Differentielle Regulation der postprandialen Jejunummotilität des Menschen durch CCK und durch das cholinerge Nervensystem
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Philipps-Universität Marburg
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Abstract
Summary of Study Protocol "Differential
Regulation of Postprandial Human Jejunal Motility by CCK and
the Cholinergic System". This study was designed to assess the
role of endogenous CCK and cholinergic neural inputs as
physiological regulators of human postprandial jejunal motility
and transit. Therefore, CCK-A and muscarinic regulators were
blocked by their specific antagonists loxiglumide and atropine.
Methods: 9 healthy male volunteers were studied on 3 separate
days in random order with background IV infusions of a) saline
0,9%, b) atropine [5µg / (kg x h)] or c) loxiglumide [10 mg /
(kg x h)]. After an interdigestive period of at least 20 min a
mixed liquid meal (49% carbohydrate, 35%liquid, 16%protein) was
intrajejunally perfused for 240 min through the most proximal
port of the manometry catheter (8 ports spaced at 2
cm-intervals) located just distally the ligament of Treitz.
Intestinal transit time was measured by the hydrogen breath
test with 15 g lactulose intrajejunally administered 1 min
after start of nutrition perfusion. Results: Mean ± SEM ; * : p
< 0,05 vs saline 0,9% ; # : p< 0,01 loxiglumid vs
atropine. The results in following sequence of the parameter:
Saline ; Atropin ; Loxiglumide. Summery of contraktions / 240
min: 5434 ±568 ; 5140 ± 768 ; 3414 ± 629*#. Mean amplitude
(mmHg): 18,9 ± 0,9 ; 23,9 ± 1,1* ; 16,3 ± 1,0 *#. Mean
duration(s): 3,7 ± 0,2 ; 3,4 ± 0,1* ; 3,2 ± 0,1*. Motility
index (mmHg x s/240 min): 229248 ± 28446 ; 261446 ± 46120 ;
117587 ± 30879*#. summery of propagated peaks/240min: 3957 ±
448 ; 2798 ± 522* ; 1824 ± 479*. % propagated peaks / 240 min:
58,7 ± 2,4 ; 40,2 ± 3,2* ; 39,8± 4,4*. Summery of propagation
over 2 cm: 920 ± 10 ; 785 ± 147 ; 505 ± 130*. Summery of
propagation over 4 ?6 cm: 423 ± 50 ; 266 ± 56* ; 180 ±
59*. Summery of propagation over 8 ?12cm: 117 ± 24 ; 61 ±
10* ; 37 ± 10*. Intestinal transit time (min): 54,4 ± 11,3 ;
123,3 ± 24,8* ; 164,4 ± 24,1*. Summary of results: Atropine did
not alter overall contraction frequency and motility index. It
increased amplitude but shortened duration of contractions. It
markedly reduced the proportion of propagated contractions and
especially propagation over longer distandes in the jejunum.
Loxiglumide clearly diminished frequency, amplitude and
duration of contractions, absolute number and percentage of
propagated contractions. Both atropine and loxiglumide,
markedly delayed small intestinal transit. Conclusions: Both,
endogenous CCK and cholinergic neural input are important
determinants of intestianl transit. However, they differently
affect human postprandial jejunal motility. CCK is an important
stimulatory regulator of motility activity (frequency,
amplitude and duration) and its spatial temporal organization
(wave propagation). Cholinergic input is not a major
stimulatory regulator of motility activity but is required for
prograde wave propagation, especially over longer distances.
Intestinal transit depends clearly more on organization than on
activity of the contractile pattern. The differential effects
of loxiglumide and atropine would be compatible with the notion
that endogenous CCK does not primarily affect jejunal motility
via receptors on cholinergic neurons but mainly interacts with
CCK-A receptors directly located on smooth
muscle.
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Dates
Created: 2003Issued: 2004-04-20Updated: 2011-08-10
Faculty
Medizin
Publisher
Philipps-Universität Marburg
Language
ger
Data types
DoctoralThesis
Keywords
CCK-A RezeptorLoxiglumid , H2-TransitAtropinePostprandial ,Loxiglumide , ManometryMotility
DFG-subjects
CholecystokininLactuloseAcetylcholinrezepMotilitätAtropin , PlaceboGastrointestinales Hormon , GastrointestinaltraktLeerdarm
DDC-Numbers
610
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Böker, Kornelia: Differentielle Regulation der postprandialen Jejunummotilität des Menschen durch CCK und durch das cholinerge Nervensystem. : Philipps-Universität Marburg 2004-04-20. DOI: https://doi.org/10.17192/z2004.0222.
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This item has been published with the following license: In Copyright