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本文引用的文献

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Central inhibition of nitric oxide synthase modulates upper gastrointestinal motor activity.一氧化氮合酶的中枢抑制调节上消化道运动活性。
Am J Physiol. 1997 Mar;272(3 Pt 1):G417-24. doi: 10.1152/ajpgi.1997.272.3.G417.
2
Nitrergic inhibition of migrating myoelectric complex in the rat is mediated by vasoactive intestinal peptide.血管活性肠肽介导了大鼠移行性肌电复合波的一氧化氮能抑制作用。
Neurogastroenterol Motil. 1996 Dec;8(4):299-306. doi: 10.1111/j.1365-2982.1996.tb00268.x.
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The effect of acute hyperglycaemia on small intestinal motility in normal subjects.急性高血糖对正常受试者小肠运动的影响。
Diabetologia. 1996 Aug;39(8):984-9. doi: 10.1007/BF00403919.
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Nitric oxide inhibits the myoelectric activity of the small intestine in dogs.一氧化氮抑制犬小肠的肌电活动。
J Physiol Pharmacol. 1993 Mar;44(1):31-42.
5
Identification of mechanisms and sites of actions of mu and delta opioid receptor activation in the canine intestine.犬肠道中μ和δ阿片受体激活的作用机制及作用位点的鉴定
J Pharmacol Exp Ther. 1994 Feb;268(2):689-700.
6
Is nitric oxide involved in the tonic inhibition of central sympathetic outflow in humans?一氧化氮是否参与对人体中枢交感神经输出的紧张性抑制?
Hypertension. 1994 Oct;24(4):439-44. doi: 10.1161/01.hyp.24.4.439.
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Tonic inhibition of small intestinal motility by nitric oxide.一氧化氮对小肠蠕动的紧张性抑制作用。
J Auton Nerv Syst. 1993 Aug-Sep;44(2-3):179-87. doi: 10.1016/0165-1838(93)90030-x.
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The effects of recombinant human hemoglobin on esophageal motor functions in humans.重组人血红蛋白对人体食管运动功能的影响。
Gastroenterology. 1995 Oct;109(4):1241-8. doi: 10.1016/0016-5085(95)90584-7.
9
Is nitric oxide the final mediator regulating the migrating myoelectric complex cycle?一氧化氮是调节移行性肌电复合波周期的最终介质吗?
Am J Physiol. 1995 Feb;268(2 Pt 1):G207-14. doi: 10.1152/ajpgi.1995.268.2.G207.
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Effects of a nitric oxide synthase inhibitor in humans with septic shock.一氧化氮合酶抑制剂对感染性休克患者的影响。
Cardiovasc Res. 1994 Jan;28(1):34-9. doi: 10.1093/cvr/28.1.34.

一氧化氮机制调节人类小肠运动的证据。

Evidence that nitric oxide mechanisms regulate small intestinal motility in humans.

作者信息

Russo A, Fraser R, Adachi K, Horowitz M, Boeckxstaens G

机构信息

Department of Medicine, Royal Adelaide Hospital, North Terrace, Adelaide, South Australia 5000.

出版信息

Gut. 1999 Jan;44(1):72-6. doi: 10.1136/gut.44.1.72.

DOI:10.1136/gut.44.1.72
PMID:9862828
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1760071/
Abstract

BACKGROUND

Non-cholinergic non-adrenergic neural mechanisms involving nerves containing NO have been shown to modulate smooth muscle in the gastrointestinal tract, and it has been suggested that release from tonic NO inhibition may be important in the regulation of cyclical fasting small intestinal motility.

AIMS

To evaluate the role of NO mechanisms in the regulation of fasting small intestinal motor activity in humans using a specific NO synthase inhibitor, NG-monomethyl-L-arginine ( L-NMMA).

METHODS

In seven healthy male volunteers, duodenal and jejunal pressures were measured for four hours with a nine lumen manometric catheter. Volunteers attended on four separate days on which they received an intravenous infusion either saline or L-NMMA (0.5, 2, or 4 mg/kg/h) in random order. Intravenous infusions began 10 minutes after completion of phase III of the migrating motor complex (MMC).

RESULTS

The first episode of phase III activity occurred earlier after infusion of 2 and 4 mg/kg/h L-NMMA than after infusion of 0.5 mg/kg/h L-NMMA or saline (mean (95% confidence interval) 52 (36-68) and 57 (18-97) v 116 (69-193) and 145 (64-226) minutes respectively) with a resultant MMC cycle length of 82 (59-105) and 86 (46-126) v 132 (49-198) and 169 (98-240) minutes respectively. The total number of phase III activities during the four hour recording was increased (p<0.05) by L-NMMA at a dose of 4 mg/kg/h (2 (1-3)) but not at 2 mg/kg/h (1.5 (1-2)) or 0.5 mg/kg/h (1.3 (1-2)) compared with saline (1.3 (0.6-2)). L-NMMA had no effect on the duration, velocity, number of contractions per minute, length of migration, or site of origin of phase III of the MMC. The duration of phase I activity was shorter (p<0.05) with 4 mg/kg/h L-NMMA than with saline (12 (1-23) v 31 (19-44) minutes).

CONCLUSIONS

These observations suggest that NO mechanisms play a role in the regulation of fasting small intestinal motor activity in humans.

摘要

背景

涉及含一氧化氮(NO)神经的非胆碱能非肾上腺素能神经机制已被证明可调节胃肠道平滑肌,并且有人提出,从持续性NO抑制中释放出来可能在周期性禁食小肠运动的调节中起重要作用。

目的

使用特异性NO合酶抑制剂NG-单甲基-L-精氨酸(L-NMMA)评估NO机制在调节人类禁食小肠运动活动中的作用。

方法

在7名健康男性志愿者中,使用九腔测压导管测量十二指肠和空肠压力4小时。志愿者在四个不同的日子前来,在这些日子里他们随机接受静脉输注生理盐水或L-NMMA(0.5、2或4mg/kg/h)。静脉输注在移行运动复合波(MMC)的III期完成后10分钟开始。

结果

输注2mg/kg/h和4mg/kg/h L-NMMA后,III期活动的首次发作比输注0.5mg/kg/h L-NMMA或生理盐水后更早(平均(95%置信区间)分别为52(36-68)和57(18-97)分钟,而116(69-193)和145(64-226)分钟),MMC周期长度分别为82(59-105)和86(46-126)分钟,而132(49-198)和169(98-240)分钟。在4mg/kg/h剂量的L-NMMA作用下,4小时记录期间III期活动的总数增加(p<0.05),但在2mg/kg/h(1.5(1-2))或0.5mg/kg/h(1.3(1-2))时未增加,与生理盐水(1.3(0.6-2))相比。L-NMMA对MMC的III期的持续时间、速度、每分钟收缩次数、移行长度或起源部位没有影响。4mg/kg/h L-NMMA作用下I期活动的持续时间比生理盐水时更短(p<0.05)(12(1-23)分钟对31(19-44)分钟)。

结论

这些观察结果表明,NO机制在调节人类禁食小肠运动活动中起作用。