光气急性染毒大鼠的血液流变学变化
Changes in hemorheology of rats with acute phosgene exposure
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摘要:
目的 探讨光气染毒对大鼠血液流变学指标的影响。
方法 将健康成年雄性SD大鼠随机分为对照组、光气染毒组，每个时间点6只，每组共30只。将大鼠置于染毒箱内，对照组吸入空气5 min，染毒组吸入浓度为8.33 mg/L的光气5 min。在染毒后1、3、6、12、24 h，将大鼠用质量分数为20%的乌拉坦腹腔注射麻醉后，采集血液样本，进行血常规、血气分析及血液流变学相关指标检测。
结果 染毒组大鼠吸入光气3 h后，动脉氧分压和氧合指数出现明显下降，6 h后时达到最低点，分别为58.67、202.30 mmHg（1 mmHg=0.133 kPa），此时氧分压达临床呼吸衰竭标准（ < 60 mmHg）；氧合指数达到急性肺损伤诊断标准（ < 300 mmHg），接近急性呼吸窘迫综合征诊断标准（ < 200 mmHg）。同对照组相比，染毒组大鼠的二氧化碳分压在各个时间点均升高，pH值的变化与氧分压和氧合指数的变化大致相同。染毒组大鼠的红细胞计数在1、3 h时明显低于对照组（P < 0.01），6、12 h时与对照组无明显差异，在24 h时再次低于对照组（P < 0.05）；红细胞压积在各时间点均有升高，且在6、12 h与对照组的差异有统计学意义（P < 0.01）；血小板在各时间点均较对照组有明显降低（P < 0.05）。染毒组大鼠在不同切变率下的全血黏度均较在对照组有所升高，特别是在6 h时，除切变率为10 s-1外，其余切变率下二者的差异均有统计学意义（P < 0.01）。在1 h时，染毒组大鼠的血浆黏度有明显的升高，之后逐渐下降，在24 h时与对照组相比差异无统计学意义。染毒组大鼠的红细胞最大变形指数在1 h时已出现明显降低，12 h时达到最低值，24 h时略有回升。
结论 光气染毒可导致大鼠出现急性肺损伤及明显的血液流变学异常。
Abstract:Objective To investigate the effects of phosgene exposure on hemorheological in dicators of rats. Methods Health adult male SD rats were randomized into a control group (n=30) and a phosgene exposure group (n=30). Blood samples of rats were collected at 1, 3, 6, 12, and 24 h after 5-min air or phosgene (8.33 mg/L) inhalation and after intraperitoneal in jection with 20% urethane anesthesia. Routine blood test, blood gas analysis, and hemorheological indicator detection were performed.
Results The levels of arterial oxygen partial pressure and oxygenation index decreased at 3 h after phosgene inhalation and reached bottom at 6 h, being 58.67 and 202.30 mmHg (1 mmHg=0.133 kPa), respectively. The arterial oxygen partial pressure at 6 h reached the clinical standard of respiratory failure ( < 60 mmHg); the oxygenation index at 6 h reached the diagnostic criteria for acute lu ng injury ( < 300 mmHg) and was close to the diagnostic criteria for acute respiratory distress syndrome ( < 200 mmHg). Compared with the control group, the exposure group showed elevated partial pressure of carbon dioxide at each designed time point, and the trend of pH was aligned with oxygen partial pressure and oxygenation index. The red blood cell counts at 1, 3, and 24h were lower in the exposure group than in the control group (P < 0.01 or P < 0.05), except 6 and 12 h. Packed cell volume was increased in the exposure group and showed statistical differences at 6 and 12 h compared with the control group (P < 0.01). Platelet count was decreased in the exposure group at all time points (P < 0.05). In addition, the rats administered with phosgene showed higher whole blood viscosity than the control group at varied shear rates, especially at 6 h, and except the shear rate of 10 s-1, the whole blood viscosity at other shear rates showed statistical differences between the two groups (P < 0.01). The plasma viscosity of the exposure group was increased at 1h, then decreased, and no difference was found at 24h compared with the control group. The maximum erythrocyte deformability index of the exposure group was obviously decreased from 1h, reached bottom at 12, but rebounded slightly at 24h.
Conclusion Phosgene can induce acute lung injury and significant changes in hemorheological indicators in rats.
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