CO2 TRANSPORT AND MEDULLARY CHEMORECEPTOR PHYSIOLOGY

合理治疗呼吸系统疾病，特别是急性呼吸道疾病 慢性疾病中的衰竭和二氧化碳滞留是基于 了解二氧化碳对呼吸的控制。延髓化学感受器 在调节呼吸方面起着至关重要的作用，但 他们的活动尚未确定。二氧化碳水合的催化作用 在产生氢离子和阴离子(HCO3)跨细胞交换过程中 (缓冲这一过程)将通过以下方法在麻醉大鼠中进行研究 通过脑脊液灌流给药这些过程的阻滞剂 枕大池和测量对二氧化碳的呼吸反应。这种关系 延髓化学感受器组织中氢离子活性与 将通过测量麻醉的大鼠和猫的通气性来研究 在组织和膈神经中插入pH微电极的组织pH 动脉血二氧化碳分压和血氧分压瞬时变化时的活动。通过测量 用伺服控制的温度探头进行局部组织灌流， 同时测量组织的pH值，血流的反应 化学感受器组织对氧分压和二氧化碳分压变化的影响及其与组织的关系 将研究氢离子的活性。经小动脉穿透的可能性 二氧化碳交换将通过测量组织pH值来测试，同时改变动脉 和脑脊液超融合二氧化碳的方向相同和相反。 二氧化碳在化学感受器组织中传输的理论描述将是重点 关于阴离子交换、缓冲和微动脉交换。这些研究应该 为拒绝或接受化学感受器机制假说提供证据 这是至关重要的。

Rational treatment of respiratory disease, especially acute respiratory failure and CO2 retention in chronic diseases, is based on the understanding of CO2 control of breathing. The medullary chemoreceptors play a crucial role in regulating breathing but the mechanisms governing their activity are not established. The role of catalysis of CO2 hydration in producing hydrogen ions and of anion (HCO3) exchange across cells (buffering this process) will be studied in anesthetized rats by administering blocking agents of these processes via CSF perfusion into the cisterna magna and measuring the ventilatory response to CO2. The relation between hydrogen ion activity in medullary chemoreceptor tissue and ventilation will be studied in anesthetized rats and cats by measuring tissue pH with a pH microelectrode inserted in the tissue and phrenic nerve activity during transient changes of arterial PCO2 and PO2. By measuring local tissue perfusion with a servo controlled temperature probe, with simultaneous measure of tissue pH, the response of blood flow in the chemoreceptor tissue to changes of PO2 and PCO2 and its relation to tissue hydrogen ion activity will be studied. The possibility of trans-arteriolar CO2 exchange will be tested by measuring tissue pH while changing arterial and CSF superfusate PCO2 in the same and in opposing directions. Theoretical description of CO2 transport in chemoreceptor tissue will focus on anion exchange, buffering and arteriolar exchange. These studies should provide evidence to reject or accept hypotheses of chemoreceptor mechanisms which are of cardinal importance.