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目的：观察蛔虫变应原致喘豚鼠动物模型的血液流变学变化的动态变化、丰富变应原激发动物哮喘的内容。方法：把实验豚鼠随机分为阴性对照组、佐剂对照组和阳性激发组。用蛔虫变应原激发致喘豚鼠后，观察各实验组在激发哮喘后１小时、２４小时和７２小时的血液流变学变化。结果：由蛔虫变应原引起的过敏性哮喘豚鼠动物模型，其血液流变性出现异常，阳性激发组的血浆粘度分别为６，６２±０．２８，５１.４± ０．１１，４．８６± ０．２３，远高于阴性对照组（平均为 ４．５７± ０．２０）和佐剂对照组（平均为 ４．６３±０．１７），有显著性意义（Ｐ＜０．０１）；红细胞聚集指数和全血高切还原粘度也均较阴性对照组、佐剂对照组显著性升高（Ｐ＜０.０１）；而红细胞压积则无明显变化。结论：用蛔虫变应原致喘豚鼠后，血液出现高粘滞状态，进一步加剧气道局部的缺血、缺氧及炎性反应，导致气体交换障碍、肺功能降低。
OBJECTIVE: To observe the dynamic changes of hemorrheology in animal model of asthma induced by roundworm allergen, and to enrich the content of allergen-stimulated asthma in animals. Methods: Experimental guinea pigs were randomly divided into negative control group, adjuvant control group and positive stimulation group. Hemorrhagic asthmatic guinea pigs were induced by roundworm allergen, and the changes of hemorheology were observed at 1 hour, 24 hours and 72 hours after asthma stimulation in each experimental group. Results: The animal model of allergic asthma caused by Ascaris allergen showed abnormal hemorheology, and the plasma viscosity of the positive group was 6,62 ± 0.28,51.4 ± 0.11,4.86 ± 0.23, which was significantly higher than that in the negative control group (mean 4.57 ± 0.20) and adjuvant control group (average 4.63 ± 0.17) (P <0.01). Erythrocyte aggregation index and whole blood high shear reduction viscosity than the negative control group and the adjuvant control group were significantly increased (P <0.01), while the hematocrit had no significant change. CONCLUSION: The high viscosity state of blood caused by asthma caused by roundworm allergen further aggravates ischemia, hypoxia and inflammatory reaction in airways, resulting in gas exchange disorder and decreased pulmonary function.