Islami Hilmi, Ilazi Ali, Gashi Nijazi, Mustafa Lirim, Maloku Halit, Jashanica Adelina
Department of Pharmacology, Faculty of Medicine, University of Prishtina, Clinical Centre, Prishtina, Kosova.
Kosovo Occupationnal Health Institute, Clinical Centre, Gjakova, Kosova.
Acta Inform Med. 2014 Apr;22(2):107-10. doi: 10.5455/aim.2014.22.107-110.
In this paper, effect of the Tolazoline as antagonist of the alpha-2 adrenergic receptors in patients with bronchial asthma and chronic obstructive bronchitis was studied, and also the effect of stimulation with Hexoprenaline of beta-2 adrenergic receptor after bronchi-constriction caused with Propranolol, and Acetylcholine.
Lung function parameters are determined with Body plethysmography. In patients with bronchial asthma and chronic obstructive bronchitis was registered resistance (Raw), was determined the amount of intrathoracic gas volume (ITGV), and specific resistance was calculated as well (SRaw). Aerosolization was done with standard aerosolizing machine-Asema.
The study included a total of 21 patients. Two hours after the inhalation of Propranolol, in experimental group, it was applied the blocker of alpha-2 adrenergic receptors (Tolazoline 20 mg / ml with inhalator ways), which did not cause changes in bronchomotor tonus of tracheobronchial system (p > 1.0). Meanwhile, at the same patient, stimulation of beta-2 adrenergic receptor with Hexoprenaline (2 inh x 0.2 mg) is associated with a significant decrease of the specific resistance of airways (SRaw, p < 0.01). Control group results show that after bronchi-constriction caused by Propranolol-aerosol (20 mg / ml) in patients with bronchial asthma and chronic obstructive bronchitis, an increase of specific resistance in airways was caused (SRaw, p < 0.01), which confirms the presence of hyper-reactive bronco-constrictor effects intermediated by vagal ways. Two hours after Propranolol, inhaled Hexorenaline has blocked the action of Propranolol, but not entirely. Furthermore, two hours after acetylcholine-aerosol (1 mg /ml) was applied, inhaled Ipratropium (2 inh x 1 mg) has fully blocked the action of chemical bronchoconstrictor mediators, causing a decline of specific resistance in the airways (SRaw; p < 0.01).
This suggests that primary mechanism, which would cause reaction in patients with increased bronchial reactibility, is prevalence of the cholinergic system over adrenergic one, and not the relationship in between alpha-2 and beta-2 adrenergic receptors.
本文研究了妥拉唑啉作为α-2肾上腺素能受体拮抗剂对支气管哮喘和慢性阻塞性支气管炎患者的影响，以及在普萘洛尔和乙酰胆碱引起支气管收缩后，用海索那林刺激β-2肾上腺素能受体的效果。
用体容积描记法测定肺功能参数。记录支气管哮喘和慢性阻塞性支气管炎患者的气道阻力（Raw），测定胸腔内气体容积（ITGV），并计算比气道阻力（SRaw）。使用标准雾化器Asema进行雾化。
本研究共纳入21例患者。在吸入普萘洛尔两小时后，在实验组应用α-2肾上腺素能受体阻滞剂（妥拉唑啉20mg/ml，经吸入途径），未引起气管支气管系统支气管运动张力的变化（p>1.0）。同时，在同一患者中，用海索那林（2次吸入，每次0.2mg）刺激β-2肾上腺素能受体与气道比气道阻力显著降低相关（SRaw，p<0.01）。对照组结果显示，在支气管哮喘和慢性阻塞性支气管炎患者中，普萘洛尔气雾剂（20mg/ml）引起支气管收缩后，气道比气道阻力增加（SRaw，p<0.01），这证实了存在由迷走神经途径介导的高反应性支气管收缩效应。普萘洛尔两小时后，吸入海索那林可阻断普萘洛尔的作用，但不完全。此外，在应用乙酰胆碱气雾剂（1mg/ml）两小时后，吸入异丙托溴铵（2次吸入，每次1mg）可完全阻断化学性支气管收缩介质的作用，导致气道比气道阻力下降（SRaw；p<0.01）。
这表明，导致支气管反应性增加患者出现反应的主要机制是胆碱能系统相对于肾上腺素能系统占优势，而非α-2和β-2肾上腺素能受体之间的关系。
