de Groot B, Zuurbier C J, van Beek J H
Laboratory for Physiology, Institute for Cardiovascular Research, Vrije Universiteit, 1081 BT Amsterdam, The Netherlands.
Am J Physiol. 1999 May;276(5):H1616-24. doi: 10.1152/ajpheart.1999.276.5.H1616.
We investigated the role of myoglobin (Mb) in supplying O2 to mitochondria during transitions in cardiac workload. Isovolumic rabbit hearts (n = 7) were perfused retrogradely with hemoglobin-free Tyrode solution at 37 degrees C. Coronary venous O2 tension was measured polarographically, and tissue oxygenation was measured with two-wavelength near-infrared spectroscopy (NIRS), both at a time resolution of approximately 2 s. During transitions to anoxia, 68 +/- 2% (SE) of the NIRS signal was due to Mb and the rest to cytochrome oxidase. For heart rate steps from 120 to 190 or 220 beats/min, the NIRS signal decreased significantly by 6.9 +/- 1.3 or 11.1 +/- 2.1% of the full scale, respectively, with response times of 11.0 +/- 0.8 or 9.1 +/- 0.5 s, respectively. The response time of end-capillary O2 concentration ([O2]), estimated from the venous [O2], was 8.6 +/- 0.8 s for 190 beats/min (P < 0.05 vs. NIRS time) or 8.5 +/- 0.9 s for 220 beats/min (P > 0.05). The mean response times of mitochondrial O2 consumption (VO2) were 3.7 +/- 0.7 and 3.6 +/- 0.6 s, respectively. The deoxygenation of oxymyoglobin (MbO2) accounted for only 12-13% of the total decrease in tissue O2, with the rest being physically dissolved O2. During 11% reductions in perfusion flow at 220 beats/min, Mb was 1.5 +/- 0.4% deoxygenated (P < 0.05), despite the high venous PO2 of 377 +/- 17 mmHg, indicating metabolism-perfusion mismatch. We conclude that the contribution of MbO2 to the increase of VO2 during heart rate steps in saline-perfused hearts was small and slow compared with that of physically dissolved O2.
我们研究了肌红蛋白（Mb）在心脏工作负荷转变过程中向线粒体供应氧气的作用。在37℃下，用不含血红蛋白的台氏液逆行灌注等容的兔心脏（n = 7）。用极谱法测量冠状静脉血氧张力，并用双波长近红外光谱法（NIRS）测量组织氧合，时间分辨率均约为2秒。在转变为缺氧状态时，NIRS信号的68±2%（标准误）归因于Mb，其余归因于细胞色素氧化酶。对于心率从120次/分钟升至190或220次/分钟的情况，NIRS信号分别显著下降了满量程的6.9±1.3%或11.1±2.1%，响应时间分别为11.0±0.8秒或9.1±0.5秒。根据静脉血氧浓度（[O2]）估算的毛细血管末端血氧浓度（[O2]）的响应时间，对于190次/分钟为8.6±0.8秒（与NIRS时间相比，P < 0.05），对于220次/分钟为8.5±0.9秒（P > 0.05）。线粒体氧消耗（VO2）的平均响应时间分别为3.7±0.7秒和3.6±0.6秒。氧合肌红蛋白（MbO2）的脱氧仅占组织氧总减少量的12 - 13%，其余为物理溶解氧。在220次/分钟时灌注流量降低11%的过程中，尽管静脉血氧分压高达377±17 mmHg，但Mb的脱氧率为1.5±0.4%（P < 0.05），表明存在代谢 - 灌注不匹配。我们得出结论，在生理盐水灌注的心脏中，心率增加时MbO2对VO2增加的贡献与物理溶解氧相比小且缓慢。
