Karlström L
Acta Physiol Scand Suppl. 1986;549:1-48.
The present study was designed to test whether fluid and electrolyte secretion evoked in the small intestine by the dihydroxy bile salt sodium deoxycholate could be due to activation of a nervous reflex mechanism. The effect of the bile salt on small intestinal motility was also investigated, and an analysis was made of factors involved in passive and active transport mechanisms relevant to bile salt-induced secretion. Luminal perfusion with sodium deoxycholate changed net fluid transport from absorption to secretion. Hexamethonium, a ganglionic receptor blocker, lidocaine, a local anaesthetic and tetrodotoxin, a sodium channel blocker, inhibited the induced fluid secretion. The inhibitory effect increased in proportion to the rate of secretion. Elimination of the bile salt from the perfusate also inhibited the secretion. A minor part of the induced change in net fluid transport was resistant to nerve blockade or to bile salt elimination. The change of net fluid transport was paralleled by a change of sodium and chloride transport from absorption to secretion. The change of net sodium transport was due to both a reduced uptake and increased losses. Villus tissue hyperosmolality was reduced by the bile salt. Hexamethonium inhibited the electrolyte secretion. The bile salt caused epithelial lesions in the upper parts of the villi. The lesions persisted also after the bile salt-induced secretion had been inhibited by nerve blockade or by bile salt elimination. Lesions also appeared in intestines which failed to develop net fluid secretion. The bile salt also induced characteristic intestinal contractions which showed a good correlation with the rate of net fluid secretion. The motility was also inhibited by nerve blockade or bile salt elimination. Atropine abolished the induced motility but did not influence the secretion. Indomethacin, a prostaglandin synthesis inhibitor, or pyrilamine, a histamine 1-receptor antagonist, did not inhibit either motility or secretion. The bile salt caused a mucosal vasodilatation, total blood flow increasing about 50%. Capillary filtration coefficient remained unchanged. Lymph flow did not increase. No correlation was found between the change of intestinal blood flow and the change of net fluid transport. Hexamethonium and tetrodotoxin inhibited the induced secretion without influencing blood flow. It is concluded that sodium deoxycholate evokes intestinal secretion and motility via an enteric nervous reflex arch consisting of a presynaptic cholinergic neuron and two postganglionic neurons, one cholinergic innervating the intestinal smooth muscle cell and the other non-cholinergic, non-adrenergic influencing intestinal flu
本研究旨在测试二羟基胆盐脱氧胆酸钠在小肠中引发的液体和电解质分泌是否可能归因于神经反射机制的激活。还研究了胆盐对小肠运动的影响，并分析了与胆盐诱导的分泌相关的被动和主动转运机制中涉及的因素。用脱氧胆酸钠进行肠腔灌注使净液体转运从吸收变为分泌。神经节受体阻滞剂六甲铵、局部麻醉剂利多卡因和钠通道阻滞剂河豚毒素抑制了诱导的液体分泌。抑制作用与分泌速率成比例增加。从灌注液中去除胆盐也抑制了分泌。净液体转运诱导变化的一小部分对神经阻滞或胆盐去除具有抗性。净液体转运的变化与钠和氯的转运从吸收到分泌的变化平行。净钠转运的变化是由于摄取减少和损失增加。胆盐降低了绒毛组织的高渗性。六甲铵抑制电解质分泌。胆盐导致绒毛上部的上皮损伤。在神经阻滞或胆盐去除抑制了胆盐诱导的分泌后，损伤仍然存在。在未能产生净液体分泌的肠道中也出现了损伤。胆盐还诱导了特征性的肠道收缩，其与净液体分泌速率显示出良好的相关性。运动也受到神经阻滞或胆盐去除的抑制。阿托品消除了诱导的运动，但不影响分泌。前列腺素合成抑制剂吲哚美辛或组胺1受体拮抗剂吡咯胺既不抑制运动也不抑制分泌。胆盐导致粘膜血管扩张，总血流量增加约50%。毛细血管滤过系数保持不变。淋巴流量没有增加。未发现肠道血流量变化与净液体转运变化之间的相关性。六甲铵和河豚毒素抑制诱导的分泌而不影响血流量。结论是，脱氧胆酸钠通过由突触前胆碱能神经元和两个节后神经元组成的肠神经反射弧引发肠道分泌和运动，其中一个胆碱能神经元支配肠道平滑肌细胞，另一个非胆碱能、非肾上腺素能神经元影响肠道液体……（原文此处似乎不完整）
