Effects of inflammatory mediators on electrolyte transport across the porcine distal colon epithelium.
Effects of inflammatory mediators on electrolyte transport across the porcine distal colon epithelium.
复制标题
炎症介质对跨猪远端结肠上皮电解质转运的影响。
DOI：
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发表时间：
1993
影响因子：
3.5
通讯作者：
S. O’Grady
中科院分区：
文献类型：
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作者：
T. Traynor;David R. Brown;S. O’Grady
将来自猪远端结肠的上皮固定在Ussing室中，并浸泡在血浆样林格氏溶液中。组胺产生的电流增加不受神经传导阻滞剂河豚毒素预处理的影响。H1-组胺拮抗剂吡拉明和环氧合酶抑制剂吲哚美辛均使组胺浓度-反应曲线产生右移。用葡萄糖酸盐代替Cl或用三（羟甲基）氨基甲烷（三）-N-2-羟乙基哌嗪-N '-2-乙磺酸代替HCO 3，分别抑制了74%和23%的粘膜对组胺的反应。此外，组胺增加了浆膜-粘膜Na和Cl通量，抑制粘膜-浆膜Na通量，导致净Na和Cl吸收减少。前列腺素E2也产生短路电流的增加，但不受河豚毒素的影响。取代Cl或HCO 3抑制这些增加了85%。前列腺素E2抑制粘膜-浆膜和净氯通量。白三烯C4产生的短路电流的振荡增加，这是完全阻断河豚毒素。这些电流的增加归因于血清-粘膜Cl通量的增加，这导致净Cl吸收的减少。从这些数据可以得出结论：1）组胺与H1受体相互作用，增加Na和Cl分泌，抑制Cl吸收; 2）前列腺素E2抑制HCO 3依赖性Cl吸收途径，可能涉及Cl/HCO 3交换; 3）白三烯C4作用于肠神经，刺激Cl分泌。
The epithelium from the porcine distal colon was mounted in Ussing chambers and bathed in plasma-like Ringer's solution. Histamine produced increases in current which were not affected by pretreatment with the neural conduction blocker tetrodotoxin. Both the H1-histamine antagonist pyrilamine and the cyclooxygenase inhibitor indomethacin produced dextral shifts in the histamine concentration-response curve. Replacement of Cl with gluconate or HCO3 with tris(hydroxymethyl)aminomethane(tris)-N-2- hydroxyethylpiperazine-N'-2-ethanesulfonic acid in the bathing solution inhibited the mucosal response to histamine by 74 and 23%, respectively. In addition, histamine increased the serosal-to-mucosal Na and Cl fluxes and inhibited the mucosal-to-serosal Na flux, resulting in a reduction of net Na and Cl absorption. Prostaglandin E2 also produced increases in short-circuit current which remained unaffected by tetrodotoxin. Replacement of either Cl or HCO3 inhibited these increases by 85%. Prostaglandin E2 inhibited the mucosal-to-serosal and net Cl fluxes. Leukotriene C4 produced oscillating increases in the short-circuit current which were completely blocked by tetrodotoxin. These increases in current were attributed to an increase in the serosal-to-mucosal Cl flux which resulted in a decrease in net Cl absorption. From these data it was concluded that: 1) histamine interacts with H1-receptors to increase Na and Cl secretion and inhibit Cl absorption; 2) prostaglandin E2 inhibits a HCO3-dependent Cl absorptive pathway, possibly involving Cl/HCO3 exchange and 3) leukotriene C4 acts on enteric nerves to stimulate Cl secretion.