Falkay G, Török I, Kovács L
Department of Obstetrics and Gynaecology, University Medical School of Szeged, Hungary.
Acta Physiol Hung. 1988;71(4):503-6.
The foetal lung responds to beta-receptor agonists with a release of surfactant from alveolar cells. The aim of the present study was to investigate whether the administration of the betamimetic fenoterol could influence the desensitization - associated decrease of beta-adrenoreceptors in the rabbit foetal lung. With experiments on pregnant rabbits, this hypothesis was put to the test and found to be true. At a gestational age of 27-28 days, does were infused 7.5-10.0 mg of fenoterol or given Ringer's solution. The does and foetuses were sacrificed at 12 hours from the start of the infusion, and the number and affinity of beta-adrenergic receptors in lung tissues were determined by a direct binding technique using 3H-dihydroprenolol. These studies show that fenoterol can induce desensitization of beta-receptors in the foetal lung but not in the doe. Thus, it is concluded that desensitization of foetal pulmonary adrenoreceptors may result in diminished lung function after long-term treatment with beta-2 sympathicomimetics.
胎儿肺对β受体激动剂的反应是肺泡细胞释放表面活性物质。本研究的目的是调查β拟交感神经药非诺特罗的给药是否会影响兔胎儿肺中与脱敏相关的β肾上腺素能受体的减少。通过对怀孕兔子进行实验，对这一假设进行了检验，结果发现该假设是正确的。在妊娠27 - 28天时，给母兔输注7.5 - 10.0毫克非诺特罗或给予林格氏液。在输注开始12小时后处死母兔和胎儿，使用3H - 二氢普萘洛尔通过直接结合技术测定肺组织中β肾上腺素能受体的数量和亲和力。这些研究表明，非诺特罗可诱导胎儿肺中的β受体脱敏，但不会使母兔的β受体脱敏。因此，得出结论，长期使用β2拟交感神经药治疗后，胎儿肺肾上腺素能受体的脱敏可能导致肺功能下降。
