Eyre P, Gaviller P, Thorsen J
Res Commun Chem Pathol Pharmacol. 1982 Jul;37(1):3-10.
Groups of guinea-pigs were vaccinated with equine influenza A-1 virus and helically-cut tracheal strips were subsequently contracted to carbachol (EC50) and relaxed to isoprenaline at 3, 5 and 10 days post-vaccination. Tracheas from another group were contracted to phenylephrine in the presence of propranolol. Compared to controls, responses to isoprenaline in virus-infected tracheas were significantly potentiated at days 3 and 10. Virus infection significantly inhibited tracheal responsiveness to phenylephrine. It appears that enhancement of isoprenaline may be caused by diminished reactivity of the alpha-adrenoceptor system, thus promoting airway dilatation caused by the beta-adrenoceptor agonist.
将豚鼠分组，用甲型马流感病毒进行疫苗接种，随后在接种疫苗后第3、5和10天，将螺旋切割的气管条与卡巴胆碱（EC50）收缩，并与异丙肾上腺素舒张。另一组气管在普萘洛尔存在的情况下与去氧肾上腺素收缩。与对照组相比，病毒感染的气管在第3天和第10天对异丙肾上腺素的反应显著增强。病毒感染显著抑制气管对去氧肾上腺素的反应性。异丙肾上腺素的增强作用似乎可能是由α-肾上腺素能受体系统反应性降低引起的，从而促进β-肾上腺素能受体激动剂引起的气道扩张。
