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儿茶酚胺在流感嗜血杆菌诱导的β-肾上腺素能受体功能降低中的作用。

Involvement of catecholamines in Haemophilus influenzae induced decrease of beta-adrenoceptor function.

作者信息

Schreurs A J, Versteeg D H, Nijkamp F P

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1982 Sep;320(3):235-9. doi: 10.1007/BF00510134.

Abstract

The deeper airways of patients with asthmatic bronchitis are often infected with Haemophilus influenzae. Vaccination of guinea pigs with H. influenzae resulted in a significant impairment of the isoproterenol induced relaxation of isolated tracheal spirals by approximately 50% 4 days following vaccination. In the present study we further investigated the effects of some drugs affecting catecholamine release on the H. influenzae induced functional desensitization of tracheal spirals. Benserazide, an inhibitor of dopa-decarboxylase, completely prevented the reduction in isoproterenol-induced relaxation after H. influenzae vaccination, while no effect on relaxation of tracheal spirals from control animals was detected. On the other hand, inhibiting the re-uptake of catecholamines with desipramine did not influence the relaxation in the H. influenzae vaccinated tracheal spirals. Treatment of control animals with desipramine however resulted in a decreased relaxation of the isolated spirals by 40%. One day following vaccination with H. influenzae the level of norepinephrine in lung tissue was significantly elevated by 71%, and in plasma by 77%, while after 4 days no significant effects were observed. The spontaneous release of norepinephrine, epinephrine and dopamine of tracheal incubates was increased at days 1 and 4 following vaccination. The release of catecholamines from minced lung incubates of H. influenzae pretreated guinea pigs did not differ from that of controls. On the basis of these results it may be suggested that catecholamine metabolism is changed in lungs from H. influenzae vaccinated animals. Catecholamines, accordingly may play a role in the desensitization of beta-adrenoceptors by H. influenzae.

摘要

哮喘性支气管炎患者的深部气道常感染流感嗜血杆菌。用流感嗜血杆菌对豚鼠进行疫苗接种后4天,异丙肾上腺素诱导的离体气管螺旋条舒张功能显著受损,幅度约为50%。在本研究中,我们进一步研究了一些影响儿茶酚胺释放的药物对流感嗜血杆菌诱导的气管螺旋条功能脱敏的作用。多巴脱羧酶抑制剂苄丝肼完全阻止了流感嗜血杆菌疫苗接种后异丙肾上腺素诱导舒张功能的降低,而对对照动物气管螺旋条的舒张功能未检测到影响。另一方面,用去甲丙咪嗪抑制儿茶酚胺的再摄取对流感嗜血杆菌疫苗接种的气管螺旋条的舒张功能没有影响。然而,用去甲丙咪嗪处理对照动物会导致离体螺旋条的舒张功能降低40%。用流感嗜血杆菌疫苗接种1天后,肺组织中去甲肾上腺素水平显著升高71%,血浆中升高77%,而4天后未观察到显著影响。接种后第1天和第4天,气管孵育物中去甲肾上腺素、肾上腺素和多巴胺的自发释放增加。流感嗜血杆菌预处理的豚鼠肺组织匀浆中儿茶酚胺的释放与对照无差异。基于这些结果,可能提示流感嗜血杆菌疫苗接种动物的肺中儿茶酚胺代谢发生了变化。因此,儿茶酚胺可能在流感嗜血杆菌引起的β-肾上腺素能受体脱敏中起作用。

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