Kreutzer U, Jue T
Biological Chemistry Department, University of California, Davis 95616, USA.
Am J Physiol. 1995 Apr;268(4 Pt 2):H1675-81. doi: 10.1152/ajpheart.1995.268.4.H1675.
The 1H nuclear magnetic resonance (NMR) signal of tissue myoglobin has provided an opportunity to determine the critical O2 level in saline-perfused myocardium at room temperature. Above the intracellular PO2 of 4 mmHg, the myocardium exhibits no sign of hypoxia. At 4 mmHg, the rate pressure product (RPP) decreases, and the lactate formation rate, measured enzymatically, increases. However, O2 consumption and the 31P-NMR signal of phosphocreatine level remain relatively constant until the cellular PO2 reaches 2 mmHg. The ATP signal intensity dips only when cellular O2 reaches 0.8 mmHg, while pH remains unchanged at 7.2. The sequential nature of the cellular response to limiting O2, starting with alterations in the lactate formation rate and RPP, indicates that NADH, rather than ADP, signals tissue hypoxia. Moreover, the study suggests that the O2 gradient from capillary to cell is larger than that from cytosol to mitochondria.
组织肌红蛋白的1H核磁共振（NMR）信号为在室温下测定生理盐水灌注心肌中的临界氧水平提供了契机。在细胞内氧分压高于4 mmHg时，心肌未表现出缺氧迹象。在4 mmHg时，心率血压乘积（RPP）降低，通过酶法测定的乳酸生成速率增加。然而，直到细胞氧分压达到2 mmHg之前，氧消耗和磷酸肌酸水平的31P-NMR信号仍保持相对恒定。只有当细胞氧分压达到0.8 mmHg时，ATP信号强度才会下降，而pH值在7.2时保持不变。细胞对氧限制的反应具有顺序性，从乳酸生成速率和RPP的改变开始，这表明是NADH而非ADP发出组织缺氧信号。此外，该研究表明从毛细血管到细胞的氧梯度大于从细胞质到线粒体的氧梯度。
