Tsubone H, Suzuki A K
J Toxicol Environ Health. 1984;13(4-6):905-17. doi: 10.1080/15287398409530550.
To examine the role of the vagal pathway on the cardiopulmonary functions in NO2-exposed rats, phenyl diguanide, which stimulates type J receptors in the lungs, was injected to control and exposed rats at a constant dose. Based on a statistical test, a decrease in the heart rate (HR) after the injection was observed in the groups exposed to 20 ppm NO2 for 1.5 h and 3h, and 10 ppm for 24 h. On the other hand, an increase in respiratory rate (RR) was observed in the groups exposed to 10 ppm for 3 h and 4 ppm for 1 wk. No change in HR and RR was found in the group exposed to 0.4 ppm for 4 wk. These results suggest that the augmentation of the reflex cardiopulmonary responses due to stimulation to the type J receptors was produced by exposures with a higher concentration of NO2.
为研究迷走神经通路在二氧化氮暴露大鼠心肺功能中的作用，以恒定剂量向对照大鼠和暴露大鼠注射刺激肺部J型受体的苯基双胍。基于统计检验，在暴露于20 ppm二氧化氮1.5小时和3小时以及10 ppm 24小时的组中，注射后观察到心率（HR）下降。另一方面，在暴露于10 ppm 3小时和4 ppm 1周的组中观察到呼吸频率（RR）增加。在暴露于0.4 ppm 4周的组中未发现HR和RR有变化。这些结果表明，较高浓度二氧化氮暴露可通过刺激J型受体增强反射性心肺反应。
