jejunal perfusion
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2012 ◽  
Vol 67 (2) ◽  
pp. 202-206 ◽  
Author(s):  
K Nagy ◽  
L Ramos ◽  
M-C Courtet-Compondu ◽  
S Braga-Lagache ◽  
K Redeuil ◽  
...  

2006 ◽  
Vol 291 (3) ◽  
pp. G389-G395 ◽  
Author(s):  
Sutep Gonlachanvit ◽  
Radoslav Coleski ◽  
Chung Owyang ◽  
William L. Hasler

The actions of nutrients on gut transit of liquids and solids have been extensively studied, but the effects of meal ingestion on intestinal gas flow are unexplored. We hypothesized that meals of varying caloric content and consistency modulate gas transit to different degrees. Nine healthy volunteers underwent jejunal perfusion of physiological gas mixtures at 12 ml·min−1·3 h, with ingestion of nothing (control), water (240 ml), 240-kcal liquid meals, and 240-kcal solid meals at the end of the second hour in separate studies. Gas was quantified from an intrarectal catheter. After an initial lag phase, gas evacuation approached steady state by the end of the fasting period. Solid and liquid caloric meals increased total gas volumes evacuated from 5–40 min after ingestion vs. control studies ( P < 0.05). These increases resulted from increased numbers of bolus gas evacuations ( P < 0.05), whereas bolus volumes, pressures, and flow rates were similar for all test conditions. Solid and liquid caloric meals elicited similar effects on bolus gas dynamic parameters, whereas water did not affect these measures vs. control (NS, not significant). Both caloric meals and the noncaloric liquid meal increased continuous gas flow, which represented <2% of total gas expulsion. In conclusion, caloric meals promote bolus gas transit in healthy humans, whereas noncaloric liquids have no effect. Solids stimulate early postprandial gas dynamics to the same extent as liquid meals of similar caloric content. Thus modulatory effects of meals on intestinal gas transit depend on their caloric content but not their consistency.


2001 ◽  
Vol 14 (1) ◽  
pp. 24-30 ◽  
Author(s):  
E. Rønholm ◽  
Lars Bäckman ◽  
Styrbjørn Friman ◽  
Kari-Lie Karlsen ◽  
Lars Mjörnstedt ◽  
...  

2001 ◽  
Vol 14 (1) ◽  
pp. 24-30 ◽  
Author(s):  
E. Ronholm ◽  
L. Backman ◽  
S. Friman ◽  
L. Mjornstedt ◽  
M. Olausson ◽  
...  

Gut ◽  
1999 ◽  
Vol 44 (2) ◽  
pp. 174-179 ◽  
Author(s):  
C P Bearcroft ◽  
P Domizio ◽  
F H Mourad ◽  
E A André ◽  
M J G Farthing

BackgroundThe antineoplastic drug cisplatin has been widely used for the treatment of cancer in humans but its use has been limited by vomiting and diarrhoea. Cisplatin releases 5-hydroxytryptamine into the gut which is thought to be the major mediator of cisplatin induced vomiting.AimTo determine whether cisplatin affects fluid and electrolyte transport in rat jejunum and whether this change can be modulated by the 5-hydroxytryptamine3 receptor antagonist, ondansetron.MethodsJejunal perfusion in rats in vivo was performed one hour after intraperitoneal cisplatin (5 and 10 mg/kg) administration. The effect of pretreatment with subcutaneous ondansetron 300 μg/kg was investigated.ResultsMedian net fluid absorption after cisplatin 10 mg/kg (67 μl/min/g dry intestinal weight (interquartile range 46 to 100); n = 15) was reduced compared with controls (120 (107 to 151) μl/min/g; n = 13; p<0.001). Ondansetron reversed the impairment of jejunal fluid absorption produced by cisplatin to normal (161 (130 to 176) μl/min/g; n = 11; p<0.001). Electrolyte movement paralleled fluid movement. Jejunal histological examination of sections from cisplatin treated animals showed villus damage, which was not prevented by pretreatment with ondansetron.ConclusionThese findings suggest that diarrhoea during cisplatin therapy may be due to altered fluid transport in the small bowel. The reversal of fluid transport to normal in the presence of a 5-hydroxytryptamine3 receptor antagonist suggests that 5-hydroxytryptamine is a local mediator in the small intestine.


