Experimental Research of Mechanism of Gastrointestinal Motility Disorder of Severe Acute Pancreatitis in Rats_CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY

Authors：

WANG Qiang ¹ , WANG Xiangying ¹ , HUANG Shuo ¹ , LU Yizhan ² , ZHANG Xingwen. ³

1. Department of Hepatobiliaropancreatic Surgery， The People’s Hospital of Hunan Province， Changsha 410005， Hunan Province，China;;
2. Department of General Surgery， The People’s Hospital of Xiangxi Autonomous Prefecture， Jishou 416000，Hunan Province， China;;
3. Department of Emergency， The People’s Hospital of Hunan Province， Changsha 410005，Hunan Province， China;

Corresponding author：

Keywords：

Severe acute pancreatitis; Gastrointestinal motility; Gastrointestinal hormones; Interdigestive myoelectric complex; Motilin; Vasoactive intestinal peptide

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Objective 　To investigate the mechanism of gastrointestinal motility disorder of severe acute pancreatitis （SAP） in rats.
Methods 　SD rats were randomly divided into 2 groups：sham operation （SO） group （n=16） and SAP group （n=16）. The gastric antrum interdigestive myoelectric complex （IMC） of rat was recorded by using bipolar silver electrode recording， the concentration of serum motilin （MTL） and vasoactive intestinal peptide （VIP） were detected by enzyme-linked immunosorbent assay （ELISA） method， and determined the pancreatic pathology score.
Results 　Compared with SO group， the concentration of serum MTL obvious decreased and the concentration of VIP obvious rised in SAP group （P＜0.01）. Compared with SO group， the time of IMC cycle， andⅠand Ⅱ phase were extended， and time of Ⅲ phase was shortened， also the amplitude and frequency of peak electric of Ⅲ phase were declined in SAP group （P＜0.01）. And the concentration of MTL in SAP group showed positive correlation with the time of Ⅲ phase of IMC （r=0.967， P＜0.01）， the concentration of VIP in SAP group showed negative correlation with the time of Ⅲ phase of IMC （r=-0.592， P＜0.05）. The pancreatic organization pathological score in SAP group was higher than that in SO group （P＜0.01）.
Conclusion 　There is gastrointestinal motility disorder in SAP rats， furthermore， it may induce gastrointestinal motility disorder through effecting the gastrointestinal smooth muscle electrical activity.

Citation： WANG Qiang,WANG Xiangying,HUANG Shuo,LU Yizhan,ZHANG Xingwen.. Experimental Research of Mechanism of Gastrointestinal Motility Disorder of Severe Acute Pancreatitis in Rats. CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY, 2012, 19(4): 419-423. doi: Copy

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14.	Van Assche G， Depoortere I， Thijs T， et a1. Contractile effects and intracellular Ca2+ signalling induced by motilin and erythromycin in the circular smooth muscle of human colon [J].Neurogastroenterol Motil， 2001， 13(1)： 27-35.
15.	Feighner SD， Tan CP， McKee KK， et al. Receptor for motilin identified in the human gastrointestinal system [J]. Science，1999， 284(5423)：2184-2188.
16.	杨侠，童蕾，杨浩. 大鼠肠肌间神经元胃动素受体的表达及胃动素引起神经元内钙信号的机制 [J]. 四川大学学报( 医学版)， 2006， 37(5)：683-686.
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24.	Murthy KS， Zhang KM， Jin JG， et al. VIP-mediated G proteincoupled Ca2+ influx activates a constitutive NOS in dispersed gastric muscle cells [J]. Am J Physiol， 1993， 265(4 Pt 1)：G660-G671.
25.	Kim BJ， Lee JH， Jun JY， et al. Vasoactive intestinal polypeptide inhibits pacemaker activity via the nitric oxide-cGMP-protein kinase G pathway in the interstitial cells of Cajal of the murine small intestine [J]. Mol Cells， 2006， 21(3)： 337-342.

