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Biomedical subjects

X D Wang

Publications and source records attributed to X D Wang.

At least 91 records · Page 5Linked to original sources
PubMed1996

Cisapride prevents enteric bacterial overgrowth and translocation by improvement of intestinal motility in rats with acute liver failure.

Enteric bacterial overgrowth resulting from compromised gastrointestinal motility has been suggested to be important for the development of enteric bacterial translocation. In the present study, the effect of cisapride, a 5-hydroxytryptamine-4-receptor agonist and stimulant of intestinal motility, was evaluated concerning intestinal motility, as measured by intestinal transit time, enteric bacterial overgrowth, and bacterial translocation from the gut in rats with acute liver failure induced by 90% hepatectomy. The results demonstrated that (1) the incidence of bacterial translocation to the systemic and portal circulation as well as to the liver, spleen, kidneys, and lungs was nil, and 17-33% to MLN in hepatectomized animals treated with cisapride, i.e. significantly lower than in hepatectomized rats administered saline; (2) overgrowth of E. coli in the intestine was noted in hepatectomized animals given saline, but not following cisapride treatment; (3) cisapride improved the otherwise delayed intestinal transit time following hepatectomy as shown by an increase in the leading edge of isotopic propulsion and the linear slope of the cumulative percent of radioactivity through each intestinal segment. Thus, we conclude that intravenous administration of cisapride prevents enteric bacterial overgrowth and bacterial translocation by improving intestinal motility in rats with acute liver failure induced by subtotal hepatectomy.

Animals↗
PubMed1996

Ultrasound-guided internal radiotherapy using yttrium-90-glass microspheres for liver malignancies.

UNLABELLED: Treatment of liver malignancies, in particular hepatocellular carcinoma, remains a serious problem because of the difficulty of delivering adequate therapeutic agents to the lesions while sparing the surrounding normal tissue. In an attempt to overcome this obstacle, intratumoral injection of 90Y, a beta-emitter, was performed. METHODS: Twenty-seven hepatocellular carcinomas and six liver metastases were studied, most of which had failed other therapeutic modalities. Guided by ultrasound, 90Y-glass microspheres (GMS) were carefully injected into predetermined tumor sites. The procedure was repeated at 3--4-wk intervals where indicated. Echographic, clinical and laboratory follow-up was conducted at regular intervals. RESULTS: Twelve to 32 mo after treatment, 27 patients were still alive, with dramatic improvement of their clinical condition: 90.6% of the tumor foci became smaller, with echogenic or blood flow changes on liver sonograms. Serum titers of alpha-FP in 10 of 13 patients returned to normal levels. Repeat biopsy in nine patients showed complete tumor destruction in eight. Six patients died of either end-stage disease or wide dispersion of the tumor. CONCLUSION: The intratumoral administration of 90Y-GMS under ultrasound guidance yielded a higher cure rate for liver malignancy with no severe side effects. The higher radiation dosage delivered by injected 90Y to the periphery of the lesions (up to 28,215-75,720 cGy) was thought to account for the successful outcome. These results show that intratumoral radionuclide injection is feasible for treatment of malignant lesions inside the body.

Adult↗
PubMed1996

In vivo biosynthesis of retinoic acid from beta-carotene involves and excentric cleavage pathway in ferret intestine.

This study was done to determine whether retinoic acid can be produced by excentric cleavage of beta-carotene in vivo. By using an inhibitor of retinaldehyde oxidation, citral, either retinaldehyde or beta-carotene was incorporated in a micellar solution and perfused through the upper portion of small intestine of ferrets. After 2 h perfusion of 1 microM retinaldehyde, retinoic acid rose in portal blood (+3.5 +/- 1.3 nmol/L) and was detected in the intestinal mucosa (30 +/- 2 pmol/g). When citral was added at 2 mM along with retinaldehyde, retinoic acid decreased in the portal blood and retinoic acid was not detected in the intestinal mucosa. With or without the presence of citral (2 mM), the perfusion of beta-carotene (10 microM) during 2 h caused a significant rise of retinoic acid in portal blood (+2.6 +/- 0.6 nmol/L and + 4.1 +/- 0.6 nmol/L, respectively) and in liver; moreover, significant amounts of retinoic acid were detected in the intestinal mucosa (19 +/- 3 pmol/g and 36 +/- pmol/g, respectively. This study demonstrates that after intestinal perfusion of beta-carotene in the ferret in vivo, a substantial amount of retinoic acid is formed via an excentric cleavage pathway.

