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J Thorac Cardiovasc Surg 1995;109:1250-1251
© 1995 Mosby, Inc.

BRIEF COMMUNICATIONS

The effects of the rate of reoxygenation on the recovery of hypoxemic hearts

Antonio Corno, MDa, Michele Samaja, PhDb, Stefania Casalini, PhDb, Sonia Allibardi, PhDc


Milan, Italy

The myocardial damage induced by the "reoxygenation phenomenon" of hypoxic hearts is well known from both experimental Go Go 1-4 and clinical Go 5 reports. The surgical repair of cyanotic congenital heart defects in infants may be complicated by the problem of acute reoxygenation at the beginning of cardiopulmonary bypass (CPB). Go 5 In fact, at the onset of CPB the whole body and, therefore, the myocardium are suddenly perfused from the arterial line with an oxygen saturation and an oxygen tension (Po2 ) (generally >200 mm Hg) substantially higher than the baseline value because of the underlying cyanotic congenital heart defect. The main responsibility for the heart injury has been clinically associated with the burst of oxygen-derived free radicals when cyanotic hearts are suddenly exposed to high oxygen pressures. Go 5

To test the hypothesis that the rate of reoxygenation may be critical in the observed pattern, we performed an experimental study in which isolated rat hearts were exposed to acute hypoxia and then underwent either "fast" or "slow" reoxygenation: the recovery of ventricular performance was then compared with the mode of the reoxygenation. Isolated rat hearts, perfused with Krebs-Henseleit buffer with a coronary flow of 15 ml/min, Go 3 after a period of stabilization with 100 oxygen saturation, were exposed to 20 minutes of hypoxic perfusion (coronary flow of 15 ml/min, oxygen saturation 10% of baseline). Reoxygenation was either "fast" (Po2 increase >200 mm Hg/sec) or "slow" (Po2 increase 2 mm Hg/sec).

The results (GoTable I) indicate that both the systolic and diastolic ventricular functions were more depressed after "fast" reoxygenation than after "slow" reoxygenation. Although it is difficult to transfer results gathered in an isolated heart preparation to an in vivo situation, from this experimental study it appears that (1) gradual reoxygenation after hypoxia may contribute to the reduction of myocardial injury in infants with cyanosis who undergo cardiac repair with the use of CPB; (2) the persisting myocardial dysfunction after reoxygenation underlines the presence of factors responsible for the reoxygenation damage other than oxygen free radicals Go 3; (3) the bulk of the injury may be associated with events that occur not only during the reoxygenation, but most likely also during hypoxia, such as the high energy demand Go 4 ; and (4) other experimental and clinical studies are required to learn how to prevent or reduce the reoxygenation phenomenon.


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  		Table I.
 
We are already aware of other centers of pediatric cardiac surgical care in which CPB in infants with cyanosis is routinely initiated with an arterial Po2 (80 to 100 mm Hg) lower than that generally used and maintained at a relatively lower value (maximum 120 mm Hg) than that conventionally used (Pedro Del Nido, personal communication, 1994).

Footnotes

From Hospital "S. Donato," a University of Milan,b and Scientific Institute "S. Raffaele," c Milan, Italy. Back

J THORAC CARDIOVASC SURG 1995;109:1250-1 Back

References

  1. Guarnieri C, Flamigni F, Caldarera CM. Role of oxygen in the cellular damage induced by reoxygenation of hypoxemic hearts. J Mol Cell Cardiol 1980;12:797-808.[Medline]
  2. Corno A, Samaja M. The reoxygenation phenomenon [Letter]. J THORAC CARDIOVASC SURG 1993;105:373.[Medline]
  3. Samaja M, Motterlini R, Santoro F, Dell'Antonio G, Corno A. Oxidative injury in reoxygenated and reperfused hearts. Free Radic Biol Med 1994;16:255-62.[Medline]
  4. Samaja M, Casalini S, Allibardi S, Corno A. Effects of energy demand in ischemic and hypoxemic isolated rat hearts. Adv Exp Med Biol 1994 (In press).
  5. Del Nido P, Mickle DAG, Wilson GJ, et al. Inadequate myocardial protection with cold cardioplegic arrest during repair of tetralogy of Fallot. J THORAC CARDIOVASC SURG 1988;95:223-9.[Abstract]




This Article
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