Basu S
Indian J Physiol Pharmacol. 1981 Jan-Mar;25(1):17-25.
A single breath of 100% CO2 produces depression of the monosynaptic reflexes, recorded from L7 or S1 ventral root, after stimulation of the Posterior Biceps and Semitendinosus nerve (PBST) in anaesthetised cats. As the depression could not be attributed to the J-reflex(1), the possible site of action of the CO2 induced depression of monosynaptic reflexes was worked out. PBST nerve threshold did not change after CO2 introduction and the depression persisted in paralysed cats under controlled ventilation, thus eliminating the possibility of movement effect of the spinal cord due to tachypnoea. Spinal cord sections at the level of L1 and C1 abolished the depression, whereas the depression persisted in the decerebrate preparation. Thus it is concluded that a single-breath of 100% CO2 depresses the monosynaptic reflexes at the supraspinal level. Blood gas tensions (PO2 and pCO2) measured before and after CO2 introduction showed a shortlasting increase in pCO2 and not much significant change in pO2 compared to the long lasting depression of monosynaptic reflexes.
在麻醉猫中，吸入一口100%的二氧化碳后，刺激肱二头肌后束和半腱肌神经（PBST），从L7或S1腹根记录到的单突触反射会受到抑制。由于这种抑制不能归因于J反射(1)，因此确定了二氧化碳诱导单突触反射抑制的可能作用部位。引入二氧化碳后，PBST神经阈值没有变化，并且在控制通气的瘫痪猫中这种抑制持续存在，从而排除了因呼吸急促导致脊髓运动效应的可能性。L1和C1水平的脊髓横断消除了这种抑制，而在去大脑制备中这种抑制仍然存在。因此得出结论，吸入一口100%的二氧化碳会在脊髓以上水平抑制单突触反射。引入二氧化碳前后测量的血气张力（PO2和pCO2）显示，与单突触反射的长期抑制相比，pCO2有短暂升高，而pO2变化不大。
