Reibel D K, Rovetto M J
Am J Physiol. 1978 May;234(5):H620-4. doi: 10.1152/ajpheart.1978.234.5.H620.
The relationship between oxygen deficiency-reduced high energy phosphate levels and their resynthesis upon return to aerobic conditions was investigated in the isolated perfused rat heart. Any net adenosine triphosphate (ATP) hydrolysis during anoxia tended to impair ATP resynthesis with subsequent aerobic perfusion. Thirty minutes of ischemia reduced myocardial ATP 50%, and with restoration of aerobic conditions ATP increased to only 60% of control levels. The major source of postischemic and postanoxic ATP was adenosine 5'-monophosphate and adenosine 5'-disphosphate. Loss of purine base from oxygen-deficient cells limited restoration of ATP. The inclusion of adenosine, ATP, or creatine phosphate (CP) in the perfusate did not enhance postischemic tissue adenine-nucleotide concentrations. Postischemic and postanoxic CP concentrations returned to control values and were independent of ischemic and anoxic ATP and CP concentrations. Complete resynthesis of CP suggests that cellular energy-producing pathways were functional. Ventricular performance was directly related to tissue ATP concentration in aerobic control, postischemic, and postanoxic hearts. Thus, loss of adenine nucleotides during oxygen deficiency may impair subsequent aerobic synthesis of ATP and mechanical function.
在离体灌注大鼠心脏中研究了缺氧导致高能磷酸水平降低及其在恢复有氧条件时重新合成之间的关系。缺氧期间任何三磷酸腺苷（ATP）的净水解都倾向于损害随后有氧灌注时ATP的重新合成。30分钟的缺血使心肌ATP减少50%，恢复有氧条件后ATP仅增加到对照水平的60%。缺血后和缺氧后ATP的主要来源是5'-单磷酸腺苷和5'-二磷酸腺苷。缺氧细胞中嘌呤碱的丢失限制了ATP的恢复。在灌注液中加入腺苷、ATP或磷酸肌酸（CP）并没有提高缺血后组织腺嘌呤核苷酸的浓度。缺血后和缺氧后CP浓度恢复到对照值，且与缺血和缺氧时的ATP及CP浓度无关。CP的完全重新合成表明细胞能量产生途径是有功能的。在有氧对照、缺血后和缺氧后的心脏中，心室功能与组织ATP浓度直接相关。因此，缺氧期间腺嘌呤核苷酸的丢失可能损害随后ATP的有氧合成和机械功能。