1. Warshaw AL. Improving the treatment of necrotizing pancreatitis——a step up [J]. N Engl J Med， 2010， 362(16)：1535-1537.
2. Herberta MK， Holzer P. Standardized concept for the treatment of gastrointestinal dysmotility in critically ill patients—— Currentstatus and future options [J]. Clin Nutr， 2008， 27(1)：25-41.
3. Liu H， Li W， Wang X， et al. Early gut mucosal dysfunction in patients with acute pancreatitis [J]. Pancreas， 2008， 36(2)：192-196.
4. Flint RS， Windsor JA. The role of the intestine in the pathophysiology and management of severe acute pancreatitis [J]. HPB (Oxford)， 2003， 5(2)： 69-85.
5. Wang X， Gong Z， Wu K， et al. Gastrointestinal dysmotility in patients with acute pancreatitis [J]. J Gastroenterol Hepatol，2003， 18(1)： 57-62.
6. 王强，王湘英. 胃肠激素紊乱与重症急性胰腺炎胃肠动力障碍的机制 [J]. 中华全科医师杂志， 2012， 11(1)： 85-87.
7. Schmidt J， Lewandrowsi K， Warshaw AL， et al. Morphometric characteristics and homogeneity of a new model of acute pancreatitis in the rat [J]. Int J Pancreatol， 1992， 12(1)：41-51.
8. 刘劲松，侯晓华. 激素与胃肠道运动 [J]. 胃肠病学和肝病学杂志， 2004， 13， (4)：335-336.
9. 周吕. 胃肠激素与胃肠动力 [J]. 中国实用内科杂志， 2006，26 (10)： 733-736.
10. 徐敏，王兴鹏，等. 急性胰腺炎病人胃肠动力的变化及其机制研究 [J]. 中华急诊医学杂志， 2002， 11(5)：327-330.
11. 侯冰宗，石磊，房思炼，等. 清胰汤保留灌肠对急性重症胰腺炎患者胃肠动力学变化机制的研究 [J]. 中山大学学报( 医学科学版)， 2008， 29(4)：20-22.
12. Shi XZ， Choudhury BK， Pasricha PJ， et al. A novel role of VIP in colonic motility function：induction of excitation-transcription coupling in smooth muscle cells [J]. Gastroenterology， 2007，132(4)： 1388-1400.
13. Ogawa A， Mochiki E， Yanai M， et al. Interdigestive migrating contractions are coregulated by ghrelin and motilin in conscious dogs [J]. Am J Physiol Regul Integr Comp Physiol， 2012，302(2)： R233-R241.
14. Van Assche G， Depoortere I， Thijs T， et a1. Contractile effects and intracellular Ca2+ signalling induced by motilin and erythromycin in the circular smooth muscle of human colon [J].Neurogastroenterol Motil， 2001， 13(1)： 27-35.
15. Feighner SD， Tan CP， McKee KK， et al. Receptor for motilin identified in the human gastrointestinal system [J]. Science，1999， 284(5423)：2184-2188.
16. 杨侠，童蕾，杨浩. 大鼠肠肌间神经元胃动素受体的表达及胃动素引起神经元内钙信号的机制 [J]. 四川大学学报( 医学版)， 2006， 37(5)：683-686.
17. Fang P， Dong L， Luo JY. Effects of motilin on intracellular free calcium in cultured smooth muscle cells from the antrum of neonatal rats [J]. Acta Physiol (Oxf)， 2010， 199(1)：53-61.
18. Biancani P. Diversity of Ca2+-mobilizing mechanisms focus on “cGMP-mediated Ca2+ release from IP3-insensitive Ca2+ stores in smooth muscle” [J]. Am J Physiol， 1998， 274(5 Pt 1)： C1196-C1198.
19. Zietlow A， Nakajima H， Taniguchi H， et al. Association between plasma ghrelin and motilin levels during MMC cycle in conscious dogs [J]. Regul Pept， 2010， 164(2-3)：78-82.
20. Ohno T， Mochiki E， Kuwano H. The roles of motilin and ghrelin in gastrointestinal motility [J]. Int J Pept， 2010， 2010. pii：820794. Epub 2010 Feb 3.[ 21] Lu Y， Owyang C. Secretin-induced gastric relaxation is mediated by vasoactive intestinal polypeptide and prostaglandin pathways[J]. Neurogastroenterol Motil， 2009， 21(7)：754-e47-759-e47.
21. Van Geldre LA， Lefebvre RA. Interaction of NO and VIP in gastrointestinal smooth muscle relaxation [J]. Curr Pharm Des，2004， 10(20)： 2483-2497.
22. Hagen BM， Bayguinov O， Sanders KM. VIP and PACAP regulate localized Ca2+ transients via cAMP-dependent mechanism [J]. Am J Physiol Cell Physiol， 2006， 291(2)： C375-C385.
23. Matsuda NM， Miller SM. Non-adrenergic non-cholinergic inhibition of gastrointestinal smooth muscle and its intracellular mechanism(s) [J]. Fundam Clin Pharmacol， 2010， 24(3)： 261-268.
24. Murthy KS， Zhang KM， Jin JG， et al. VIP-mediated G proteincoupled Ca2+ influx activates a constitutive NOS in dispersed gastric muscle cells [J]. Am J Physiol， 1993， 265(4 Pt 1)：G660-G671.
25. Kim BJ， Lee JH， Jun JY， et al. Vasoactive intestinal polypeptide inhibits pacemaker activity via the nitric oxide-cGMP-protein kinase G pathway in the interstitial cells of Cajal of the murine small intestine [J]. Mol Cells， 2006， 21(3)： 337-342.

CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY

Experimental Research of Mechanism of Gastrointestinal Motility Disorder of Severe Acute Pancreatitis in Rats

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