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J Thorac Cardiovasc Surg 1997;114:304-305
© 1997 Mosby, Inc.

LETTERS TO THE EDITOR

Hyperoxic cardiopulmonary bypass causes reoxygenation injury and lipid peroxidation

Kai Ihnken, MD

Stanford University Hospital
Department of Surgery
Room H3680
300 Pasteur Dr.
Stanford, CA 94305

To the Editor:

With great interest I read the brief communication "Contribution of Hyperoxia to Lipid Peroxidation in Coronary Artery Operations: Should We Keep a Low Oxygen Tension?" by Hadjinikolaou and colleagues (J Thorac Cardiovasc Surg 1997;113:212-3). However, I have to disagree with several of their statements.

First, the comment that "the contribution of hyperoxia to oxygen free radical generation and consequent lipid peroxidation in cardiac operations has to date not been addressed" is wrong. We intensively studied the effect of hyperoxic cardiopulmonary bypass (CPB) on oxygen-derived free radical–induced lipid peroxidation in hypoxic immature hearts Go Go Go 1–4,6 and in normoxic adult hearts.Go 5 The results show that hyperoxic CPB causes reoxygenation damage, leading to lipid peroxidation, reduced antioxidant reserve capacity, creatine kinase release, and impaired postbypass contractility in hypoxic immature hearts.Go Go Go 1–4,6 Reports by other groups also address the issue.Go 7 Additionally, in normoxic adult hearts, hyperoxic CPB causes lipid peroxidation, creatine kinase and lactate dehydrogenase release, and an increase in polymorphonuclear leukocyte elastase.Go 5

Second, the authors further state that lipid peroxidation is absent during CPB. Additionally, they did not find a relationship between the degree of hyperoxia and levels of lipid peroxidation. The results of our studies clearly indicate the existence of lipid peroxidation as early as 5 minutes after the start of CPB. We measured conjugated dienes as a marker of lipid peroxidation. Compared with results in control subjects without hypoxia, hyperoxic CPB (oxygen tension [Po2] = 400 mm Hg) caused a 13-fold increase in myocardial conjugated diene production during cardioplegic induction (5 minutes after the start of CPB) in hypoxic immature hearts.Go Go 2,3 Reduction of Po2 during CPB to normoxic levels (100 mm Hg) resulted in significantly (73%) lower production of myocardial conjugated dienes.Go Go 2,3

Furthermore, for the first time, we described a new method of "controlled reoxygenation," in which CPB is started with ambient Po2 (30 mm Hg) and normoxic reoxygenation is begun at the time of cardioplegic arrest.Go 4 Applying this method, we were able to avoid biochemical evidence of reoxygenation injury and to present almost complete functional recovery in previously hypoxic hearts.Go 4

In normoxic adult hearts we demonstrated a beneficial effect in terms of enzyme release, polymorphonuclear leukocyte elastase production, and especially lipid peroxidation, by lowering oxygen levels (150 mm Hg) in the extracorporeal circuitGo 5 (Fig. 1).



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  		Fig. 1. Malondialdehyde (MDA) as a measure of lipid peroxidation from systemic venous blood at the start and end of CPB. The hyperoxic group included 10 patients during coronary artery bypass graft operations in which CPB was conducted in a hyperoxic fashion (Po2 = 450 mm Hg). The normoxic group consisted of 10 patients also undergoing coronary artery bypass graft operations in which CPB was run with reduced oxygen levels (Po2 150 mm Hg). The groups did not differ in terms of age, sex, severity of disease, contractility, number of grafts, length of CPB, or ischemic time. *p < 0.05 versus hyperoxic group (analysis of variance).

 
We were also able to show that treatment with oxygen-derived free radical scavengers can limit reoxygenation injury and avoid lipid peroxidation during CPB.Go 6 I therefore partly agree with the authors, although we found convincing evidence that reduced Po2 during CPB is more important and is indeed absolutely vital. Hyperoxia is not physiologic, it is damaging to all organs, and above all it is absolutely not necessary. I truly believe that within 5 to 10 years, CPB in hypoxic immature hearts, as well as in normoxic adult hearts, will be instituted only in a normoxic fashion to avoid oxygenation damage and lipid peroxidation.

12/8/82359

References

  1. Ihnken K, Morita K, Buckberg GD, Matheis G, Sherman MP, Allen BS, et al. Studies of hypoxemic/reoxygenation injury: without aortic clamping. II. Evidence for reoxygenation damage. J Thorac Cardiovasc Surg 1995;110:1171-81.
  2. Morita K, Ihnken K, Buckberg GD, Sherman MP, Young HH. Studies of hypoxemic/reoxygenation injury: without aortic clamping. IX. Importance of avoiding perioperative hyperoxemia in the setting of previous cyanosis. J Thorac Cardiovasc Surg 1995;110:1235-44.
  3. Ihnken K, Morita K, Buckberg GD, Young HH. Studies of hypoxemic/reoxygenation injury: with aortic clamping. XI. Cardiac advantages of normoxemic versus hyperoxemic management during cardiopulmonary bypass. J Thorac Cardiovasc Surg 1995;110:1255-64.
  4. Morita K, Ihnken K, Buckberg GD. Studies of hypoxemic/reoxygenation injury: with aortic clamping. XII. Delay of cardiac reoxygenation damage in the presence of cyanosis: a new concept of controlled cardiac reoxygenation. J Thorac Cardiovasc Surg 1995;110:1265-73.
  5. Ihnken K, Winkler A, Beyersdorf F, Neidhart G, Winkelmann B, Unkelbach U, et al. Reduction of oxidative damage and nitric oxid on cardiopulmonary bypass by controlling Po2 during open heart surgery. Circulation 1995;92(Suppl):I763-4.
  6. Ihnken K, Morita K, Buckberg GD, Sherman MP, Young HH. Studies of hypoxemic/reoxygenation injury: without aortic clamping. VI. Counteraction of oxidant damage by exogenous antioxidants: N-(2-mercaptopropionyl) glycine and catalase. J Thorac Cardiovasc Surg 1995;110:1212-20.
  7. Del Nido PJ, Mickle DAG, Wilson GJ, Benson LN, Coles JG, Trusler GA, et al. Evidence of myocardial free radical injury during elective repair of tetralogy of Fallot. Circulation 1987;76(Suppl):V174-9.




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