Zhu N, Weiss H R
University of Medicine and Dentistry of New Jersey/Robert Wood Johnson Medical School, Department of Physiology and Biophysics, Piscataway 08854, USA.
Microvasc Res. 1995 May;49(3):253-67. doi: 10.1006/mvre.1995.1022.
The hypothesis tested was that myocardial venous O2 saturation (SvO2) heterogeneity, a measure of microregional O2 supply/consumption balance, would increase under hypoxic and CO-hypoxia conditions. Since we are able to determine both O2 supply and the O2 supply/consumption ratio, we could also determine whether regional myocardial O2 consumption was heterogeneous. Twenty open-chest anesthetized dogs were studied under control and four hypoxic conditions, hypoxic hypoxia induced by ventilation with either an 8% O2 (SaO2 = 56%) or a 6% O2 (SaO2 = 40%) gas mixture for 20 min, or CO hypoxia induced by ventilation with a 1% CO gas mixture for either 7 min (SaO2 = 67%) or 20 min (SaO2 = 40%). Regional myocardial blood flow was measured using radioactive microspheres in 40 pieces (approximately 0.5 g) of the left ventricular free wall. Arterial and venous O2 saturations were determined with a four-wavelength microspectrophotometric method. A total of 28 veins (20-100 microns) were examined to determine SvO2 for each condition within each animal. The coefficient of variation (CV = SD/mean x 100), an index of heterogeneity, was calculated for both flow and SvO2 under each condition. Flow increased with increasing severity of hypoxia but its heterogeneity did not change with hypoxic or CO hypoxia. However, SvO2 heterogeneity significantly increased with increasing severity of hypoxia. A linear regression of SvO2 CV and mean SvO2 showed a significant correlation (CV = -0.84 (mean SvO2) + 51.1, R = 0.59). All possible myocardial O2 consumptions were calculated by multiplying all of the flows and O2 extractions. In 53 subepicardial and subendocardial measurements, only 10% of the flow and O2 supply/consumption heterogeneity observations could be explained by uniform O2 consumption if our acceptance criterion was 0.06-0.1 ml O2/min/100 g, and 50% could be explained with an acceptance criterion of 0.3-0.4 ml O2/min/100 g. Therefore, there must be some regional myocardial O2 consumption heterogeneity. The increase in venous O2 saturation heterogeneity during hypoxia may be due to increased variation in regional myocardial O2 consumption or variation in the control of O2 supply/consumption coupling.
所检验的假设是，作为微区域氧供应/消耗平衡指标的心肌静脉血氧饱和度（SvO2）异质性在缺氧和一氧化碳缺氧条件下会增加。由于我们能够测定氧供应以及氧供应/消耗比率，因此我们也能够确定局部心肌氧消耗是否存在异质性。对20只开胸麻醉犬在对照及四种缺氧条件下进行了研究，这四种缺氧条件分别为：用含8%氧气（动脉血氧饱和度[SaO2]=56%）或6%氧气（SaO2=40%）的混合气体通气20分钟诱导的低氧性缺氧，或用含1%一氧化碳的混合气体通气7分钟（SaO2=67%）或20分钟（SaO2=40%）诱导的一氧化碳缺氧。使用放射性微球测量左心室游离壁40个组织块（约0.5克）的局部心肌血流量。采用四波长显微分光光度法测定动脉和静脉血氧饱和度。检查每只动物每种条件下总共28条静脉（20 - 100微米）以确定SvO2。计算每种条件下血流量和SvO2的变异系数（CV =标准差/平均值×100），作为异质性指标。血流量随缺氧严重程度增加而增加，但其异质性并不随缺氧或一氧化碳缺氧而改变。然而，SvO2异质性随缺氧严重程度增加而显著增加。SvO2变异系数与平均SvO2的线性回归显示出显著相关性（CV = -0.84（平均SvO2）+ 51.1，R = 0.59）。通过将所有血流量和氧摄取量相乘计算所有可能的心肌氧消耗量。在53次心外膜下和心内膜下测量中，如果我们的接受标准为0.06 - 0.1毫升氧/分钟/100克，则只有10%的血流量和氧供应/消耗异质性观察结果可以用均匀的氧消耗来解释，而如果接受标准为0.3 - 0.4毫升氧/分钟/100克，则50%可以得到解释。因此，必然存在一些局部心肌氧消耗异质性。缺氧期间静脉血氧饱和度异质性的增加可能是由于局部心肌氧消耗变化增加或氧供应/消耗耦合控制的变化所致。
