Localization of quantitative changes in pulmonary beta-receptors in ovalbumin-sensitized guinea pigs.

Localization of quantitative changes in pulmonary beta-receptors in ovalbumin-sensitized guinea pigs.
复制标题

卵清蛋白致敏豚鼠肺β受体定量变化的定位。

DOI:
10.1164/ajrccm/136.1.150
复制
发表时间:
1987
期刊:
The American review of respiratory disease
影响因子:
--
通讯作者:
Johnson,DE
Johnson,DE
中科院分区:
--
文献类型:
--
作者:
Gatto,C;Green,TP;Johnson,MG;Marchessault,RP;Seybold,V;Johnson,DE

文献摘要

被引文献

相似文献

~受体功能受损被认为是哮喘患者气道高反应性的一个因素。尽管许多间接研究对这一理论提出了质疑,但这些先前的研究都无法直接测量能够影响这种疾病状态下所见的生理变化的肺内结构上ii受体数量的变化。为了帮助明确肺内变化的位置,我们在实验前2周通过腹腔给卵清蛋白致敏来制备过敏性支气管收缩模型(S组)。第二组动物对卵清蛋白致敏,然后2周后部分脱敏(D组),在4至6周的时间内反复暴露于不断增加剂量的雾化卵清蛋白和肾上腺素救援。对照动物单独给予ip和雾化生理盐水。肺功能容积描图显示,暴露于卵清蛋白雾化后,S组气道阻力增加至对照组的294±42%(p< 0.005),动态顺应性下降至对照组的76±8% (p< 0.002), S组为39±10% (p< 0.002)。使用L-[HI]二氢阿普萘洛尔([HI] DHA),对3组肺切片的3-受体进行放射自定位和定量。卵清蛋白暴露动物肺泡和导气管上皮、细支气管和血管平滑肌中'H-DHA结合显著降低(p< 0.02)。观察到~受体密度降低的结构表明,ii -肾上腺素能功能受损可能部分解释了卵清蛋白暴露豚鼠肺功能的变化,并且可能确实参与了某些类型的人类反应性气道疾病的病理生理学。我于1987年重新呼吸;136: 150 - 154
Impaired~-receptor function has been postulated as one factor contributing to airway hyperreactivity in asthmatic patients. Although numerous indirect studies have cast doubt on this theory, none of these previous investigations has been able to directly measure changes in II-receptor number on intrapulmonary structures capable of affecting the physiologic changes seen in this disease state. Tohelp clarify the intrapulmonary location of such changes, a model of allergic bronchoconstriction was prepared by sensitizing guinea pigs to ovalbumin intraperitoneally (ip) 2 wk prior to testing (Group S). A second group of animals was sensitized to ovalbumin, then 2 wk later partially desensitized (Group D) during a 4-to 6-wk period by repeated exposure to increasing doses of nebulized ovalbumin with epinephrine rescue. Control animals received ip administered and nebulized normal saline alone. Pulmonary function assessed by plethysmography revealed an increase in airway resistance to 294±42%(SE) of control in Group S (p< 0.005) and a decrease in dynamic compliance to 76±8% of control in Group D and 39±10% of control in Group S (p< 0.002) after exposure to nebulized ovalbumin. Using L-['HI dihydroalprenolol (['HI DHA),(3-receptorswere autoradiographically localized and quantitated in lung sections from all 3 groups. Significant decreases (p< 0.02) in'H-DHA binding were noted in alveolar and conducting airway epithelium, and bronchiolar and vascular smooth muscle in ovalbumin-exposed animals. The structures where decreases in~-receptor density were observed suggest that impaired II-adrenergic function could be partially accountable for the changes in pulmonary function observed in the ovalbumin-exposed guinea pigs, and may indeed be involved in the pathophysiology of certain types of reactive airway disease in humans. AM REV RESPIR DIS 1987; 136: 150-154