Nyhof R A, Chou C C
Am J Physiol. 1983 Sep;245(3):H437-46. doi: 10.1152/ajpheart.1983.245.3.H437.
The role of local intestinal nerves in the nutrient-induced intestinal hyperemia was investigated in jejunal segments of anesthetized dogs by comparing the hyperemic effect of intraluminal glucose and oleic acid solutions before and after mucosal anesthesia and infusions of methysergide, hexamethonium, and tetrodotoxin. Methysergide, hexamethonium, and tetrodotoxin all failed to alter either the vascular or metabolic responses to luminal placement of glucose or oleic acid. The increases in blood flow and oxygen uptake produced by glucose or oleic acid, however, were blocked or attenuated after exposing the mucosa to dibucaine. The effect was norepinephrine due to an altered vascular response to vasoactive substances as dibucaine did not alter vascular responses to isoproterenol or norepinephrine. Dibucaine, however, inhibited active transport and increased passive transport of glucose across rat intestinal sacs in vitro. Oxygen consumption of the canine jejunal mucosa was also inhibited by dibucaine in vitro. It seems that inhibition of the nutrient-induced intestinal hyperemia by dibucaine is due, at least in part, to its effect on oxygen consumption and glucose transport of the mucosal epithelial cells. Nutrient-induced hyperemia appears not to be neurally mediated but more closely related to metabolism.
通过比较黏膜麻醉前后以及注射麦角新碱、六甲溴铵和河豚毒素后腔内葡萄糖和油酸溶液的充血效应，研究了局部肠神经在营养物质诱导的肠充血中的作用。实验对象为麻醉犬的空肠段。麦角新碱、六甲溴铵和河豚毒素均未能改变对腔内放置葡萄糖或油酸的血管或代谢反应。然而，在黏膜暴露于丁卡因后，葡萄糖或油酸所引起的血流增加和氧摄取增加受到阻碍或减弱。这种效应并非由去甲肾上腺素引起，因为丁卡因并未改变对异丙肾上腺素或去甲肾上腺素的血管反应。然而，丁卡因在体外抑制了大鼠肠囊对葡萄糖的主动转运并增加了被动转运。在体外，犬空肠黏膜的氧消耗也受到丁卡因的抑制。丁卡因对营养物质诱导的肠充血的抑制作用似乎至少部分归因于其对黏膜上皮细胞氧消耗和葡萄糖转运的影响。营养物质诱导的充血似乎并非由神经介导，而是与代谢更为密切相关。
