Pathophysiology of specific bronchial hyperresponsiveness

1.乙醇引起的豚鼠支气管收缩(1)乙醇的代谢产物乙醛引起支气管收缩，而乙醇不引起。(2)乙醛引起的支气管收缩是通过组胺释放介导的。(3)低剂量的乙醛不引起支气管收缩，但增强非特异性的支气管反应性。(4)血栓素A2参与了乙醛诱导的非特异性支气管高反应性。心得安诱发支气管收缩的豚鼠大模型及自主神经系统、化学介质和神经肽的作用(1)被动致敏的豚鼠吸入心得安后20分钟吸入心得安引起支气管收缩。这是第一个心得安引起的支气管收缩的动物模型。(2)副病理性或α-肾上腺素能神经活动不参与这种反应。(3)P物质和神经激肽A等神经肽不参与这种…。更多的反应。(4)脂质介质，尤其是血栓素A2，在这种反应中起着重要作用。一种非超声雾化蒸馏水诱导的豚鼠支气管收缩模型及自主神经系统、化学介质和神经肽的作用(1)吸入蒸馏水在被动致敏的豚鼠雾化抗原激发20分钟后吸入，可产生急性支气管收缩。这是第一个雾化吸入蒸馏水引起的支气管收缩的动物模型。(2)副交感神经活动不参与这种反应。(3)组胺和P物质，而不是神经激动素A，在这种反应中起很大作用。(4)血栓素A2在这种反应中没有作用。结论上述结果提示过敏性气道反应或过敏性气道炎症过程在特异性支气管反应性的形成中起重要作用。此外，特异性支气管高反应性的机制可能彼此不同，提示哮喘中几种特异性支气管高反应性的致病因素是不同的。较少

1. Alcohol-induced bronchoconstriction in guinea pigs(1) Acetaldehyde, a metabolite of ethanol, causes bronchoconstriction but ethanol does not.(2) The acetaldehyde-induced bronchoconstriction is mediated via histamine release.(3) A low dose of acetaldehyde, which does not cause bronchoconstriction, enhances non-specific bronchial responsiveness.(4) Thromboxane A2 is involved in the acetaldehyde-induced non-specific bronchial hyperresponsiveness.2. A guinea big model of propranolol-induced bronchoconstriction and the role of autonomic nerve system, chemical mediators and neuropeptides(1) An inhalation of propranolo causes bronchoconstriction when it is inhaled 20 minutes after an aerosolized antigen provocation in passively sensitized guinea pigs.This is the first animal model or propranolol-induced bronchoconstriction.(2) Parasympathctic or alpha-adrenergic nerve activity is not involved in this response.(3) Ncuropeptides such as substance P and neurokinin A do not take a part in this … More response.(4) Lipid mediators, especially thromboxane A2, have an important role in this response.3. A guinea-pig model of untrasonically nebulized distillled water (UNDW) -induced bronchoconstriction and the role of autonomic nerve system, chemical mediators and neuropeptides(1) An inhalation of UNDW produces acute bronchoconstriction when it is inhaled 20 mimutes after an aerosolized antigen provocation in passively sensitized guinea pigs.This is the first animal model of UNDW-induced bronchoconstriction.(2) Parasympathetic nerve activity is not involved in this response.(3) Histamine and substance P,but not neurokinin A,take a large part in this response.(4) Thromboxane A2 does not have a role in this response.4. ConclusionForm these results, it is suggested that allergic airway response, or allergic airway inflammatory process, is important in development of specific bronchial responsiveness. Furthermore, the mechanism of specific bronchial hyperresponsiveness may be different each other, suggesting heterogeneity of contributing factors between several specific bronchial hyperresponsiveness in asthma. Less