Maginniss L A, Szewczak J M, Troup C M
Environ Health Perspect. 1987 Jun;72:35-8. doi: 10.1289/ehp.877235.
Whole blood oxygen equilibrium curves (O2 ECs), blood buffer lines, and several hematologic properties were determined for adult guinea pigs exposed to 700 ppm methyl isocyanate (MIC) for 15 min. MIC inhalation effected a significant reduction of blood O2 affinity; the half-saturation pressure (P50) at 38 degrees C increased from the control (untreated) level of 22.8 +/- 0.1 mm Hg to values ranging from 28.5 to 43.7 mm Hg for experimental animals. MIC exposure had no apparent influence on O2 EC shape or CO2 Bohr effect. Erythrocyte volume, [metHb], O2 binding capacity, and combined red cell organic phosphate concentration (DPG + ATP) were not affected by MIC treatment. However, experimental animals experienced a severe metabolic acid-base disturbance; blood lactate concentration ranged from 8.6 to 24.0 mmole/L. Results indicate that lactic acidosis was solely responsible for increased blood P50 of MIC-treated animals. No direct effects of MIC on hemoglobin function were observed. Reduced Hb-O2 affinity, in conjunction with severe hypoxemia, compromised the guinea pigs' capacity for pulmonary O2 loading; at PaO2 of 30 mm Hg, Hb-O2 saturation (S) decreased from 66% S for controls to 42% S for MIC-treated animals.
对暴露于700 ppm异氰酸甲酯(MIC)15分钟的成年豚鼠测定了全血氧平衡曲线(O2 ECs)、血液缓冲线和若干血液学特性。吸入MIC导致血液O2亲和力显著降低;38℃时的半饱和压力(P50)从对照(未处理)水平的22.8±0.1 mmHg升高至实验动物的28.5至43.7 mmHg。暴露于MIC对O2 EC形状或CO2波尔效应没有明显影响。红细胞体积、[高铁血红蛋白]、O2结合能力和红细胞有机磷酸盐联合浓度(DPG + ATP)不受MIC处理的影响。然而,实验动物出现了严重的代谢性酸碱紊乱;血液乳酸浓度范围为8.6至24.0 mmol/L。结果表明,乳酸酸中毒是MIC处理动物血液P50升高的唯一原因。未观察到MIC对血红蛋白功能的直接影响。Hb-O2亲和力降低,加上严重低氧血症,损害了豚鼠的肺O2加载能力;在PaO2为30 mmHg时,Hb-O2饱和度(S)从对照的66% S降至MIC处理动物的42% S。