The effects of the rate of reoxygenation on the recovery of hypoxemic hearts
1995; Elsevier BV; Volume: 109; Issue: 6 Linguagem: Inglês
10.1016/s0022-5223(95)70212-1
ISSN1097-685X
AutoresAntonio F. Corno, Michele Samaja, Stefania Casalini, Sonia Allibardi,
Tópico(s)Mechanical Circulatory Support Devices
ResumoThe myocardial damage induced by the "reoxygenation phenomenon" of hypoxic hearts is well known from both experimental 1Guarnieri C Flamigni F Caldarera CM Role of oxygen in the cellular damage induced by reoxygenation of hypoxemic hearts.J Mol Cell Cardiol. 1980; 12: 797-808Abstract Full Text PDF PubMed Scopus (452) Google Scholar, 2Corno A Samaja M The reoxygenation phenomenon [Letter].J THORAC CARDIOVASC SURG. 1993; 105: 373PubMed Google Scholar, 3Samaja M Motterlini R Santoro F Dell'Antonio G Corno A Oxidative injury in reoxygenated and reperfused hearts.Free Radic Biol Med. 1994; 16: 255-262Crossref PubMed Scopus (36) Google Scholar, 4Samaja 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)PubMed Google Scholar and clinical 5Del 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: 223-229Abstract Full Text PDF PubMed Google Scholar 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). 5Del 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: 223-229Abstract Full Text PDF PubMed Google Scholar 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. 5Del 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: 223-229Abstract Full Text PDF PubMed Google Scholar 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, 3Samaja M Motterlini R Santoro F Dell'Antonio G Corno A Oxidative injury in reoxygenated and reperfused hearts.Free Radic Biol Med. 1994; 16: 255-262Crossref PubMed Scopus (36) Google Scholar 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 (Table 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 3Samaja M Motterlini R Santoro F Dell'Antonio G Corno A Oxidative injury in reoxygenated and reperfused hearts.Free Radic Biol Med. 1994; 16: 255-262Crossref PubMed Scopus (36) Google Scholar; (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 4Samaja 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)PubMed Google Scholar ; and (4) other experimental and clinical studies are required to learn how to prevent or reduce the reoxygenation phenomenon.Table IFastp ValueSlown55Rate of reoxygenation (mm Hg/sec)2002Recovery (% of baseline) Developed pressure46± 70.162 ± 5 + dP/dt48± 50.00570 ± 3 - dP/dt48± 10NS61 ± 4 Oxygen uptake57± 8NS68 ± 9Change over baseline End-diastolic pressure (mm Hg)40± 90.0922 ± 3 Coronary pressure (mm Hg)37± 18NS28 ± 7dP/dt, Rate of pressure rise; NS, not significant. Open table in a new tab dP/dt, Rate of pressure rise; NS, not significant. 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).
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