Studies of hypoxemic/reoxygenation injury: without aortic clamping. IX. Importance of avoiding perioperative hyperoxemia in the setting of previous cyanosis.

[1]  G. Buckberg,et al.  Studies of hypoxemic/reoxygenation injury: without aortic clamping. II. Evidence for reoxygenation damage. , 1995, The Journal of thoracic and cardiovascular surgery.

[2]  G. Buckberg.  Studies of hypoxemic/reoxygenation injury: I. Linkage between cardiac function and oxidant damage. , 1995, The Journal of thoracic and cardiovascular surgery.

[3]  G. Buckberg,et al.  Role of controlled cardiac reoxygenation in reducing nitric oxide production and cardiac oxidant damage in cyanotic infantile hearts. , 1994, The Journal of clinical investigation.

[4]  A. Feinstein,et al.  Oxygen as a cause of blindness in premature infants: "autopsy" of a decade of errors in clinical epidemiologic research. , 1992, Journal of clinical epidemiology.

[5]  W. Williams,et al.  Effect of oxygen tension and cardiovascular operations on the myocardial antioxidant enzyme activities in patients with tetralogy of Fallot and aorta-coronary bypass. , 1992, The Journal of thoracic and cardiovascular surgery.

[6]  G. Buckberg,et al.  Role of L-arginine-nitric oxide pathway in myocardial reoxygenation injury. , 1992, The American journal of physiology.

[7]  W. Little,et al.  Comparison of measures of left ventricular contractile performance derived from pressure-volume loops in conscious dogs. , 1989, Circulation.

[8]  R. Kloner,et al.  Deleterious Effects of Oxygen Radicals in Ischemia/Reperfusion Resolved and Unresolved Issues , 1989, Circulation.

[9]  D. Godin,et al.  Altered antioxidant status in the ischemic/reperfused rabbit myocardium: effects of allopurinol. , 1989, Canadian Journal of Cardiology.

[10]  G. Buckberg,et al.  Studies on prolonged acute regional ischemia. II. Implications of progression from dyskinesia to akinesia in the ischemic segment. , 1989, The Journal of thoracic and cardiovascular surgery.

[11]  M. Duvelleroy,et al.  Enzyme release and mitochondrial activity in reoxygenated cardiac muscle: relationship with oxygen-induced lipid peroxidation. , 1989, General physiology and biophysics.

[12]  P. Menasche,et al.  Free radicals and myocardial protection: a surgical viewpoint. , 1989, The Annals of thoracic surgery.

[13]  J. Mayer,et al.  Myocardial protection in cyanotic neonatal lambs. , 1988, The Journal of thoracic and cardiovascular surgery.

[14]  Kiichi Sagawa,et al.  Cardiac Contraction and the Pressure-Volume Relationship , 1988 .

[15]  W. Hörl,et al.  Plasma levels of main granulocyte components during cardiopulmonary bypass. , 1988, Journal of Thoracic and Cardiovascular Surgery.

[16]  W. Williams,et al.  Inadequate myocardial protection with cold cardioplegic arrest during repair of tetralogy of Fallot. , 1988, The Journal of thoracic and cardiovascular surgery.

[17]  W. Williams,et al.  Evidence of myocardial free radical injury during elective repair of tetralogy of Fallot. , 1987, Circulation.

[18]  P. J. Simpson,et al.  Free radical scavengers in myocardial ischemia. , 1987, Federation proceedings.

[19]  M. Hess,et al.  PGH Synthase and Lipoxygenase Generate Superoxide in the Presence of NADH or NADPH , 1986, Circulation research.

[20]  T. Orszulak,et al.  Oxygen free radical generation during cardiopulmonary bypass: correlation with complement activation. , 1986, Circulation.

[21]  P. Menasché,et al.  A comparative study of free radical scavengers in cardioplegic solutions. Improved protection with peroxidase. , 1986, The Journal of thoracic and cardiovascular surgery.

[22]  J. Hammon,et al.  Pathophysiology of chronic cyanosis in a canine model. Functional and metabolic response to global ischemia. , 1985, The Journal of thoracic and cardiovascular surgery.

[23]  S. Levitsky,et al.  Chronic hypoxemia depresses global ventricular function and predisposes to the depletion of high-energy phosphates during cardioplegic arrest: implications for surgical repair of cyanotic congenital heart defects. , 1984, The Annals of thoracic surgery.

[24]  J. Crapo,et al.  Hyperoxia increases H2O2 release by lung mitochondria and microsomes. , 1982, Archives of biochemistry and biophysics.

[25]  J. Crapo,et al.  Hyperoxia increases oxygen radical production in rat lung homogenates. , 1982, Archives of biochemistry and biophysics.

[26]  J. Jarmakani,et al.  Mechanism of tissue Ca2+ gain during reoxygenation after hypoxia in rabbit myocardium. , 1982, The American journal of physiology.

[27]  G. Bullock,et al.  The oxygen paradox and the calcium paradox: two facets of the same problem? , 1978, Journal of molecular and cellular cardiology.

[28]  L. Opie,et al.  Myocardial Metabolism in Cyanotic Congenital Heart Disease Studied by Arteriovenous Differences of Lactate, Phosphate, and Potassium at Rest and during Atrial Pacing , 1977, Circulation.

[29]  C. Markert,et al.  Myocardial LDH Isozyme Distribution in the Ischemic and Hypoxic Heart , 1976, Circulation.

[30]  L. Mela,et al.  Cardiac mitochondrial activity in acute and chronic cyanosis. , 1973, The Journal of surgical research.

[31]  I. T. Oliver.  A spectrophotometric method for the determination of creatine phosphokinase and myokinase. , 1955, The Biochemical journal.

[32]  R. Bartlett,et al.  Severe myocardial dysfunction during extracorporeal membrane oxygenation. , 1992, Journal of pediatric surgery.

[33]  A. Boveris,et al.  Mitochondrial production of superoxide radical and hydrogen peroxide. , 1977, Advances in experimental medicine and biology.

[34]  W. Rudolph.  Myocardial metabolism in cyanotic congenital heart disease. , 1971, Cardiology.

[35]  J. Shaver,et al.  Myocardial metabolism in cyanotic congenital heart disease. , 1970, Cardiology.