Background-Nitric oxide (NO) is an unstable vasodilator formed by NO synthetase (NOS) from L-arginine (L-Arg) in various cells but its role in the control of pancreatic secretion in humans has not been examined. Aims-This study was designed to determine the role of endogenous NO in the control ofexocrine and endocrine pancreas using NOS inhibitor, NG-monomethyl-L-Arg (L-NMMA). Methods-Pancreatic secretion was stimulated by intravenous infusion of secretin (80 pmol/kglh) plus caerulein (50 pmollkglh) and duodenal content was aspirated by gastroduodenal tube. Two series of tests with secretagogue infusion were performed, one, with addition of graded doses of L-NMMA and, another, with addition of a constant dose of L-Arg alone followed by L-NMMA alone and finally by a combination of L-Arg and L-NMMA. Results-Addition of L-NMMA in graded doses (2-8 ,imol/kg/h) reduced dose dependently the secretin-caerulein stimulated pancreatic enzyme secretion without alterations in the volume flow and bicarbonate outputs. The addition of L-Arg to L-NMMA reversed the inhibitory action of L-NMMA on protein enzyme response to secretin-caerulein in these subjects. Secretin-caerulein infusion caused significant increase in plasma insulin and pancreatic polypeptide levels but without changes in plasma glucagon or somatostatin levels. L-NMMA alone resulted in a significant fall in plasma insulin and pancreatic polypeptide levels, while L-Arg added to pancreatic secretagogue infusion caused a significant increase of plasma insulin and pancreatic polypeptide levels above those attained with secretagogues alone. After the addition of L-Arg to L-NMMA, both plasma insulin and pancreatic polypeptide levels rose significantly above the levels observed with L-NMMA plus secretin-CCK stimulation.Conclusion-This study provides evidence that the suppression of NOS reduces pancreatic enzyme secretion and the plasma insulin and pancreatic polypeptide levels suggesting that endogenous NO affects both exocrine and endocrine pancreatic secretion in humans. (Gut 1997; 40: 86-91) Keywords: pancreas, nitric oxide, L-NMMA, secretin, caerulein, insulin, pancreatic polypeptide.Nitric oxide (NO), originally known as endothelium derived relaxing factor,' is an unstable vasodilator released by endothelial cells2 3 and neurons4 5 to act as local hormone in the vicinity of these cells. It is formed from the terminal guanitidine nitrogen atom of L-argmnine
The effects of loxiglumide, a potent cholecystokinin (CCK)-receptor antagonist, and atropine, a muscarinic receptor blocker, on exocrine pancreatic secretion stimulated by hormones (secretin plus CCK) and a Lundh test meal were studied in healthy young volunteers. Loxiglumide infused intravenously in gradually increasing doses (2-16 mumol/kg-h) caused a dose-dependent inhibition of pancreatic enzyme secretion induced by intravenous infusion of a constant dose of secretin (82 pmol/kg-h) plus CCK-8 (85 pmol/kg-h) but had relatively smaller influence on duodenal volume flow and bicarbonate output. Atropine (20 nmol/kg) also caused a significant reduction in pancreatic enzyme secretion but failed to affect the volume flow or bicarbonate secretion induced by secretin plus CCK, possibly owing to the high doses of secretin and CCK used in these tests. Both loxiglumide and atropine inhibited the pancreatic enzyme response to a Lundh meal, but atropine was more effective in the early phase and loxiglumide in the late phase of the postprandial secretion. Neither loxiglumide nor atropine affected the plasma gastrin and CCK levels, but both antagonists reduced plasma pancreatic polypeptide responses to the Lundh meal. We conclude that 1) loxiglumide results in a relatively stronger suppression of the pancreatic enzyme than aqueous-alkaline secretion induced by secretin plus CCK, whereas atropine inhibits only enzyme secretion; and 2) both loxiglumide and atropine suppress the pancreatic enzyme responses to the meal stimulation without affecting the postprandial plasma gastrin and CCK responses.
Kulesza E.,Sochi J .,Dzi.rzana. sh D.,Podl.snr J., Bogon ia.sh Z. IIOllth of ag., hiu. bun exilili ned.The children were divided into groups iccording to th. b.o. or nOl'llal gut flora/n/:CObo=27,COn=I9, DPbo=33, DPn=36.lo duodtnil fluid aerobes,anaerobes and yusts wert .s t illibd.Smn h.a, were lIusvred by RIA, duodtnil b.a. -TlC,fuul b.i.-Sb r"9"05t 3-P!Io. Ru!!l..!i :Bacltriil overgr",th WiS found in 47.B:! in DP and 5B.7',( in CO, lIiinlr cnstd by Enltrobacltriacue and DOIlg thM E.Col i.E.CoIi was isolab d in. 6.l.7',( in OPbo iIld 69.7'1. in COho.ln duodfnal fl uid uncOlljuQi ted and sfCondiry h.a , were found in~of children.lo all the inuesti gab d groups nahbsorption of h.a, was found-heul b.i. ov.r 270 \ROI/IOOg .ln 34' 1. fasti ng duodenal b.a, wtre bela. the cr itiulllicellil' concentritionl2lno11lJ.FastinglO '/smB b.i. wtre eleuabd in 567. in DP and CD considered together and postprandiilrll20 '1 in 467.. Conclus ions : I. Bacbriil ouergra.th is i pitngenic hctor in DP and CD. 2. E.CoIi in duod.na1 flu id UUst prolongat ion iIld aggriviition of inhnt's diir rhu. 3. In both OP and CD bile ic ids malabsorpt ion and l iuer failure are observed. 4. The est illit ion of lIicroflora and b.a, giue infOl'llati ons concern ing prognosis and trnbltnt ilIIOng other HCT,but do not diHerent iite chronic diirrhu.
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