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[甲烷对大鼠近端结肠运动及离子通道机制的影响]

[Effects of methane on proximal colon motility of rats and ion channel mechanisms].

作者信息

Liu Ying, Luo He-sheng, Liang Cheng-bo, Tan Wei, Xia Hong, Xu Wen-juan

机构信息

Department of Gastroenterology, Renmin Hospital, Wuhan University, Wuhan, China.

出版信息

Zhonghua Yi Xue Za Zhi. 2013 Feb 5;93(6):459-63.

Abstract

OBJECTIVE

To explore the effects of methane on proximal colon motility and elucidate its ion channel mechanisms.

METHODS

The circular muscle and longitudinal muscle strips of proximal colon were isolated from rats. An isometric force transducer and a biology signal collection system were employed to observe the effects of methane on spontaneous contractile activity of muscle strips. The effects of methane on longitudinal muscle strips were observed after pre-treatment of these strips with tetrodotoxin (TTX) or N-nitro-L-arginine methylester (L-NAME). Single cell of colonic smooth muscle was isolated by collagenase and then whole-cell patch clamp technique was used to record voltage dependent potassium current (IKV) and large conductance Ca(2+)-activated K(+) current (IBKca) in the absence or presence of methane.

RESULTS

Methane significantly attenuated the contractile amplitude of longitudinal muscle strips (from (1.12 ± 0.27) to (0.99 ± 0.31) g, n = 19, P = 0.013) whereas there were no changes in some longitudinal muscle strips (n = 6) in the presence of methane. The inhibitory effect of methane persisted after the pre-treatment of longitudinal muscle strips with TTX or L-NAME. Methane had no effects on the contractile cycle time of longitudinal muscle strips and contractile activity of circular muscle strips. And 3% methane solution significantly increased the density of IKV (from (13.3 ± 1.0) pA/pF to (18.5 ± 1.4) pA/pF, at +60 mV, n = 11, P = 0.001) versus the control group whereas methane had no effect on IBKca (all P > 0.05).

CONCLUSION

Methane can inhibit contractile activity of proximal colonic longitudinal muscle by activating voltage dependent potassium channel and increasing IKV.

摘要

目的

探讨甲烷对近端结肠动力的影响并阐明其离子通道机制。

方法

从大鼠分离出近端结肠的环形肌条和纵行肌条。使用等长力传感器和生物信号采集系统观察甲烷对肌条自发收缩活动的影响。用河豚毒素(TTX)或N-硝基-L-精氨酸甲酯(L-NAME)预处理纵行肌条后,观察甲烷对其的影响。用胶原酶分离结肠平滑肌单细胞,然后在有无甲烷存在的情况下,使用全细胞膜片钳技术记录电压依赖性钾电流(IKV)和大电导钙激活钾电流(IBKca)。

结果

甲烷显著降低纵行肌条的收缩幅度(从(1.12±0.27)降至(0.99±0.31)g,n = 19,P = 0.013),而在存在甲烷的情况下,一些纵行肌条(n = 6)没有变化。用TTX或L-NAME预处理纵行肌条后,甲烷的抑制作用持续存在。甲烷对纵行肌条的收缩周期时间和环形肌条的收缩活动没有影响。与对照组相比,3%甲烷溶液显著增加了IKV的密度(在+60 mV时,从(13.3±1.0)pA/pF增加到(18.5±1.4)pA/pF,n = 11,P = 0.001),而甲烷对IBKca没有影响(所有P>0.05)。

结论

甲烷可通过激活电压依赖性钾通道并增加IKV来抑制近端结肠纵行肌的收缩活动。

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