Runold M, Cherniack N S, Prabhakar N R
Department of Medicine, University Hospitals, Case Western Reserve University, Cleveland, Ohio.
Respir Physiol. 1990 May-Jun;80(2-3):299-306. doi: 10.1016/0034-5687(90)90090-l.
Adenosine, which is released during hypoxia, increases carotid chemoreceptor discharge. It is not known if adenosine also may stimulate the aortic chemoreceptors. The purpose of this study was to investigate if adenosine also can stimulate aortic chemoreceptors. The effect of adenosine (0.01, 0.1 and 1.0 mumol/kg) on aortic chemoreceptor discharge was studied in seven anesthetized, paralyzed and artificially ventilated adult cats. Intra-aortic injections of adenosine produced an increase in chemoreceptor discharge, which reached its peak between 10 and 20 s. The chemoreceptor augmentation increased with higher doses of adenosine. Adenosine also caused a fall in blood pressure. The increase of chemoreceptor discharge was not related to fall in arterial blood pressure. Since adenosine is released during hypoxia, it is suggested that part of the cardiovascular changes induced by hypoxia is due to stimulation of aortic chemoreceptors by adenosine.
缺氧时释放的腺苷会增加颈动脉化学感受器的放电。目前尚不清楚腺苷是否也能刺激主动脉化学感受器。本研究的目的是调查腺苷是否也能刺激主动脉化学感受器。在七只麻醉、麻痹并人工通气的成年猫中，研究了腺苷（0.01、0.1和1.0 μmol/kg）对主动脉化学感受器放电的影响。主动脉内注射腺苷会使化学感受器放电增加，在10至20秒之间达到峰值。化学感受器增强作用随腺苷剂量增加而增强。腺苷还导致血压下降。化学感受器放电的增加与动脉血压下降无关。由于缺氧时会释放腺苷，因此提示缺氧引起的部分心血管变化是由于腺苷刺激主动脉化学感受器所致。
