AIM:To study the alterations of brain-gut peptides followingtraumatic brain injury(TBI)and to explore the underlyingsignificance of these peptides in the complicated gastrointestinaldysfunction.METHODS:Rat models of focal traumatic brain injury wereestablished by impact insult method,and divided into 6groups(6 rats each group)including control group withsham operation and TBI groups at postinjury 3,12,24,72 h,and d 7.Blood and proximal jejunum samples were takenat time point of each group and gross observations ofgastrointestinal pathology were recorded simultaneously.The levels of vasoactive intestinal peptide(VIP)in plasma,calcitonin gene-related peptide(CGRP)and cholecystokinin(CCK)in both plasma and jejunum were measured byenzyme immunoassay(EIA).Radioimmunoassay(RIA)wasused to determine the levels of VIP in jejunum.RESULTS:Gastric distension,delayed gastric emptying andintestinal dilatation with a large amount of yellowish effusionand thin edematous wall were found in TBI rats through12 h and 72 h,which peaked at postinjury 72 h.As comparedwith that of control group(247.84-29.5 ng/L),plasma VIPlevels were significantly decreased at postinjury 3,12 and24 h(106.74-34.1 rig/L,148.74-22.8 ng/L,132.84-21.6 ng/L,respectively),but significantly increased at 72 h(405.04±29.8ng/L)and markedly declined on d 7(130.74±19.3 ng/L).However,Plasma levels CCK and CGRP were significantlyincreased through 3 h and 7 d following TBI(126-691%increases),with the peak at 72 h.Compared with control(VIP,13.64-1.4 ng/g;CGRP,70.64-17.7 ng/g);VIP and CGRPlevels in jejunum were significantly increased at 3 h afterTBI (VIP,35.44±5.0 ng/g;CGRP,103.84±22.1 ng/g),anddeclined gradually at 12 h and 24 h(VIP,16.5±1.8 ng/g,5.54±1.4 nglg;CGRP,34.94±9.7 ng/g,18.54±7.7 ng/g),butwere significantly increased again at 72 h(VIP,48.74±9.5ng/g;CGRP,142.14±24.3 ng/g),then declined in various degrees on d 7(VIP,3.8±1.1ng/g;CGRP,102.5±18.1ng/g).The CCK levels in jejunum were found to change in a similartrend as that in plasma with the concentrations of CCKsignificantly increased following TBI(99-517% increases)and peaked at 72 h.CONCLUSION:Traumatic brain injury can lead to significantchanges of brain-gut peptides in both plasma and smallintestine,which may be involved in the pathogenesis ofcomplicated gastrointestinal dysfunction. AIM: To study the alterations of brain-gut peptides following traumatic brain injury (TBI) and to explore the underlyingsignificance of these peptides in the complicated gastrointestinal dysfunction. METHODS: Rat models of focal traumatic brain injury wereestablished by impact insult method, and into 6groups ( 6 rats each group) including control group withsham operation and TBI groups at postinjury 3,12,24,72 h, and d 7. Blood and proximal jejunum samples were taken at time point of each group and gross observations of gastrotrointestinal pathology were recorded simultaneously. levels of vasoactive intestinal peptide (VIP) in plasma, calcitonin gene-related peptide (CGRP) and cholecystokinin (CCK) in both plasma and jejunum were measured by enzyme immunoassay (EIA) .Radioimmunoassay (RIA) wasused to determine the levels of VIP in jejunum .RESULTS: Gastric distension, delayed gastric emptying and intestinal dilatation with a large amount of yellowish effusion and thin edematous wall were found in TBI rats thr ough12 h and 72 h, which peaked at postinjury 72 h.As comparedwith that of control group (247.84-29.5 ng / L), plasma VIPlevels were significantly decreased at postinjury 3,12 and24 h (106.74-34.1 rig / L, 148.74- 22.8 ng / L, 132.84-21.6 ng / L, respectively) but significantly increased at 72 h (405.04 ± 29.8 ng / L) and markedly declined on d 7 (130.74 ± 19.3 ng / L) CGRP were significantly increased by 3 h and 7 d following TBI (126-691% increases) with the peak at 72 h. Compared with control (VIP, 13.64-1.4 ng / g; CGRP, 70.64-17.7 ng / g); VIP and CGRPlevels in jejunum were significantly increased at 3 h after TBI (VIP, 35.44 ± 5.0 ng / g; CGRP, 103.84 ± 22.1 ng / g), and induced completion gradually at 12 h and 24 h (VIP, 16.5 ± 1.8 ng / g, ± 1.4 nglg; CGRP, 34.94 ± 9.7 ng / g, 18.54 ± 7.7 ng / g), butwere markedly increased again at 72 h (VIP, 48.74 ± 9.5 ng / g; CGRP, 142.14 ± 24.3 ng / g) in various degrees on d 7 (VIP, 3.8 ± 1.1 ng / g; CGRP, 102.5 ± 18.1 ng / g). The CCK levels in jejunum were found to change in a si milartrendas that in plasma with the concentration of CCKsificantly increased following TBI (99-517% increases) and peaked at 72 h.CONCLUSION: Traumatic brain injury can lead to significant changes in brain-gut peptides in both plasma and smallintestine, which may be involved in the pathogenesis ofcomplicated gastrointestinal dysfunction