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手术去自主神经支配导致结肠动力改变:对低位前切除术综合征的一种解释?

Surgical autonomic denervation results in altered colonic motility: an explanation for low anterior resection syndrome?

作者信息

Lee Woo Yong, Takahashi Toku, Pappas Theodore, Mantyh Christopher R, Ludwig Kirk A

机构信息

Department of Surgery, Sungkyunkwan University, Samsung Medical Center, Seoul, Korea.

出版信息

Surgery. 2008 Jun;143(6):778-83. doi: 10.1016/j.surg.2008.03.014. Epub 2008 May 9.

Abstract

BACKGROUND

We hypothesized that the bowel dysfunction known as low anterior resection syndrome is caused by denervation of the left colon. The purpose of this study is to determine how surgical denervation changes left colon motility and to identify the mechanism of this change.

MATERIALS AND METHODS

Strain gauge transducers were implanted on the serosal surface of the descending colon of male SD rats (250-300 g). After a 2-h baseline recording, motility was recorded for another 2 h after either simple left colon manipulation (n = 6) or surgical left colon denervation (n = 6). Various pharmacologic agents were then administered before denervation to determine the mechanism by which denervation changed left colon motility. Changes in motility were calculated by determining a % motility index (MI) (%MI = MI posttreatment/MI baseline) with significance defined as P < .05.

RESULT

Denervation resulted in an increased mean %MI (128.8 +/- 15.4) compared with simple manipulation of the bowel, which decreased mean %MI (87.9 +/- 25.3) (P < .05). In the second set of experiments, both guanethidine and phentolamine increased mean %MI after injection (P < .05), but no additional increase of %MI occurred after denervation (P < .05). However, propranolol produced no increase of motility after injection and it did not affect the increase in motility observed after denervation (P < .05).

CONCLUSION

Surgical denervation of the left colon results in a significant increase in motility. Pharmacologically, this increase seems to be the result of destruction of an inhibitory alpha-sympathetic pathway. This increased motility may contribute to low anterior resection syndrome.

摘要

背景

我们推测,被称为低位前切除综合征的肠道功能障碍是由左半结肠去神经支配引起的。本研究的目的是确定手术去神经支配如何改变左半结肠的运动,并确定这种变化的机制。

材料与方法

将应变片式传感器植入雄性SD大鼠(250 - 300克)降结肠的浆膜表面。在进行2小时的基线记录后,在单纯左半结肠操作(n = 6)或手术左半结肠去神经支配(n = 6)后再记录2小时的运动情况。然后在去神经支配前给予各种药物,以确定去神经支配改变左半结肠运动的机制。通过计算运动变化的百分比运动指数(MI)(%MI = 治疗后MI/基线MI)来评估运动变化,显著性定义为P <.05。

结果

与单纯肠道操作相比,去神经支配导致平均%MI增加(128.8 +/- 15.4),而单纯肠道操作使平均%MI降低(87.9 +/- 25.3)(P <.05)。在第二组实验中,胍乙啶和酚妥拉明注射后均使平均%MI增加(P <.05),但去神经支配后%MI没有进一步增加(P <.05)。然而,普萘洛尔注射后未引起运动增加,且不影响去神经支配后观察到的运动增加(P <.05)。

结论

左半结肠手术去神经支配导致运动显著增加。从药理学角度来看,这种增加似乎是抑制性α-交感神经通路被破坏的结果。这种运动增加可能导致低位前切除综合征。

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