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大鼠门腔静脉吻合术后及四氯化碳诱导肝硬化后运动传导束的功能异常

Functional abnormalities of the motor tract in the rat after portocaval anastomosis and after carbon tetrachloride induction of cirrhosis.

作者信息

Oria Marc, Raguer Nuria, Chatauret Nicolas, Bartolí Ramón, Odena Gemma, Planas Ramón, Córdoba Juan

机构信息

Liver Unit, Hospital Universitari Vall d'Hebron, Department of Medicine, Universitat Autònoma de Barcelona, Passeig Vall d'Hebron 119-129, 08035, Barcelona, Spain.

出版信息

Metab Brain Dis. 2006 Dec;21(4):297-308. doi: 10.1007/s11011-006-9036-z. Epub 2006 Nov 30.

Abstract

INTRODUCTION

Hepatic encephalopathy is a neurologic syndrome secondary to liver failure that causes cognitive and motor abnormalities. Impairment in the function of the first neuron of the motor tract (corticospinal tract) has been demonstrated in patients with cirrhosis and minimal hepatic encephalopathy.

AIM

Investigate the function of the first neuron of the motor tract in experimental models of minimal hepatic encephalopathy.

MATERIAL AND METHODS

Rats with portocaval anastomosis (n = 8) and rats with carbon tetrachloride induced cirrhosis (n = 11) underwent neurophysiological recording under light anesthesia with propofol. Motor evoked potentials were elicited applying a transcranial electric pulse and were recorded in the tibialis anterior muscle. The effect of the dose of anesthesia was assessed in a group of normal rats (n = 10).

RESULTS

Rats with portocaval anastomosis exhibited a decrease in motor evoked potentials amplitude following surgery (67 +/- 11 to 41 +/- 16%, P < 0.001). Cirrhotic rats exhibited an increase in motor evoked potentials latency after the appearance of ascites (4.65 +/- 0.43 to 5.15 +/- 0.67 ms., P = 0.04). Increasing doses of propofol produced a decrease in the amplitude and an increase in the latency of motor evoked potentials.

CONCLUSION

It is possible to reproduce functional abnormalities of the central motor tract in rats with portocaval anastomosis and carbon tetrachloride induced cirrhosis. The development of motor abnormalities in experimental models of minimal hepatic encephalopathy offers the possibility to investigate the mechanisms involved in the pathogenesis of hepatic encephalopathy and test therapeutic strategies.

摘要

引言

肝性脑病是继发于肝功能衰竭的一种神经综合征,可导致认知和运动异常。在肝硬化和轻微肝性脑病患者中已证实运动传导通路(皮质脊髓束)的第一级神经元功能受损。

目的

在轻微肝性脑病实验模型中研究运动传导通路第一级神经元的功能。

材料与方法

对门腔静脉吻合术大鼠(n = 8)和四氯化碳诱导肝硬化大鼠(n = 11)在丙泊酚轻度麻醉下进行神经生理学记录。通过经颅电脉冲诱发运动诱发电位,并记录于胫前肌。在一组正常大鼠(n = 10)中评估麻醉剂量的影响。

结果

门腔静脉吻合术大鼠术后运动诱发电位幅度降低(从67±11降至41±16%,P < 0.001)。肝硬化大鼠出现腹水后运动诱发电位潜伏期延长(从4.65±0.43毫秒增至5.15±0.67毫秒,P = 0.04)。丙泊酚剂量增加导致运动诱发电位幅度降低和潜伏期延长。

结论

在门腔静脉吻合术和四氯化碳诱导肝硬化大鼠中可以重现中枢运动传导通路的功能异常。轻微肝性脑病实验模型中运动异常的发生为研究肝性脑病发病机制及测试治疗策略提供了可能。

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