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首页> 外文期刊>Life sciences >Guinea-pig lung adenylyl and guanylyl cyclase and PDE activities associated with airway hyper- and hypo-reactivity following LPS inhalation.
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Guinea-pig lung adenylyl and guanylyl cyclase and PDE activities associated with airway hyper- and hypo-reactivity following LPS inhalation.

机译：吸入LPS后，豚鼠肺腺苷酸和鸟苷酸环化酶和PDE活性与气道高反应性和低反应性有关。

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摘要

The relationships between changes in in vivo airway reactivity and levels cyclicAMP and cyclicGMP were determined in guinea-pig lungs after exposure to inhaled lipopolysaccharide (LPS). After LPS (30 mug.ml(-1), 1 h), guinea-pigs displayed in vivo airway hyperreactivity (AHR) at 1 h and hyporeactivity (AHOR) at 48 h, to inhaled (20 s) histamine (1 or 3 mM, respectively). Isoprenaline-stimulated cAMP or SNAP-stimulated cGMP were determined in the lungs isolated from guinea-pigs exposed to LPS inhalation to determine whether there was a relationship between AHR or AHOR and adenylyl/guanylyl cyclase and phosphodiesterase (PDE) activities. Assays were performed in the absence and presence of the non-selective PDE inhibitor, 3-isobutyl-1-methylxanthine (IBMX). Levels of cAMP and cGMP in its presence indicated adenylyl and guanylyl cyclase activities, respectively. The difference between cAMP and cGMP levels, in the absence and presence of IBMX, reflected relevant PDE activity. In vivo AHR was associated with increased PDE activity towards cAMP and cGMP (67 and 278%, respectively) and also increased adenylyl (47%) and guanylyl (210%) cyclase activities. In vivo AHOR at 48 h after LPS inhalation was also associated with raised cyclase activity (p < 0.05), whereas relevant PDE activity declined by 79 and 68%, compared with 48 h after vehicle. Although net stimulated cGMP levels increased during AHR and AHOR and net stimulated cAMP increased during AHOR, our index of PDE activity increased during AHR and decreased during AHOR. These results therefore support the rationale for the use of PDE-inhibitors in the treatment of respiratory diseases associated with AHR.
机译：暴露于吸入脂多糖（LPS）后的豚鼠肺中，确定了体内气道反应性的变化与Cyclamp和Cycling GMP水平之间的关系。 LPS（30 mug.ml（-1），1 h）后，豚鼠对吸入（20 s）组胺（1或3）表现出1 h的体内气道高反应性（AHR）和48 h的低反应性（AHOR）。毫米）。在暴露于LPS吸入的豚鼠的肺中，测定了异丙肾上腺素刺激的cAMP或SNAP刺激的cGMP，以确定AHR或AHOR与腺苷酸/鸟苷酸环化酶和磷酸二酯酶（PDE）活性之间是否存在关系。在不存在和存在非选择性PDE抑制剂3-异丁基-1-甲基黄嘌呤（IBMX）的情况下进行测定。在其存在的情况下，cAMP和cGMP的水平分别表明腺苷酸和鸟苷酸环化酶的活性。在不存在IBMX的情况下，cAMP和cGMP水平之间的差异反映了相关的PDE活性。体内AHR与针对cAMP和cGMP的PDE活性增加（分别为67％和278％）以及腺苷酸环化酶活性（47％）和鸟苷酸环化酶（210％）相关。吸入LPS后48小时的体内AHOR也与环化酶活性升高有关（p <0.05），而相关PDE活性与溶媒后48 h相比分别下降了79％和68％。尽管在AHR和AHOR期间净刺激的cGMP水平升高，而在AHOR期间净刺激的cAMP水平升高，但我们的PDE活性指数在AHR期间升高，而在AHOR期间降低。因此，这些结果支持了在与AHR相关的呼吸道疾病的治疗中使用PDE抑制剂的基本原理。

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