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梗阻性黄疸对周围神经的影响:大鼠超微结构研究

Effects of obstructive jaundice on the peripheral nerve: an ultrastructural study in rats.

作者信息

Can B, Saray A, Caglikulekçi M, Saran Y

机构信息

Department of Histology and Embryology, Ankara University School of Medicine, Ankara, Turkey.

出版信息

Eur Surg Res. 2004 Jul-Aug;36(4):226-33. doi: 10.1159/000078857.

Abstract

Obstructive jaundice (OJ) and hepatic disorders have been shown to be associated with peripheral neuropathy in several clinical studies. The study evaluated the effect of OJ on the ultrastructure of the rat sciatic nerve. In the OJ group, jaundice was created by ligation of common bile duct in Wistar-Albino rats. In the sham-operated control group the same procedure was performed without ligation of the bile duct. On day 7, all rats were re-operated and sciatic nerves were explored to harvest 2-cm-long nerve segments for quantitative and qualitative histopathological analysis by light and electron microscopy. Bilirubin was measured on serum samples. Bilirubin levels were significantly higher in jaundiced rats compared with that of controls (8.46 +/- 0.45 vs. 0.80 +/- 0.14 mmol/l, means +/- SD, p < 0.01). Control nerves did not show anything other than the normal histology. In the OJ group, degenerative changes such as irregularities, thinning, ruffling and invaginations, irregularshaped bodies, vacuolizations and focal segmental demyelination were observed in the myelin sheath. Myelin clusters were noted in the axoplasm. A varying degree of swelling was noted in the nucleus and cytoplasm of the Schwann cells. Morphometric analysis of specimens obtained from sciatic nerves showed that myelin injury (370.9 +/- 51.3 vs. 11.6 +/- 0.5 axons), axonal edema (142.1 +/- 24.2 vs. 10.6 +/- 0.5 edematous axons) and Schwann cell degeneration (50.3 +/- 11.6 vs. 3.2 +/- 0.2 Schwann cells) was significantly higher in the jaundiced rats than in the control group (p < 0.01). The ultrastructural alterations spotted in the rat peripheral nerve were attributed to hyperbilirubinemia and increased concentrations of several neurotoxic substances released from the Kupffer cells in OJ. Neuropathy in jaundiced patients seems to result from accompanying degenerative changes in the peripheral nervous system. However, the exact nature and initiating factors of this nerve injury remains to be unveiled.

摘要

多项临床研究表明,阻塞性黄疸(OJ)和肝脏疾病与周围神经病变有关。本研究评估了OJ对大鼠坐骨神经超微结构的影响。在OJ组中,通过结扎Wistar - 白化大鼠的胆总管来制造黄疸。在假手术对照组中,进行相同的手术操作,但不结扎胆管。在第7天,所有大鼠再次手术,探查坐骨神经,获取2厘米长的神经节段,用于光镜和电镜下的定量和定性组织病理学分析。检测血清样本中的胆红素。与对照组相比,黄疸大鼠的胆红素水平显著更高(8.46±0.45 vs. 0.80±0.14 mmol/l,均值±标准差,p < 0.01)。对照神经除了正常组织学外未显示其他异常。在OJ组中,观察到髓鞘出现退行性变化,如不规则、变薄、起皱和内陷、不规则形状的物体、空泡化和局灶性节段性脱髓鞘。轴浆中可见髓鞘簇。雪旺细胞的细胞核和细胞质出现不同程度的肿胀。对从坐骨神经获取的标本进行形态计量分析表明,黄疸大鼠的髓鞘损伤(370.9±51.3 vs. 11.6±0.5轴突)、轴突水肿(142.1±24.2 vs. 10.6±0.5水肿轴突)和雪旺细胞变性(50.3±11.6 vs. 3.2±0.2雪旺细胞)显著高于对照组(p < 0.01)。在大鼠周围神经中发现的超微结构改变归因于高胆红素血症以及OJ中库普弗细胞释放的几种神经毒性物质浓度增加。黄疸患者的神经病变似乎是由周围神经系统伴随的退行性变化引起的。然而,这种神经损伤的确切性质和起始因素仍有待揭示。

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