Cholecystokinin increases small intestinal motility and reduces enteric bacterial overgrowth and translocation in rats with surgically induced acute liver failure.
Enteric bacterial translocation into extraintestinal sites has been proposed as a potential route for bacterial infection in acute liver failure. Bacterial overgrowth in the intestine plays an important role in the etiology of bacterial translocation from the gut. The aim of the present study was to evaluate the influence of exogenous cholecystokinin (CCK) on intestinal transit time, enteric bacterial overgrowth and translocation in experimental acute liver failure induced by 90% hepatectomy. A delayed intestinal transit time was noted in animals subjected by subtotal hepatectomy after 1 h, followed by enteric bacterial overgrowth and translocation into the systemic circulation, mesenteric lymph nodes, and systemic organs at 2 and 4 h. Intravenous infusion of CCK stimulated intestinal transit time in animals with sham operation and subtotal hepatectomy, though a restoration to sham levels could not be obtained in the later. Moreover, enteric bacterial overgrowth and translocation were prevented in hepatectomized animals. The present data imply that impaired intestinal motility, followed by enteric bacterial overgrowth and translocation in experimental acute liver failure, could be prevented by CCK infusion.
Wang
X
X
Department of Surgery, Lund University Hospital, Sweden.
Soltesz
V
V
Axelson
J
J
Andersson
R
R
D000818:Animals; D018988:Bacterial Translocation / Q000187:drug effects*; D002766:Cholecystokinin / Q000494:pharmacology*; D004926:Escherichia coli / Q000502:physiology; D005769:Gastrointestinal Motility / Q000187:drug effects*; D006498:Hepatectomy; D007421:Intestine, Small / Q000187:drug effects / Q000382:microbiology / Q000503:physiopathology*; D017114:Liver Failure, Acute / Q000382:microbiology* / Q000503:physiopathology*; D008297:Male; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley
D002766:Cholecystokinin