体内百日咳毒素治疗可降低大鼠阻力动脉的收缩，但不影响小鼠气管的收缩。

In vivo pertussis toxin treatment reduces contraction of rat resistance arteries but not that of mouse trachea.

作者信息

van Meijeren Cornelia E, Vleeming Wim, van de Kuil Ton, Manni Javotte, Kegler Diane, Hendriksen Coenraad F M, de Wildt Dick J

机构信息

National Institute for Public Health and Environment, Laboratory of Toxicology, Pathology and Genetics, P.O. Box 1, 3720 BA Bilthoven, The Netherlands.

出版信息

Eur J Pharmacol. 2004 Mar 19;488(1-3):127-35. doi: 10.1016/j.ejphar.2004.02.003.

DOI:10.1016/j.ejphar.2004.02.003

PMID:15044044

Abstract

In order to develop an in vitro method for detecting residual pertussis toxin activity in acellular pertussis vaccines, the effects of in vivo pertussis toxin treatment on contraction and relaxation properties of isolated mouse trachea and of isolated rat small mesenteric resistance arteries were studied. In vivo pertussis toxin treatment (24 or 72 microg/kg, intraperitoneally (i.p.)) did not affect contraction and relaxation properties of isolated BALB/c or NIH mouse trachea. In vivo pertussis toxin treatment (30 microg/kg, intravenously) significantly reduced noradrenaline- or KCl-induced maximal contraction and reduced sensitivity to noradrenaline in isolated male Wistar rat small mesenteric resistance arteries. However, in vivo pertussis toxin treatment did not affect relaxation properties of isolated rat small mesenteric resistance arteries. These results support the hypothesis that vasoconstriction-regulating mechanisms and not airway constriction mechanisms are involved in pertussis toxin-induced histamine sensitisation. The vasoconstriction-regulating mechanisms may provide a lead for further development of an in vitro method for measuring biologically active pertussis toxin in acellular pertussis vaccines based on mechanisms involved in the histamine sensitisation test.

摘要

为了开发一种体外检测无细胞百日咳疫苗中残留百日咳毒素活性的方法，研究了体内百日咳毒素处理对分离的小鼠气管以及分离的大鼠小肠系膜阻力动脉收缩和舒张特性的影响。体内百日咳毒素处理（24或72微克/千克，腹腔注射（i.p.））不影响分离的BALB/c或NIH小鼠气管的收缩和舒张特性。体内百日咳毒素处理（30微克/千克，静脉注射）显著降低了去甲肾上腺素或氯化钾诱导的分离雄性Wistar大鼠小肠系膜阻力动脉的最大收缩，并降低了对去甲肾上腺素的敏感性。然而，体内百日咳毒素处理不影响分离的大鼠小肠系膜阻力动脉的舒张特性。这些结果支持以下假设，即百日咳毒素诱导的组胺致敏涉及血管收缩调节机制而非气道收缩机制。血管收缩调节机制可能为基于组胺致敏试验所涉及机制进一步开发体外测量无细胞百日咳疫苗中生物活性百日咳毒素的方法提供线索。