Nylander O, Sjöblom M
Department of Neuroscience, Division of Physiology, Biomedical Center, Uppsala University, Uppsala, Sweden.
Acta Physiol (Oxf). 2007 Apr;189(4):325-35. doi: 10.1111/j.1748-1716.2006.01649.x.
To examine whether modulation of paracellular solute permeability affects the capability of the duodenum to adjust luminal osmolality.
Proximal duodenum was perfused with a hypotonic NaCl solution and effects on paracellular permeability to (51)Cr-EDTA, motility, anion secretion, net fluid flux and perfusate osmolality determined in anaesthetized rats in the absence and presence of the COX-2 inhibitor parecoxib. Vasoactive intestinal peptide (VIP) was used to reduce and lidocaine to augment the hypotonicity-induced increase in paracellular permeability.
Luminal hypotonicity slightly increased paracellular permeability in control animals. Parecoxib induced motility, increased electrolyte and fluid secretion, potentiated the hypotonicity-induced rise in paracellular permeability and enhanced the capability to adjust luminal osmolality. VIP, given to control animals stimulated electrolyte and fluid secretion and augmented the capability to adjust luminal osmolality. Administration of VIP to parecoxib-treated animals increased secretion further, markedly reduced the hypotonicity-induced increase in permeability but did not change the osmolality-adjusting capability. Luminal lidocaine potentiated the hypotonicity-induced increase in permeability, reduced the hypotonicity-induced net fluid absorption and the osmolality-adjusting capability was 50% greater than in controls. Lidocaine, given to parecoxib-treated animals potentiated the hypotonicity-induced increase in permeability, reduced the hypotonicity-induced net fluid absorption but did not change the osmolality-adjusting capability.
Vasoactive intestinal peptide reduces the osmolality-adjusting capacity of the duodenum by inhibiting paracellular solute permeability but improves this capacity by stimulating active electrolyte and fluid secretion. In contrast, lidocaine improves the osmolality-adjusting capability by augmenting paracellular solute transport but depresses it by reducing the hypotonicity-induced net fluid absorption.
研究细胞旁溶质通透性的调节是否会影响十二指肠调节管腔渗透压的能力。
用低渗氯化钠溶液灌注十二指肠近端，在麻醉大鼠中，于不存在和存在COX-2抑制剂帕瑞昔布的情况下，测定对细胞旁对（51）铬-乙二胺四乙酸的通透性、运动性、阴离子分泌、净液体通量和灌注液渗透压的影响。使用血管活性肠肽（VIP）降低，利多卡因增强低渗诱导的细胞旁通透性增加。
管腔低渗在对照动物中轻微增加细胞旁通透性。帕瑞昔布诱导运动，增加电解质和液体分泌，增强低渗诱导的细胞旁通透性增加，并增强调节管腔渗透压的能力。给予对照动物VIP刺激电解质和液体分泌，并增强调节管腔渗透压的能力。给予帕瑞昔布处理的动物VIP进一步增加分泌，显著降低低渗诱导的通透性增加，但不改变渗透压调节能力。管腔内利多卡因增强低渗诱导的通透性增加，降低低渗诱导的净液体吸收，渗透压调节能力比对照高50%。给予帕瑞昔布处理的动物利多卡因增强低渗诱导的通透性增加，降低低渗诱导的净液体吸收，但不改变渗透压调节能力。
血管活性肠肽通过抑制细胞旁溶质通透性降低十二指肠的渗透压调节能力，但通过刺激主动电解质和液体分泌改善该能力。相反，利多卡因通过增加细胞旁溶质转运改善渗透压调节能力，但通过减少低渗诱导的净液体吸收降低该能力。
