Wasicko M J, Melton J E, Neubauer J A, Krawciw N, Edelman N H
Department of Medicine, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, New Brunswick 08903-0019.
J Appl Physiol (1985). 1990 Jan;68(1):53-8. doi: 10.1152/jappl.1990.68.1.53.
To determine if depression of central respiratory output during progressive brain hypoxia (PBH) can be generalized to other brain stem outputs, we examined the effect of PBH on the tonic (tSCS) and inspiratory-synchronous (iSCS) components of preganglionic superior cervical sympathetic (SCS) nerve activity. Peak phrenic and SCS activity were measured in nine anesthetized, paralyzed, peripherally chemodenervated, vagotomized cats. PBH was produced by inhalation of 0.5% CO in 40% O2 while blood pressure and end-tidal CO2 were maintained constant. A progressive reduction in arterial O2 content from 14.3 +/- 0.6 to 4.5 +/- 0.3 vol% caused a 79 +/- 7% depression of peak phrenic activity and an 84 +/- 10% reduction of iSCS activity, but tSCS activity increased 42 +/- 21%. During CO2 rebreathing, iSCS activity increased in parallel with peak phrenic activity while tSCS activity was unchanged. The slopes of the CO2 responses of both phrenic (6.3 +/- 1.2%max/mmHg) and iSCS (4.6 +/- 0.8%max/mmHg) activity were unaffected by PBH. In four of nine hypocapnic and three of nine hypoxic studies, inspiratory activity in the SCS nerve was observed even after completely silencing the phrenic neurogram.(ABSTRACT TRUNCATED AT 250 WORDS)
为了确定进行性脑缺氧（PBH）期间中枢呼吸输出的抑制是否可推广至其他脑干输出，我们研究了PBH对颈上交感神经节前神经活动的紧张性（tSCS）和吸气同步性（iSCS）成分的影响。在9只麻醉、麻痹、外周化学去神经支配、迷走神经切断的猫中测量膈神经和颈上交感神经的峰值活动。通过吸入40%氧气中的0.5%一氧化碳来产生PBH，同时维持血压和呼气末二氧化碳恒定。动脉血氧含量从14.3±0.6降至4.5±0.3容积%，导致膈神经峰值活动降低79±7%，iSCS活动降低84±10%，但tSCS活动增加42±21%。在二氧化碳重复呼吸期间，iSCS活动与膈神经峰值活动平行增加，而tSCS活动不变。PBH不影响膈神经（6.3±1.2%最大值/毫米汞柱）和iSCS（4.6±0.8%最大值/毫米汞柱）活动的二氧化碳反应斜率。在9项低碳酸血症研究中的4项和9项低氧血症研究中的3项中，即使在膈神经电图完全沉默后，仍观察到颈上交感神经中的吸气活动。（摘要截断于250字）