1995 ◽  
Vol 268 (6) ◽  
pp. G959-G967
Author(s):  
J. J. Cullen ◽  
J. C. Eagon ◽  
F. S. Hould ◽  
R. B. Hanson ◽  
K. A. Kelly

The hypothesis was that orally moving pacesetter potentials distal to a site of jejunal transection and anastomosis would slow transit through jejunum containing them and that reoperation with excision of bowel containing these pacesetter potentials would restore transit to the control. In six conscious dogs with jejunal serosal electrodes for recording myoelectric activity and a jejunal perfusion/aspiration catheter for measuring transit, jejunal pacesetter potential frequency decreased distal to a midjejunal transection and anastomosis from 18.7 +/- 0.3 (SE) cycles/min (cpm) proximal to the site to 14.4 +/- 0.6 cpm distal to the site (P < 0.05). In addition, orally propagating pacesetter potentials occurred > 25% of the time in a 37 +/- 7 cm length of bowel distal to the site during fasting and after feeding. Transit through the segment with the orally moving pacesetter potentials was slowed during feeding (half time before and after transection, 7.7 +/- 1.1 and 13 +/- 2.0 min, respectively, P < 0.05). Resection of the segment with the abnormal pacesetter potentials shortened the length of bowel containing them to 24 +/- 2 cm (P > 0.05) and restored transit to the control. In conclusion, orally moving pacesetter potentials distal to a canine jejunal transection and anastomosis slowed transit through the segment of bowel containing them. Resection of the segment restored transit to the control.


1993 ◽  
Vol 35 (3) ◽  
pp. 243-250 ◽  
Author(s):  
H. Lennernas ◽  
D. Nilsson ◽  
SM Aquilonius ◽  
O. Ahrenstedt ◽  
L. Knutson ◽  
...  
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1992 ◽  
Vol 72 (2) ◽  
pp. 468-475 ◽  
Author(s):  
N. J. Rehrer ◽  
A. J. Wagenmakers ◽  
E. J. Beckers ◽  
D. Halliday ◽  
J. B. Leiper ◽  
...  

This study was designed to examine aspects of digestive function that may limit assimilation of water and oxidation of orally ingested carbohydrate (CHO) during exercise. Eight males completed a crossover study in which each cycled on four occasions for 80 min at 70% maximal O2 consumption. Beverage was consumed at 0, 20, 40, and 60 min. Beverages were water, 4.5% glucose (4.5G), 17% glucose (17G), and 17% maltodextrin (17MD). CHO beverages contained 20 meq/l NaCl and were 13C enriched to measure exogenous CHO oxidation. Gastric (beverage) volume was measured at 80 min. Water uptake was estimated by including 2H2O in the beverage and measuring 2H accumulation in blood. Jejunal perfusion tests were conducted at rest with the same subjects and beverages. In 60 min, 1,294 +/- 31 (SE) ml were ingested; at 80 min, volumes emptied with H2O (1,257 +/- 32 ml) and 4.5G (1,223 +/- 32 ml) were greater than with 17G (781 +/- 56 ml) and 17MD (864 +/- 71 ml; P less than 0.05). Total CHO oxidized was similar with all beverages, but there was a greater increase in exogenous CHO oxidation over time with 17G and 17MD than with 4.5G; 54, 19, and 18% of the CHO ingested with 4.5G, 17G, and 17MD, respectively, was oxidized. This represents 57, 32, and 27%, respectively, of the CHO emptied from the stomach. 2H accumulation in the blood was more rapid with H2O and 4.5G than with 17G or 17MD. Net jejunal water absorption was greater from 4.5G than from water. Net water absorption was also observed from 17MD, whereas net secretion was observed with 17G.(ABSTRACT TRUNCATED AT 250 WORDS)


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