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迷走神经阻断对犬食物和激素刺激的胰多肽及胃动素释放的影响。

Effect of vagal blockade on food- and hormone-stimulated release of pancreatic polypeptide and motilin in dogs.

作者信息

Greenberg G R, Chan B, Nordgren S R, Alleyne J

出版信息

Dig Dis Sci. 1985 Oct;30(10):946-53. doi: 10.1007/BF01308294.

Abstract

Vagal control of food- and hormone-stimulated release of pancreatic polypeptide (PP) and motilin was investigated in four conscious dogs by examining the effect of cryogenic vagosympathetic blockade. The postprandial PP response of 189 +/- 7 pM was totally, although reversibly, inhibited to 58 +/- 11 pM with the vagi blocked. Similarly, bombesin-, CCK-OP-, or neurotensin-stimulated PP release was abolished. Although the PP response to intraduodenal perfusion of an elemental diet was also reduced by blockade, the 52 +/- 15% inhibition was less than observed with the meal. In contrast to PP, plasma motilin fell after the meal from a fasting level of 128 +/- 16 pM to a nadir of 52 +/- 7 pM. Vagal blockade reversed this decline as plasma motilin rose to a peak of 121 +/- 18 pM with a pattern resembling the motilin response in the interdigestive state. This motilin increment during blockade was inhibited by atropine and by infusion of porcine PP. Plasma motilin also fell with the elemental diet, but this response was not affected by blockade. During infusion of bombesin, plasma motilin rose by 60 +/- 9 pM; vagal blockade augmented this increment twofold. Thus, the PP response to a meal and to hormonal stimulation is controlled by a vagal cholinergic excitatory pathway. However, intestinal release of PP is mediated in part by the vagus and in part by a vagally independent mechanism which may be neural or hormonal. Alternatively, vagal noncholinergic inhibition is a major mechanism modulating the motilin response after oral food but motilin release exclusively from intestinal nutriments is mediated by nonvagal, noncholinergic mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

通过检测低温迷走交感神经阻滞的效果,在四只清醒犬中研究了迷走神经对食物和激素刺激的胰多肽(PP)及胃动素释放的控制。阻断迷走神经后,餐后PP反应从189±7 pM完全(尽管是可逆的)抑制至58±11 pM。同样,蛙皮素、胆囊收缩素八肽或神经降压素刺激的PP释放也被消除。虽然阻断迷走神经也降低了十二指肠内灌注要素饮食引起的PP反应,但52±15%的抑制程度低于进食时观察到的情况。与PP相反,餐后血浆胃动素从空腹水平128±16 pM降至最低点52±7 pM。迷走神经阻滞逆转了这种下降,血浆胃动素升至121±18 pM的峰值,其模式类似于消化间期的胃动素反应。阻断期间这种胃动素的增加被阿托品和输注猪PP所抑制。要素饮食时血浆胃动素也下降,但这种反应不受阻断的影响。输注蛙皮素期间,血浆胃动素升高60±9 pM;迷走神经阻滞使这种升高增加了两倍。因此,PP对进食和激素刺激的反应受迷走胆碱能兴奋途径控制。然而,肠内PP的释放部分由迷走神经介导,部分由与迷走神经无关的机制介导,该机制可能是神经或激素机制。或者,迷走神经非胆碱能抑制是调节口服食物后胃动素反应的主要机制,但仅从肠内营养物质释放胃动素是由非迷走神经、非胆碱能机制介导的。(摘要截短于250字)

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