Atzori L, Corriga A M, Congiu L
Dipartimento Tossicologia-Sez. Patologia Generale, Università degli Studi, Cagliari, Italia.
G Ital Med Lav. 1995 Jan-Nov;17(1-6):65-70.
In the present investigation a possible involvement of tachykinins during sulfur dioxide-(SO2) and metabisulfite-(MBS) induced bronchoconstriction, and paraquat (PQ)-induced mortality was studied. SO2 (250ppm) inhalation and MBS (3mM) perfusion induced a marked decrease of compliance and conductance in the isolated and perfused lung. SO2-induced bronchoconstriction was associated with release of Calcitonin Gene Related Peptide, suggesting activation of capsaicin sensitive sensory nerves. Pretreatment of animals with capsaicin, in order to deplete the tachykinin content of sensory nerves, significantly reduced SO2- and MBS-induced bronchoconstriction. PQ (25mg/Kg) treatment induced high mortality (75%) after 3 weeks. Pretreatment with capsaicin significantly protected versus PQ induced mortality (25%). The results suggest that tachykinin content in the respiratory airways participate to SO2- and MBS-induced bronchoconstriction and PQ mortality.
在本研究中,研究了速激肽在二氧化硫(SO2)和焦亚硫酸盐(MBS)诱导的支气管收缩以及百草枯(PQ)诱导的死亡过程中可能的参与情况。吸入SO2(250ppm)和灌注MBS(3mM)导致离体灌注肺的顺应性和传导性显著降低。SO2诱导的支气管收缩与降钙素基因相关肽的释放有关,提示辣椒素敏感感觉神经被激活。用辣椒素预处理动物以耗尽感觉神经中的速激肽含量,可显著降低SO2和MBS诱导的支气管收缩。PQ(25mg/Kg)处理3周后诱导高死亡率(75%)。辣椒素预处理对PQ诱导的死亡有显著保护作用(25%)。结果表明,呼吸道中的速激肽含量参与了SO2和MBS诱导的支气管收缩以及PQ导致的死亡。