Fedde M R, Dodd D E, Troup C M, Fowler E H
Environ Health Perspect. 1987 Jun;72:29-33. doi: 10.1289/ehp.877229.
The influence of methyl isocyanate (MIC) inhalation on the gas exchange function of the lungs in guinea pigs was studied by measuring arterial blood gases, pH, and tracheal pressure during constant-volume, artificial ventilation with air or 100% O2 at 40 and 120 min after exposure. A 15 min exposure to MIC at concentrations of 240 to 628 ppm caused a marked reduction in PaO2 and pHa and an elevated tracheal pressure during artificial ventilation. The low PaO2 was only slightly elevated when the animals were ventilated with 100% O2. Although the dry-wet lung weight ratio was reduced at the highest exposure concentration, the effect was not severe and no significant increase in lung water was found at the lower concentrations. MIC inhalation caused severe pulmonary blood shunting and ventilation/perfusion imbalance. This, in turn, led to hypoxemia, metabolic acidosis, and tissue hypoxia, which could produce death. The pulmonary gas exchange deficit likely resulted from bronchial and bronchiolar obstruction caused by sloughed epithelium and other debris from intra- and extrapulmonary airways.
通过在暴露后40分钟和120分钟时,在定容条件下用空气或100%氧气进行人工通气期间测量动脉血气、pH值和气管压力,研究了豚鼠吸入甲基异氰酸酯(MIC)对肺气体交换功能的影响。暴露于浓度为240至628 ppm的MIC 15分钟,会导致人工通气期间动脉血氧分压(PaO2)和动脉血pH值(pHa)显著降低,以及气管压力升高。当动物用100%氧气通气时,低PaO2仅略有升高。尽管在最高暴露浓度下干湿肺重量比降低,但影响并不严重,在较低浓度下未发现肺水显著增加。吸入MIC会导致严重的肺内血液分流和通气/灌注失衡。这进而导致低氧血症、代谢性酸中毒和组织缺氧,可能导致死亡。肺气体交换不足可能是由于肺内和肺外气道脱落的上皮细胞和其他碎屑引起的支气管和细支气管阻塞所致。