Diener M, Bridges R J, Knobloch S F, Rummel W
Institut für Pharmakologie und Toxikologie, Universität des Saarlandes, Federal Republic of Germany.
Naunyn Schmiedebergs Arch Pharmacol. 1988 Jan;337(1):74-8. doi: 10.1007/BF00169480.
Two preparations of rat colon descendens were used in order to localize the action sites of iloprost and prostaglandin E2 (PGE2). One preparation, the mucosa-submucosa preparation contained the submucosal and mucosal plexus whereas for the mucosa preparation in addition the submucosa with the submucosal plexus was removed. Iloprost (10(-6) mol.l-1) caused an increase in short-circuit current (Isc), potential difference (Pd) and tissue conductance (Gt) of the mucosa-submucosa preparation reflecting net Cl- secretion as confirmed by unidirectional ion flux measurements. The Cl- secretion was due to an increase in JClsm and a decrease in JClms. These effects were completely abolished by addition of 5 X 10(-5) mol.l-1 atropine. Iloprost had only small and inconsistent effects in the mucosa preparation. In contrast PGE2 (10(-6) mol.l-1) increased Isc, Pd and Gt due to Cl- secretion in both preparations. The Cl- secretion was caused by an increase in JClsm and a decrease in JClms. Only the PGE2 effect in the mucosa-submucosa preparation but not in the mucosa preparation was inhibited by about 50% by atropine. The results suggest that the prostacyclin derivative iloprost induces a Cl- secretion only by an activation of submucosal neurons whereas PGE2 acts both on the epithelium and the submucosal plexus. The neuronal effects of prostaglandins appear to be, at least in part, mediated by muscarinic receptors.
为了确定伊洛前列素和前列腺素E2（PGE2）的作用位点，使用了两种大鼠降结肠制剂。一种制剂是黏膜-黏膜下层制剂，包含黏膜下层和黏膜丛；而对于黏膜制剂，还去除了带有黏膜下丛的黏膜下层。伊洛前列素（10⁻⁶ mol·L⁻¹）导致黏膜-黏膜下层制剂的短路电流（Isc）、电位差（Pd）和组织电导（Gt）增加，这反映了净Cl⁻分泌，单向离子通量测量证实了这一点。Cl⁻分泌是由于JClsm增加和JClms减少。加入5×10⁻⁵ mol·L⁻¹阿托品后，这些作用完全被消除。伊洛前列素在黏膜制剂中的作用很小且不一致。相比之下，PGE2（10⁻⁶ mol·L⁻¹）在两种制剂中均因Cl⁻分泌而使Isc、Pd和Gt增加。Cl⁻分泌是由JClsm增加和JClms减少引起的。阿托品仅使黏膜-黏膜下层制剂中的PGE2作用受到约50%的抑制，而黏膜制剂中的不受影响。结果表明，前列环素衍生物伊洛前列素仅通过激活黏膜下神经元诱导Cl⁻分泌，而PGE2既作用于上皮细胞，也作用于黏膜下丛。前列腺素的神经元作用似乎至少部分是由毒蕈碱受体介导的。
