Ling L, Olson E B, Vidruk E H, Mitchell G S
Department of Comparative Biosciences, University of Wisconsin, Madison 53706, USA.
Respir Physiol. 1997 Nov;110(2-3):261-8. doi: 10.1016/s0034-5687(97)00091-1.
This paper will describe recent studies concerning the existence of developmental plasticity in the hypoxic ventilatory control system and the locus of the functional impairment following perinatal sensory suppression. Suppression of peripheral arterial chemoreceptor activity was achieved by exposing rats to hyperoxia (60% O2) for the first month of life; all measurements were conducted 2-5 months after the exposure (perinatal treated rats). Hypoxic (but not hypercapnic) ventilatory responses were severely attenuated in awake perinatal treated rats, but not in rats exposed to hyperoxia as adults, indicating that the persistent effect is unique to development and is not the nonspecific result of O2 toxicity. Impairments of the hypoxic ventilatory response due to changes in pulmonary mechanics, gas exchange or central integration of carotid chemoafferent inputs were all ruled out as primary causal factors. However, a persistent impairment of carotid chemotransduction in perinatal treated rats was apparent. These studies suggest that the hypoxic ventilatory response is susceptible to developmental plasticity, and that a carotid chemoreceptor deficit is the primary cause. These findings may have important clinical implications for patients subjected to excessive O2 therapy during neonatal intensive care.
本文将描述近期有关低氧通气控制系统发育可塑性的存在以及围产期感觉抑制后功能损伤部位的研究。通过在出生后的第一个月将大鼠暴露于高氧环境（60%氧气）来抑制外周动脉化学感受器的活动；所有测量均在暴露后2至5个月进行（围产期处理的大鼠）。在清醒的围产期处理大鼠中，低氧（而非高碳酸血症）通气反应严重减弱，但在成年后暴露于高氧的大鼠中则未减弱，这表明这种持续效应是发育所特有的，并非氧气毒性的非特异性结果。由于肺力学、气体交换或颈动脉化学传入输入的中枢整合变化导致的低氧通气反应受损均被排除为主要因果因素。然而，围产期处理的大鼠中颈动脉化学转导存在持续损伤是明显的。这些研究表明，低氧通气反应易受发育可塑性影响，且颈动脉化学感受器缺陷是主要原因。这些发现可能对新生儿重症监护期间接受过度氧气治疗的患者具有重要的临床意义。
