Hedner J, Hedner T, Jonason J
J Neural Transm. 1985;61(3-4):239-52. doi: 10.1007/BF01251915.
The neuropharmacological effects of capsaicin (CAPS) (8-methyl-N-vanillyl-6-nonenamide) have been closely linked to the peptide neurotransmitter substance P (SP). In order to elucidate SP mechanisms in peripheral and central control of breathing we have studied the respiratory effects of CAPS and SP administration to neonatal and adult rats using a whole body plethysmographic method. CAPS (3 and 30 micrograms) induced an immediate apnea after intravenous injection. This effect could be reduced by vagotomy but not further changed by combined vagotomy and glossopharyngectomy. The apnoic periods were followed by periods of tachypnea. Intracerebroventricular (i.c.v.) administration of CAPS resulted in an increased tidal volume (VT) and a decreased respiratory frequency (f), i.e. a respiratory response similar to that seen after i.c.v. SP. No apnoic episodes were seen after i.c.v. injection. The respiratory pattern after acute i.c.v. CAPS administration was not significantly changed by neonatal CAPS pretreatment. However, while saline pretreated control animals responded to an i.c.v. injection of SP with an increase in VT and inspiratory drive (VT/TI), animals pretreated with CAPS responded with a shortening of inspiratory and expiratory time in combination with an increase in VT. Similar changes have been observed in vagotomized animals after SP administration. It is concluded that CAPS elicits apnea via mechanisms located outside the CNS, which cannot be fully deafferented by combined vagotomy and glossopharyngectomy. Furthermore, CAPS i.c.v. induces a stimulation of respiration by a central mechanism of action, possibly due to a release of SP. Neonatal pretreatment with CAPS modifies the respiratory response to i.c.v. SP. This effect might be due to an impairment in tonical afferent SP mechanisms to the central respiratory regulating system and possibly also to an impairment of central SP mechanisms involved in respiration.
辣椒素（CAPS，8 - 甲基 - N - 香草基 - 6 - 壬酰胺）的神经药理学效应与肽类神经递质P物质（SP）密切相关。为了阐明SP在外周和中枢呼吸控制中的机制，我们采用全身体积描记法研究了向新生大鼠和成年大鼠注射CAPS和SP后的呼吸效应。静脉注射CAPS（3微克和30微克）后立即诱发呼吸暂停。迷走神经切断术可减轻这种效应，但迷走神经切断术联合舌咽神经切断术不会使其进一步改变。呼吸暂停期之后是呼吸急促期。脑室内（i.c.v.）注射CAPS导致潮气量（VT）增加，呼吸频率（f）降低，即产生了与脑室内注射SP后相似的呼吸反应。脑室内注射后未见呼吸暂停发作。急性脑室内注射CAPS后的呼吸模式，经新生期CAPS预处理后无明显改变。然而，生理盐水预处理的对照动物脑室内注射SP后，潮气量和吸气驱动（VT/TI）增加，而经CAPS预处理的动物则表现为吸气和呼气时间缩短，同时潮气量增加。SP给药后在迷走神经切断的动物中也观察到了类似变化。结论是，CAPS通过位于中枢神经系统之外的机制引发呼吸暂停，联合迷走神经切断术和舌咽神经切断术不能完全消除其传入神经。此外，脑室内注射CAPS通过中枢作用机制刺激呼吸，可能是由于SP的释放。新生期CAPS预处理改变了对脑室内注射SP的呼吸反应。这种效应可能是由于向中枢呼吸调节系统的紧张性传入SP机制受损，也可能是由于参与呼吸的中枢SP机制受损。
