卵清蛋白刺激对致敏豚鼠肺动脉内皮反应性的影响

B.S. Uydeş-Doǧan, F. Akar, H. Zengil, N. Abacioǧlu, İ. Kanzik
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引用次数: 4

摘要

摘要:一般已经证明,致敏过程和/或特异性抗原刺激导致气道平滑肌制剂对收缩激动剂的反应性增加。然而,没有报道阐明血管制剂中的这种修饰。在这项研究中,我们研究了卵清蛋白致敏和激发对豚鼠肺动脉对各种血管活性药物的反应性的影响。在第1、3和5天,用i p注射卵清蛋白(10 mg/kg)给豚鼠积极致敏。从末次注射后第21天开始,分别在体外和体内注射卵清蛋白。研究了致敏过程和刺激对豚鼠肺动脉内皮依赖性和非依赖性反应的影响。卵清蛋白激发而非致敏过程显著降低了内皮依赖的乙酰胆碱和组胺松弛反应。在钙离子载体a23187的反应中也观察到类似的减少。然而,在对三硝酸甘油和氯化钾的反应中没有观察到任何改变,这排除了致敏和刺激后肺动脉平滑肌松弛和收缩能力的异常。此外,与凝血素类似物u46619不同,在卵清蛋白致敏和激发后,苯肾上腺素的收缩作用增强,氯化钾诱导收缩。用肥大细胞稳定剂甘糖二钠而非自由基清除剂超氧化物歧化酶培养致敏动脉,可以保护对内皮依赖性血管扩张剂的反应性降低。我们得出结论,卵清蛋白激发引起肺血管内皮细胞反应性异常,可能是由于肥大细胞释放的破坏性酶所致。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effect of Ovalbumin Challenge on Endothelial Reactivity of Pulmonary Arteries from Sensitized Guinea-pigs

Summary: It has been generally demonstrated that sensitization process and/or specific antigen challenge causes an increase in the responsiveness of airway smooth muscle preparations to contractile agonists. However, there is no report elucidating such modifications in vascular preparations. In this study, we examined the influence of ovalbumin sensitization and challenge on the reactivity of guinea-pig pulmonary arteries to various vasoactive agents. Guinea-pigs were actively sensitized to ovalbumin (10 mg/kg) by i p injections on days 1, 3 and 5. Beginning 21 days after the last injection, animals were challenged with ovalbumin either in vitro or in vivo. The effects of sensitization process and challenge were studied on endothelium-dependent and -independent responses of guinea-pig pulmonary arteries.

Ovalbumin challenge but not sensitization process significantly reduced the endothelium-dependent relaxant responses to acetylcholine and histamine. Similar reductions were also observed in the responses of calcium ionophore, A 23187. However, no alteration was observed in the responses to glyceryl trinitrate and potassium chloride which excludes an abnormality in the relaxant and contractile capacities of pulmonary artery smooth muscle following sensitization and challenge. In addition, an enhancement was observed in the contractile effect of phenylephrine after ovalbumin sensitization and challenge different from U 46619, a thromboxane analogue, and potassium chloride induced contractions. Incubation of the sensitized arteries with the mast cell stabilizer, disodium cromoglycate but not with the free radical scavenger superoxide dismutase protected the reduced responsiveness to endothelium-dependent vasodilators following challenge.

We conclude that ovalbumin challenge causes an abnormality in endothelial cell reactivity of pulmonary vasculature possibly due to destructive enzymes released from mast cells.

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