神经肽释放会增加血清白蛋白的损失，并减少腹膜透析中的超滤。

Neuropeptide release augments serum albumin loss and reduces ultrafiltration in peritoneal dialysis.

机构信息

Institute of Biomedicine1 and Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden.

出版信息

Perit Dial Int. 2012 Mar-Apr;32(2):168-76. doi: 10.3747/pdi.2010.00254. Epub 2011 Sep 30.

DOI:10.3747/pdi.2010.00254

PMID:21965619

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3525390/

Abstract

BACKGROUND

The triggers of the acute local inflammatory response to peritoneal dialysis (PD) fluid exposure remain unknown. In the present study, we investigated the effects of neurogenic inflammation and mast cell degranulation on water and solute transport in experimental PD.

METHODS

Single 2-hour dwells in rats with PD catheters were studied. Histamine and the neuropeptides substance P and calcitonin gene-related peptide (CGRP) were measured in PD fluid samples by ELISA. Radiolabeled albumin ((125)I and (131)I respectively) was used as an intraperitoneal (IP) and intravascular tracer. Glucose and urea concentrations were measured in plasma and PD fluid. The effects of varying the volume and osmolarity of a lactate-buffered PD fluid were compared and related to the effects of pharmacologic intervention.

RESULTS

Application of 20 mL 3.9% glucose PD fluid induced an IP histamine release during the first 30 minutes, blockable by the mast cell stabilizer doxantrazole and the substance P neurokinin-1 receptor (NK1R)-blocker spantide. Histamine release was also inhibited at a reduced PD volume (14 mL), but was not affected by normalizing the PD fluid osmolarity. Blockade of NK1R also reduced plasma albumin leakage to the peritoneal cavity. Inhibition of CGRP receptors by CGRP8-37 improved osmotic (transcapillary) and net ultrafiltration and reduced the dialysate urea concentration. Neuropeptide release was not clearly related to activation of the TrpV1 receptor, the classic trigger of neurogenic inflammation.

CONCLUSIONS

Neuropeptide release exaggerated albumin loss and reduced ultrafiltration in this rat PD model. Intervention aimed at the neuropeptide action substantially improved PD efficiency.

摘要

背景

腹膜透析（PD）液暴露引起急性局部炎症反应的触发因素尚不清楚。在本研究中，我们研究了神经炎症和肥大细胞脱颗粒对实验性 PD 中水和溶质转运的影响。

方法

研究了大鼠 PD 导管单次 2 小时停留。通过 ELISA 测量 PD 液样本中的组胺和神经肽物质 P 和降钙素基因相关肽（CGRP）。放射性标记白蛋白（(125)I 和 (131)I 分别）用作腹腔内（IP）和血管内示踪剂。测量血浆和 PD 液中的葡萄糖和尿素浓度。比较了不同体积和渗透压的乳酸缓冲 PD 液的影响，并将其与药物干预的效果相关联。

结果

应用 20 mL 3.9%葡萄糖 PD 液在最初 30 分钟内引起 IP 组胺释放，可被肥大细胞稳定剂 doxantrazole 和物质 P 神经激肽-1 受体（NK1R）-阻断剂 spantide 阻断。在减少 PD 体积（14 mL）时，组胺释放也受到抑制，但 PD 液渗透压正常化不受影响。NK1R 阻断也减少了血浆白蛋白向腹腔的渗漏。用 CGRP8-37 抑制 CGRP 受体可改善渗透（跨毛细血管）和净超滤，并降低透析液尿素浓度。神经肽释放与经典神经炎症触发物 TrpV1 受体的激活没有明显关系。