Mautone A J, Katz Z, Scarpelli E M
Toxicol Ind Health. 1985 Oct;1(2):37-57. doi: 10.1177/074823378500100205.
We exposed 22 mongrel dogs to 94 ppm phosgene for 20 min from a non-rebreathing system. We expressed exposure to phosgene as ppm X VI X min X kg 1, i.e., the amount of gas containing a known phosgene concentration that was actually inhaled per min standardized to body weight, the "exposure index" (EI). In contrast, the conventional expression of exposure, i.e., ppm X min, fails to take volume inhaled (VI) and body weight into account. Five dogs received no intervention and served as controls. Fourteen dogs received basic therapy of oral cortisone (40 mg/kg) and NaHCO3 (3 mEq/kg) plus 100% O2 (FiO2 = 1.0) for 30 min after the exposure period. These animals were further divided according to the following selected additional therapies, which were started 30 min after exposure: Theophylline, 5 mg/kg iv for 20 min followed by 1 mg/kg/hr for 70 min (n = 5). Three dogs of this group were given a trial of 5 cm H2O expiratory resistance during the period of basic therapy. Because of the untoward response, expiratory resistance was discontinued and not used in other experiments. PGE2-hi, [1 microgram/kg/min] iv for 90 min (n = 3). PGE1-lo, [0.04 microgram/kg/min] iv for 90 min (n = 3). Atropine, 0.5 mg/kg iv at 30 and 50 min after exposure (n = 3). Three dogs [group 5] received oral cortisone and NaHCO3 plus inhaled supplementary surfactant, 2.7 mg/min ultrasonically nebulized (FiO2 = 0.5; phosphate buffer), for 30 min after exposure. All treated dogs, groups [1] through [4] and the surfactant group [5], received cortisone (40 mg/kg/hr iv), NaHCO3 to correct base deficit, and O2 to correct hypoxemia from 30 min to 120 min after exposure. Because of its clearly beneficial effect in group [1], theophylline was also given to all other treatment groups during this period. At the end of the study, all lungs were excised, examined and prepared for light microscopy. We found that EI, which varied among subjects because of spontaneous variations of VI during exposure, correlated significantly with the changes in base deficit induced by phosgene inhalation. We also found that the change in minute ventilation, delta VI X kg-1, correlated significantly with changes in lung compliance, peak flow and base deficit. Evaluation of the various therapeutic modalities revealed the following: Immediate therapy with O2 is vital and and FiO2 of 0.4 to 0.5 is sufficient.(ABSTRACT TRUNCATED AT 400 WORDS)
我们将22只杂种犬通过非重复呼吸系统暴露于浓度为94 ppm的光气中20分钟。我们用光气暴露量（ppm×VI×分钟×千克⁻¹）来表示光气暴露情况，即每分钟实际吸入的含有已知光气浓度的气体量，并根据体重进行标准化，此为“暴露指数”（EI）。相比之下，传统的暴露表达方式，即ppm×分钟，未考虑吸入体积（VI）和体重。5只犬未接受任何干预，作为对照。14只犬在暴露期后接受了口服可的松（40毫克/千克）和碳酸氢钠（3毫当量/千克）加100%氧气（FiO₂ = 1.0）的基础治疗30分钟。这些动物根据以下选定的附加治疗方法进一步分组，附加治疗在暴露后30分钟开始：茶碱，静脉注射5毫克/千克，持续20分钟，然后以1毫克/千克/小时的速度持续70分钟（n = 5）。该组中有3只犬在基础治疗期间进行了5厘米水柱呼气阻力试验。由于出现不良反应，呼气阻力试验停止，未在其他实验中使用。高剂量前列腺素E₂，静脉注射[1微克/千克/分钟]，持续90分钟（n = 3）。低剂量前列腺素E₁，静脉注射[0.04微克/千克/分钟]，持续90分钟（n = 3）。阿托品，在暴露后30分钟和50分钟时静脉注射0.5毫克/千克（n = 3）。3只犬[第5组]在暴露后接受口服可的松和碳酸氢钠加吸入补充表面活性剂治疗，通过超声雾化，剂量为2.7毫克/分钟（FiO₂ = 0.5；磷酸盐缓冲液），持续30分钟。所有接受治疗的犬，即第[1]组至第[4]组以及表面活性剂组[5]，在暴露后30分钟至120分钟期间接受可的松（40毫克/千克/小时静脉注射）、用于纠正碱缺失的碳酸氢钠以及用于纠正低氧血症的氧气治疗。由于茶碱在第[1]组中具有明显的有益效果，在此期间所有其他治疗组也给予了茶碱。在研究结束时，切除所有肺部，进行检查并制备用于光镜检查。我们发现，由于暴露期间VI的自发变化，不同个体的EI有所不同，EI与光气吸入引起的碱缺失变化显著相关。我们还发现，分钟通气量的变化，即δVI×千克⁻¹，与肺顺应性、峰值流量和碱缺失的变化显著相关。对各种治疗方式的评估结果如下：立即给予氧气治疗至关重要，FiO₂为0.4至0.5就足够了。（摘要截取自400字）
