Pequignot J M, Hellström S
UA CNRS 1196, Laboratoire de Physiologie, Faculté de Médecine Grange-Blanche, Lyon, France.
Biomed Biochim Acta. 1987;46(12):911-4.
Rats were exposed to hypoxia (10% O2) for 1 and 3 weeks with or without daily injections of DL-propranolol (0.66 mg/kg i.p.). The structure of the carotid bodies was analyzed by light microscopical morphometry. Hypoxia induced enlargement of the carotid body due to enhanced vascularity and hypertrophy of glomic and interstitial tissues. The contents of dopamine and norepinephrine multiplied. Propranolol abolished the vasodilatory effect of hypoxia within the first week but did not prevent the other structural changes and the rise in catecholamine content. The data suggest that 1) the vaso-dilation elicited by long-term hypoxia may be controlled by beta-adrenoceptors; 2) the structural and biochemical events occurring in rat carotid body during long-term hypoxia seem to be controlled by different mechanisms.
将大鼠暴露于低氧环境（10%氧气）1周和3周，每日注射或不注射DL-普萘洛尔（0.66毫克/千克，腹腔注射）。通过光学显微镜形态计量学分析颈动脉体的结构。低氧由于血管增多以及球细胞和间质组织肥大导致颈动脉体增大。多巴胺和去甲肾上腺素含量增加。普萘洛尔在第一周内消除了低氧的血管舒张作用，但并未阻止其他结构变化和儿茶酚胺含量的升高。这些数据表明：1）长期低氧引起的血管舒张可能受β-肾上腺素能受体控制；2）大鼠颈动脉体在长期低氧期间发生的结构和生化事件似乎受不同机制控制。
