Kupriyanov V V, Shaw R A, Xiang B, Mantsch H, Deslauriers R
Institute for Biodiagnostics, National Research Council of Canada, Winnipeg, MB, Canada.
J Mol Cell Cardiol. 1997 Sep;29(9):2431-9. doi: 10.1006/jmcc.1997.0478.
Intracellular pO2 in cardiac muscle is determined by the balance between its diffusion from vascular (VS) to intracellular space (IS) and uptake by mitochondria. Cessation of mechanical work decreases O2 demand and should reduce the O2 gradient between VS and IS. In this work, the effects of arterial pO2 (pO2a) on myoglobin (Mb) oxygenation, O2 uptake and lactate formation rates [V(O2) and V(Lac), micromol/min/g wet weight, respectively] in beating and KCl-arrested pig hearts were compared. pO2a was decreased stepwise (five steps, 10 min/step) from 528+/-24 to 54+/-19 mmHg by changing the ratio of O2/CO2 (95:5%) to N2/CO2 (95:5%) in the gas mixture from 100/0 through 50/50, 25/75, 10/90 to 0/100. While recording mechanical function, visible/near-infrared (near-IR) spectra (400-2500 nm) were acquired from the left ventricular wall every 45 s (32 scans) using a fiber-optic light guide connected to an NIRSystems spectrometer. Relative MbO2 in the epicardium + midmural layer and the epicardium was estimated from absorbance changes (second derivative) at 764 and 584 nm, respectively. In beating hearts, a decrease in pO2a resulted in a decrease in MbO2 (similar in both layers) and V(O2) (from 1.26+/-0.15 to 0.22+/-0.10) and an increase in V(Lac) from 0 to 2.43+/-0.76. In arrested hearts an increase in V(Lac) (0.55+/-0.24) was observed only at the lowest pO2a and the Mb oxygenation curve was shifted towards lower vascular pO2 [(pO2a+pO2v)/2] by ;160 mmHg. Oxygen consumption (oxygen flux) correlated linearly with calculated values of the oxygen gradients between the vascular and cytoplasmic spaces in both beating and arrested hearts. However, the diffusion rate constant was 3.5 times lower in arrested hearts.
(1) hypoxia in KCl-arrested hearts results in only moderate activation of anaerobic glycolysis; (2) oxygenation of the epicardial and midmural LV layers is similar; and (3) a large pO2 gradient exists between VS and IS in beating and arrested crystalloid-perfused hearts.
心肌细胞内的氧分压取决于其从血管空间（VS）扩散到细胞内空间（IS）与被线粒体摄取之间的平衡。机械活动停止会降低氧气需求，并应减小VS和IS之间的氧梯度。在本研究中，比较了动脉氧分压（pO2a）对跳动的和氯化钾停搏的猪心脏中肌红蛋白（Mb）氧合、氧气摄取率和乳酸生成率[分别为V（O2）和V（Lac），微摩尔/分钟/克湿重]的影响。通过将混合气体中O2/CO2（95:5%）与N2/CO2（95:5%）的比例从100/0逐步（分五步，每步10分钟）改变为50/50、25/75、10/90至0/100，将pO2a从528±24 mmHg逐步降低至54±19 mmHg。在记录机械功能的同时，每隔45秒（32次扫描）使用连接到NIRSystems光谱仪的光纤光导从左心室壁获取可见/近红外（近红外）光谱（400 - 2500 nm）。分别根据764和584 nm处的吸光度变化（二阶导数）估算心外膜 + 中层和心外膜中的相对MbO2。在跳动的心脏中，pO2a降低导致MbO2降低（两层相似）以及V（O2）降低（从1.26±0.15降至0.22±0.10），V（Lac）从0增加至2.43±0.76。在停搏的心脏中，仅在最低的pO2a时观察到V（Lac）增加（0.55±0.24），并且Mb氧合曲线向较低的血管氧分压[（pO2a + pO2v）/2]方向偏移约160 mmHg。在跳动的和停搏的心脏中，氧消耗（氧通量）与血管和细胞质空间之间的氧梯度计算值呈线性相关。然而，停搏心脏中的扩散速率常数低3.5倍。
（1）氯化钾停搏心脏中的缺氧仅导致无氧糖酵解的适度激活；（2）心外膜和左心室中层的氧合相似；（3）在跳动的和停搏的晶体灌注心脏中，VS和IS之间存在较大的氧分压梯度。
