Grider J R
Department of Medicine, Medical College of Virginia, Richmond.
Gastroenterology. 1989 Dec;97(6):1414-9. doi: 10.1016/0016-5085(89)90384-3.
The components of the intestinal peristaltic reflex in humans were examined and the neurotransmitters responsible for them identified for the first time i isolated flat sheet segments of intestine. Increasing radial stretch to the caudad end elicited increasing ascending contraction only, whereas increasing radial stretch to the orad end elicited increasing descending relaxation only. Both components were abolished by hexamethonium, implying the participation of cholinergic interneurons in each component. Atropine inhibited ascending contraction only, abolishing the response to low grades of stretch and partially inhibiting the response to high grades of stretch (69% +/- 17%, p less than 0.01). The substance P antagonist [D-Pro2, D-Trp7,9] substance P partially inhibited ascending contraction induced by high grades of stretch only (40% +/- 12%, p less than 0.02). The vasoactive intestinal peptide antagonist [4-Cl-D-Phe6, Leu17]vasoactive intestinal peptide inhibited descending relaxation, abolishing the response to low grades of stretch and partially inhibiting the response to high grades of stretch (40% +/- 4%, p less than 0.001). Release of vasoactive intestinal peptide increased significantly by 91% during descending relaxation only, whereas release of both substance P and substance K increased significantly by 107% during ascending contraction only, supporting the participation of vasoactive intestinal peptide motor neurons in descending relaxation and tachykinin motor neurons as well as cholinergic motor neurons in ascending contraction. The components of the human peristaltic reflex and transmitters regulating them were identical to those found in rat and guinea pig intestine.
首次在分离出的肠扁平片状节段中,对人类肠道蠕动反射的组成部分进行了研究,并确定了与之相关的神经递质。向尾端增加径向拉伸仅引起升支收缩增强,而向口腔端增加径向拉伸仅引起降支舒张增强。六甲铵可消除这两种成分,这意味着胆碱能中间神经元参与了每个成分。阿托品仅抑制升支收缩,消除对低程度拉伸的反应,并部分抑制对高程度拉伸的反应(69%±17%,p<0.01)。P物质拮抗剂[D-脯氨酸2,D-色氨酸7,9]P物质仅部分抑制高程度拉伸诱导的升支收缩(40%±12%,p<0.02)。血管活性肠肽拮抗剂[4-氯-D-苯丙氨酸6,亮氨酸17]血管活性肠肽抑制降支舒张,消除对低程度拉伸的反应,并部分抑制对高程度拉伸的反应(40%±4%,p<0.001)。仅在降支舒张期间,血管活性肠肽的释放显著增加91%,而仅在升支收缩期间,P物质和K物质的释放均显著增加107%,这支持血管活性肠肽运动神经元参与降支舒张,速激肽运动神经元以及胆碱能运动神经元参与升支收缩。人类蠕动反射的组成部分及其调节递质与在大鼠和豚鼠肠道中发现的相同。