Cisternal Na+ transport inhibition and the ventilatory response to CO2.
Cisternal Na+ transport inhibition and the ventilatory response to CO2.
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脑池Na转运抑制和对CO2的通气反应。
DOI：
10.1152/jappl.1994.77.6.2572
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Adams,JM
中科院分区：
文献类型：
--
作者：
Sullivan,MP;Adams,JM
当PCO 2短暂升高时，神经胶质细胞或神经元可能会移动离子穿过细胞膜以恢复细胞内pH值，在此过程中改变细胞外pH值。抑制离子转运将导致不同的细胞外液pH值（对髓化学感受器的假定刺激），因此，改变通气量以响应PCO 2。我们将两种离子转运抑制剂阿米洛利和布美他尼注入麻醉家兔的小脑延髓池，并将其对再呼吸动作的反应与未接受抑制剂的假家兔进行比较。阿米洛利（10（-5）-10（-3）M）没有影响; 10（-2）M阿米洛利3小时增加呼吸频率和减少潮气量，但对分钟通气量没有净影响。布美他尼（10（-3）M）在输注1小时后没有影响，但在3小时时，在再呼吸期间，潮气量和每分钟通气量分别在6和7%潮气末CO2分数下降低。阿米洛利和布美他尼输注3小时并不影响通气，这与我们先前对脑脊液离子变化的研究预测一致。在第1小时，当延髓腹外侧区神经元和胶质细胞的离子转运被抑制时，我们没有发现离子转运抑制的效果。我们的结论是，在短暂的高碳酸血症的再呼吸演习，Na+/H+交换和Na（+）-K（+）-2Cl-共转运没有发挥重要作用，立即快速pH稳态细胞离子转运的微环境中的延髓化学感受器。
When PCO2 rises transiently, glia or neurons may move ions across their cell membranes to restore intracellular pH, in the process changing extracellular pH. Inhibiting ion transport would result in a different extracellular fluid pH (a putative stimulus for the medullary chemoreceptors) and, therefore, in an altered ventilation in response to PCO2. We infused two ion transport inhibitors, amiloride and bumetanide, into the cisterna magna of anesthetized rabbits and compared their ventilatory response to a rebreathing maneuver with sham rabbits receiving no inhibitor. Amiloride (10(-5)-10(-3) M) had no effect; 3 h of 10(-2) M amiloride increased the frequency of breathing and decreased tidal volume but had no net effect on minute ventilation. Bumetanide (10(-3) M) had no effect after 1 h of infusion, but by 3 h it had decreased tidal volume and minute ventilation at 6 and 7% end-tidal CO2 fraction, respectively, during the rebreathe. Three hours of infusion of amiloride and bumetanide did not affect ventilation in a manner consistent with our predictions from previous studies of ionic changes in cerebrospinal fluid. During the 1st h, when neuronal and glial ion transport in the ventrolateral medulla should be inhibited, we found no effect of ion transport inhibition. We conclude that, during the transient hypercapnia of a rebreathing maneuver, Na+/H+ exchange and Na(+)-K(+)-2Cl- cotransport do not play a significant role in immediate rapid pH homeostasis by cellular ion transport in the microenvironment of the medullary chemoreceptors.