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• W2002170463 abstract "The study of Bolling and associates1Bolling K Kronon M Allen BS Ramon S Wang T Hartz RS et al.Myocardial protection in normal and hypoxically stressed neonatal hearts: the superiority of hypocalcemic versus normocalcemic blood cardioplegia.J Thorac Cardiovasc Surg. 1996; 112: 1193-1201Abstract Full Text Full Text PDF PubMed Scopus (45) Google Scholar on myocardial protection in normal and hypoxically stressed hearts in this Journal concluded that good myocardial protection is independent of cardioplegic calcium concentration in nonhypoxic hearts and that hypoxic hearts are extremely sensitive to the cardioplegic calcium concentration. The authors lamented the absence of a clinically relevant hypoxic model. This is an important consideration, because many children who undergo cardiac operations in the first year of life have cyanotic heart disease, and the myocardium may be chronically perfused with hypoxic blood. Clearly it would be desirable to alter current techniques of myocardial management during surgery to provide better myocardial protection for children with cyanotic congenital heart disease and to further determine whether such techniques might also be applied to adults with acyanotic acquired heart disease. If the impact of prolonged periods of hypoxia on tolerance to subsequent ischemia could be elucidated, cardioprotection in these patients could be better understood and improved. The model of acute hypoxia described by Bolling and colleagues,1Bolling K Kronon M Allen BS Ramon S Wang T Hartz RS et al.Myocardial protection in normal and hypoxically stressed neonatal hearts: the superiority of hypocalcemic versus normocalcemic blood cardioplegia.J Thorac Cardiovasc Surg. 1996; 112: 1193-1201Abstract Full Text Full Text PDF PubMed Scopus (45) Google Scholar which was originally described by Buckberg,2Buckberg GD Studies of hypoxemic/reoxygenation injury. I. Linkage between cardiac function and oxidant damage.J Thorac Cardiovasc Surg. 1995; 110: 1164-1170Abstract Full Text Full Text PDF PubMed Scopus (62) Google Scholar Ihnken,3Ihnken K Morita K Buckberg GD Matheis G Sherman MP Allen BS et al.Studies of hypoxemic/reoxygenation injury. II. Evidence for reoxygenation damage.J Thorac Cardiovasc Surg. 1995; 110: 1171-1181Abstract Full Text Full Text PDF PubMed Scopus (53) Google Scholar and their associates, does not allow for the development of adaptive mechanisms in response to chronic hypoxia that occur in children with cyanotic heart disease. In addition, it is unknown whether reoxygenation is a real source of cardiac dysfunction in the chronically hypoxic immature heart. Preexisting injury caused by acute hypoxia may be a prerequisite for reoxygenation injury in the studies described by Bolling's group.1Bolling K Kronon M Allen BS Ramon S Wang T Hartz RS et al.Myocardial protection in normal and hypoxically stressed neonatal hearts: the superiority of hypocalcemic versus normocalcemic blood cardioplegia.J Thorac Cardiovasc Surg. 1996; 112: 1193-1201Abstract Full Text Full Text PDF PubMed Scopus (45) Google Scholar Our laboratory has developed a rabbit model of hypoxia from birth that simulates the essential characteristics of cyanotic heart disease: decreased arterial oxygen levels, polycythemia, increased right ventricular mass, decreased weight gain, and overall failure to thrive.4Baker EJ Boerboom LE Olinger GN Baker JE Tolerance of the developing heart to ischemia: impact of hypoxemia from birth.Am J Physiol. 1995; 268: H1165-H1173PubMed Google Scholar We have demonstrated that hypoxia from birth increases the tolerance of the heart to ischemia compared with that of age-matched normoxic control subjects.4Baker EJ Boerboom LE Olinger GN Baker JE Tolerance of the developing heart to ischemia: impact of hypoxemia from birth.Am J Physiol. 1995; 268: H1165-H1173PubMed Google Scholar The mechanism for adaptation to prolonged hypoxia that confers increased tolerance to subsequent myocardial ischemia is currently unknown. We have also examined the calcium content of St. Thomas' Hospital II cardioplegic solution and found in our model that the existing calcium content of 1.2 mmol/L is suboptimal to protect the ischemic immature myocardium. Optimal myocardial protection occurred with a calcium concentration of 0.4 mmol/L in hearts chronically hypoxic from birth5Baker EJ Baker JE Calcium and cardioplegic protection of the ischemic immature heart: impact of hypoxemia from birth.Ann Thorac Surg. 1994; 58: 1123-1130Abstract Full Text PDF PubMed Scopus (10) Google Scholar and 0.3 mmol/L in hearts normoxic from birth.6Baker EJ Olinger GN Baker JE Calcium content of St. Thomas' II cardioplegic solution damages ischemic immature myocardium.Ann Thorac Surg. 1991; 52: 993-999Abstract Full Text PDF PubMed Scopus (28) Google Scholar These previously published data may place in perspective the study by Bolling and coworkers, confirming their hypothesis of hypocalcemic cardioplegia being superior to normocalcemic cardioplegia in protection of immature myocardium. The response, however, of immature myocardium to acute versus chronic hypoxia before reoxygenation, with and without surgical ischemia, is speculative because neither we nor Bolling and his associates addressed this particular issue. 12/8/80740" @default.
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• W2002170463 title "Myocardial protection of the hypoxic heart" @default.
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