Delbro D, Lisander B, Andersson S A
Acta Physiol Scand. 1984 Dec;122(4):621-7. doi: 10.1111/j.1748-1716.1984.tb07552.x.
Experiments were performed in chloralosed cats where gastric motility was recorded by the "volume method". Mucosal and serosal nociceptive stimulations were accomplished by local heating to 45-52 degrees C. Heating generally elicited gastric relaxations, mainly due to activation of extrinsic inhibitory reflexes, but mucosal heating sometimes caused contractile responses which were resistant to nicotinic and adrenergic blockade. The contractions were, however, blocked by atropine and, further, could not be demonstrated after degeneration of splanchnic afferents. On the basis of these and earlier results it is suggested that the gastric contractions induced by mucosal nociceptive stimulation are due to axon reflexes, conveyed by splanchnic afferents that, possibly via release of substance P, make non-nicotinic reflex contacts with intramural excitatory cholinergic neurons.
实验在水合氯醛麻醉的猫身上进行，采用“容积法”记录胃动力。通过局部加热至45 - 52摄氏度来实现黏膜和浆膜的伤害性刺激。加热通常会引起胃舒张，主要是由于外在抑制性反射的激活，但黏膜加热有时会引起对烟碱和肾上腺素能阻断有抗性的收缩反应。然而，这些收缩可被阿托品阻断，并且在内脏传入神经变性后无法再表现出来。基于这些以及早期的结果，提示黏膜伤害性刺激诱导的胃收缩是由于轴突反射，由内脏传入神经传导，这些传入神经可能通过P物质的释放，与壁内兴奋性胆碱能神经元形成非烟碱样反射性联系。
