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Evidence for free-radical mediated injury during coronary artery bypass surgery

A Movahed1, K G Nair, T F Ashavaid

  • 1PD Hinduja National Hospital & Medical Research Centre, Bombay.

Indian Heart Journal
|March 1, 1995
PubMed

Insights

Coronary artery bypass graft surgery causes oxygen free-radical bursts, leading to myocardial impairment. This study shows increased malondialdehyde and cardiac damage markers during reperfusion, indicating free-radical mediated cardiac membrane damage.

Area of Science:

  • Cardiology
  • Biochemistry
  • Free Radical Biology

Background:

  • Coronary artery bypass graft (CABG) surgery involves ischemia and reperfusion, which can cause myocardial damage.
  • Oxygen free-radical generation increases during reperfusion following CABG.
  • This oxidative stress may lead to cardiac membrane damage and impaired heart function.

Purpose of the Study:

  • To investigate the role of oxygen free radicals in myocardial impairment during CABG surgery.
  • To measure free-radical activity and cardiac damage markers at different reperfusion times.
  • To correlate these markers with the duration of ischemia.

Main Methods:

  • Blood samples were collected from 55 patients undergoing CABG surgery.
  • Thiobarbituric acid reactive species (TBARS), primarily malondialdehyde (MDA), were measured to assess free-radical activity.
  • Creatine phosphokinase (CPK), CPK-MB, and Troponin-T levels were measured to indicate myocardial damage.

Main Results:

  • MDA levels significantly increased at 1 and 10 minutes post-reperfusion (p < 0.001), correlating with aortic cross-clamp time.
  • CPK and CPK-MB activities doubled post-reperfusion (p < 0.001).
  • Plasma Troponin-T levels significantly increased at 1 and 10 minutes post-reperfusion (p < 0.01), correlating with ischemia severity.

Conclusions:

  • The study demonstrates a significant increase in free-radical activity and cardiac damage markers during reperfusion after CABG surgery.
  • The findings suggest that free radicals mediate cardiac membrane damage during CABG.
  • This highlights the potential for therapeutic interventions targeting oxidative stress in CABG patients.

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