MB-CPK levels remained stable in the GSH group, unlike the non-treated group.
- Increases in serum m-GOT levels were significantly reduced in the GSH-treated group.
Conclusions:
- Pretreatment with GSH offers significant myocardial protection against ischemic insult during CPB.
- GSH mitigates biochemical markers of cardiac damage following cardiopulmonary bypass and cardioplegia.
Abstract:
Glutathion (GSH) plays an important role in maintenance of the redox state of the myocardium and acts as the membrane stabilizer. Seventeen patients who underwent cardiac surgery were subjected to cardiopulmonary bypass (CPB) and ischemic cardioplegia. The effect of GSH on ischemic myocardium was evaluated by serum lysosomal enzymes (acid phosphatase, beta-glucuronidase), isoenzymes of creatine phosphokinase (MB-CPK) and aspartate aminotransferase (m-GOT). standard CPB was instituted and systemic hypothermia was employed. GSH was administered to 8 patients in a dose of 200 mg/kg i.v. prior to institution of CPB. Mixed venous blood was sampled before administration of GSH, 10 min after institution of CPB and 0, 1, 6, 24 and 48 hr of reperfusion period following cardioplegia. Activity of acid phosphatase and beta-glucuronidase were significantly suppressed in the GSH-treated group compared to the non-treated group at 24 hours of reperfusion and immediately after aortic unclamping, respectively. Serum MB-CPK levels remained stable during reperfusion, but in the non-treated group, the level increased significantly at 6 hours of reperfusion. Increment of serum m-GOT levels was significantly suppressed at 1, 6 and 24 hours of reperfusion, compared to the non-treated group. These data suggest that pretreatment of GSH can protect the myocardium subjected to CPB from ischemic insult.