Yuan S Y, Brookes S J, Costa M
Department of Human Physiology, Flinders University, Adelaide, Australia.
J Auton Nerv Syst. 1997 Jan 12;62(1-2):94-102. doi: 10.1016/s0165-1838(96)00115-4.
Distension-evoked gastric reflexes were studied by intracellular recording from circular muscle cells in the gastric fundus, corpus and antrum in the isolated guinea-pig stomach. Localised electrical stimulation, 2 mm circumferential to the recording electrode, evoked inhibitory junctions potentials in all three gastric regions, sometimes followed by depolarisations in the antrum. In the mid corpus, the inhibitory responses were substantially reduced by Nw-nitro-L-arginine (100 microM), unmasking excitatory junction potentials. Residual hyperpolarisations were blocked by apamin (0.5 microM) which also enhanced the amplitude of excitatory junction potentials. These excitatory junction potentials were abolished by hyoscine (1 microM). Thus transmission from inhibitory motor neurons is mediated by both nitric oxide and an apamin-sensitive mechanism. Transmission from excitatory motor neurons to the circular muscle is mediated by acetylcholine via muscarinic receptors. Balloon distension of 10 s duration of the fundus or antrum elicited inhibitory junction potentials in circular muscle cells of the mid corpus. These inhibitory junction potentials were blocked by tetrodotoxin (0.6 microM) and were greatly reduced by Nw-nitro-L-arginine (100 microM). The residual hyperpolarisations were blocked by apamin (0.5 microM). This indicates the presence of ascending and descending inhibitory reflex pathways in the stomach. In 3 out of 7 experiments, following blockade of inhibitory transmission, small nerve-mediated excitatory junction potentials were evoked by antral distension indicating the presence of an additional ascending excitatory reflex pathway. Distension of the corpus elicited prominent inhibitory junction potentials, sometimes followed by large depolarisations, in circular muscle cells in the fundus, but not in the antrum. This suggests that there is also an ascending inhibitory reflex pathway from the corpus to the fundus but no distension-sensitive descending reflex pathway from the corpus to the antrum. These results demonstrate that within the stomach there are reflex pathways which can be activated by localised distension and project at some distance orally and aborally within the gastric wall. It is likely that the inhibitory reflex pathways are involved in gastric adaptive relaxation which occurs when the intact, isolated stomach is distended. The excitatory reflex pathways from the antrum to the corpus are likely to be involved in the intrinsic excitatory reflex responses observed in the isolated intact stomach to distension and thus be involved in the mixing and emptying of gastric contents.
通过对分离的豚鼠胃的胃底、胃体和胃窦环形肌细胞进行细胞内记录,研究了扩张诱发的胃反射。在记录电极周围2毫米圆周处进行局部电刺激,在所有三个胃区域均诱发抑制性接头电位,有时随后胃窦出现去极化。在胃体中部,Nω-硝基-L-精氨酸(100微摩尔)可使抑制性反应显著降低,从而暴露出兴奋性接头电位。残余的超极化被蜂毒明肽(0.5微摩尔)阻断,蜂毒明肽还增强了兴奋性接头电位的幅度。这些兴奋性接头电位被东莨菪碱(1微摩尔)消除。因此,抑制性运动神经元的传递由一氧化氮和蜂毒明肽敏感机制介导。兴奋性运动神经元向环形肌的传递由乙酰胆碱通过毒蕈碱受体介导。胃底或胃窦持续10秒的球囊扩张在胃体中部的环形肌细胞中诱发抑制性接头电位。这些抑制性接头电位被河豚毒素(0.6微摩尔)阻断,并被Nω-硝基-L-精氨酸(100微摩尔)大大降低。残余的超极化被蜂毒明肽(0.5微摩尔)阻断。这表明胃中存在上行和下行抑制性反射通路。在7个实验中的3个实验中,在抑制性传递被阻断后,胃窦扩张诱发了小的神经介导的兴奋性接头电位,表明存在额外的上行兴奋性反射通路。胃体扩张在胃底的环形肌细胞中诱发了明显的抑制性接头电位,有时随后出现大的去极化,但在胃窦中未出现。这表明从胃体到胃底也存在上行抑制性反射通路,但不存在从胃体到胃窦的扩张敏感下行反射通路。这些结果表明,在胃内存在可被局部扩张激活并在胃壁内口侧和肛侧一定距离投射的反射通路。抑制性反射通路可能参与了完整分离胃扩张时发生的胃适应性舒张。从胃窦到胃体的兴奋性反射通路可能参与了在分离的完整胃中观察到的对扩张的内在兴奋性反射反应,从而参与胃内容物的混合和排空。