Foutz A S, Champagnat J, Denavit-Saubié M
Laboratoire de Physiologie Nerveuse, C.N.R.S., Gif-sur-Yvette, France.
Eur J Pharmacol. 1988 Sep 13;154(2):179-84. doi: 10.1016/0014-2999(88)90095-7.
The effects on respiration of MK-801, an N-methyl-D-aspartate (NMDA) non-competitive antagonist, were studied in awake chronic cats by means of the plethysmographic technique. MK-801 (0.01-3.0 mg/kg) was first given i.v. in cumulative doses. The protocol was repeated 10-15 days later in the same animals after bilateral vagotomy. MK-801 selectively increased the duration of inspiration, causing an apneustic respiration but had no effect on the duration of expiration. The maximal inspiratory duration brought about by MK-801 in the intact cat (4.3 s; control 0.9 s) increased 4-fold after bilateral vagotomy (16.4 s; control 1.7 s). Such results suggest that the termination of the inspiratory phase in normal awake cats results from an interaction of pulmonary vagal afferent inputs (inactive on NMDA receptors) with a central mechanism in which NMDA-type glutamate receptors are activated by dicarboxylic amino acid neurotransmission.
采用体积描记技术，在清醒慢性猫中研究了N-甲基-D-天冬氨酸（NMDA）非竞争性拮抗剂MK-801对呼吸的影响。首先静脉注射累积剂量的MK-801（0.01 - 3.0毫克/千克）。10 - 15天后，在同一动物双侧迷走神经切断后重复该实验方案。MK-801选择性地增加吸气持续时间，导致长吸式呼吸，但对呼气持续时间没有影响。MK-801在完整猫中引起的最大吸气持续时间（4.3秒；对照0.9秒）在双侧迷走神经切断后增加了4倍（16.4秒；对照1.7秒）。这些结果表明，正常清醒猫吸气相的终止是由肺迷走神经传入输入（对NMDA受体无活性）与一种中枢机制相互作用导致的，在该中枢机制中，NMDA型谷氨酸受体通过二羧酸氨基酸神经传递被激活。
