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Myocardial apoptosis prevention by radical scavenging in patients undergoing cardiac surgery
Uwe M Fischer1, Paschalis Tossios, Astrid Huebner
1Department of Cardiothoracic Surgery, University of Cologne, Germany.
Background:
Reactive oxygen-derived species, including those generated during myocardial ischemia and reperfusion induced by cardioplegia, have been suggested to be involved in myocardial apoptosis induction. The purpose of our study was to investigate (1) whether cardioplegic arrest initiates apoptosis in the hearts of cardiac surgery patients and (2) whether reactive oxygen-derived species scavenging with N-acetylcysteine attenuates myocardial apoptosis initiation.
Methods:
In transmural left ventricular biopsy samples collected before and at the end of cardiopulmonary bypass, we densitometrically determined cardiac myocyte staining intensity for active caspases-3 and -7, the apoptosis signal pathway central effector enzymes. The left ventricular biopsy samples had been obtained from 36 coronary artery bypass graft patients randomized in a double-blind fashion to receive either N-acetylcysteine (100 mg/kg into cardiopulmonary bypass prime followed by infusion at 20 mg.kg(-1).h(-1); n = 18) or placebo (n = 18).
Results:
The change in left ventricular cardiac myocyte staining (end of cardiopulmonary bypass minus before cardiopulmonary bypass) differed significantly between groups for both measures: caspase-3, -3.1 +/- 4.5 gray units (mean +/- SD; N-acetylcysteine group) versus 7.1 +/- 8.1 gray units (placebo); 95% confidence interval, 6.4 to 14.4; P <.0001; caspase-7, -5.1 +/- 6.1 gray units (N-acetylcysteine) versus 5.1 +/- 5.7 gray units (placebo); 95% confidence interval, 6.3 to 15.0; P <.0001. Clinical outcome did not differ between N-acetylcysteine and placebo.
Conclusions:
Our data show that cardioplegic arrest initiates the apoptosis signal cascade in human left ventricular cardiac myocytes. This apoptosis induction can effectively be prevented by N-acetylcysteine.
Insights
Cardioplegic arrest triggers apoptosis in heart cells during cardiac surgery. N-acetylcysteine effectively prevents this apoptosis, safeguarding cardiac myocytes from programmed cell death.
Area of Science:
- Cardiology
- Cell Biology
- Biochemistry
Background:
- Reactive oxygen species (ROS) are implicated in myocardial apoptosis during ischemia-reperfusion injury from cardioplegia.
- Investigating the role of cardioplegic arrest in initiating cardiac apoptosis is crucial for cardiac surgery patients.
Purpose of the Study:
- To determine if cardioplegic arrest initiates apoptosis in human cardiac myocytes.
- To assess if N-acetylcysteine (ROS scavenger) can attenuate this apoptosis.
Main Methods:
- Left ventricular biopsy samples from 36 coronary artery bypass graft patients were analyzed.
- Staining intensity for active caspases-3 and -7 (apoptosis markers) was densitometrically determined.
- Patients were randomized to receive N-acetylcysteine or placebo during cardiopulmonary bypass.
Main Results:
- Cardioplegic arrest significantly increased caspase-3 and -7 activity in placebo group compared to N-acetylcysteine group.
- N-acetylcysteine administration significantly attenuated the increase in caspase activity, indicating reduced apoptosis initiation.
- No significant difference in clinical outcomes was observed between the groups.
Conclusions:
- Cardioplegic arrest initiates the apoptosis signal cascade in human left ventricular cardiac myocytes.
- N-acetylcysteine effectively prevents apoptosis induction during cardioplegic arrest in cardiac surgery.
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