Acyclic Monoterpenes↗
PubMed1996

[Study on relationship of lipid peroxide in coronary heart disease with and without diabetes].

Activity of erythrocyte superoxide dismutase (RBC-SOD), levels of serum malondialdehyde (MDA), plasma 6-keto-prostaglandin F 1 alpha (6-keto-PGF 1 alpha) and thromboxane B2(TXB2) were measured in 30 healthy subjects and 57 coronary heart desease (CHD) patients inoluding 21 cases complicated with diabetes and 36 without. Their characteristics of Syndrome Differentiation and typing were observed. The results showed that the activity of RBC-SOD, 6-keto-PGF 1 alpha in CHD patients were significantly lower than those in the healthy subjects, but the levels of TXB2, MDA were significantly higher. The levels of TXB2 in CHD patients with diabetes were significantly higher than tose without, but the activity of RBC-SOD were significantly lower. There were remarkably positive correlations between the levels of serum MDA and that of blood sugar, TXB2, TG and BMI in CHD patients with diabetes. There were remarkably negative correlations between the levels of serum MDA and plasma 6-keto-PGF 1 alpha. The results suggested that the metabolic abnormality of lipoperoxides was more serious in CHD patients with diabetes than without. The main Syndrome of CHD with diabetes was Qi-Yin Deficiency with Blood Stasis, while that of without diabetes was Qi Deficiency with Blood Stasis.

6-Ketoprostaglandin F1 alpha↗
PubMed1996

Evidence for the involvement of protein kinase C isoforms in alpha-1 adrenergic activation of phospholipase A2 in FRTL-5 thyroid cells.

BACKGROUND: FRTL-5 thyroid cells are a cell line extensively used for the investigation of thyroid functions. Activation of alpha-1 adrenergic receptors stimulates both arachidonic acid (AA) release and cytosolic Ca2+ increase in this cell line. Cytosolic Ca2+ and arachidonic acid are known to be important second messengers regulating a variety of thyroid functions. The generation of these messengers is regulated primarily by two different types of phospholipases, phospholipase C (PLC) and phospholipase A2 (PLA2). METHODS: Norepinephrine (NE, 10 mumol/L) was used as an alpha-1 adrenergic activator, and cytosolic-free Ca2+ concentration ([Ca2+]i) was determined using the fluorescent dye indo-1. Arachidonic acid release was measured as an indicator of PLA2 activation, and protein kinase C (PKC) activity determination and isoforms identification were performed using commercial kits. RESULTS: Norepinephrine increased [Ca2+]i and AA release. Prevention of NE-induced cytosolic Ca2+ influx, either by removal of extracellular Ca2+ or by use of Ca2+ channel blockers, NiCl2 or CoCl2, inhibited AA generation entirely. Inhibition of NE-induced increase in [Ca2+]i by the Ca2+ chelator, 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), also significantly suppressed NE-induced AA release. Inhibition of PKC activity by PKC inhibitors (H-7 or staurosporine) or downregulation induced by prolonged treatment with phorbol 12-myristate 13-acetate (PMA) or thyleametoxin (TX) significantly blocked the NE-induced AA release, which indicates PKC is involved in mediating NE-induced AA release. Protein kinase C activity measurement indicated that NE induced an activation of PKC in 5 minutes. To further characterize the role of PKC or Ca2+ in regulation of AA release, we identified PKC isoforms by immunoblotting with specific antibodies against 8 different Protein kinase C isoforms. PKC-alpha, -beta I, -beta II, -gamma, delta, -epsilon, -zeta, and -eta isoforms were identified. Norepinephrine induced translocation of PKC-alpha, -beta I, -beta II, -gamma, -delta, and -epsilon isoforms but not -zeta and -eta from cytosol to membrane. Chelation of intracellular Ca2+, prevention of Ca2+ influx, or prolonged treatment with thymeleatoxin (TX) completely blocked the NE-induced translocation of PKC-alpha. CONCLUSIONS: These results, taken together with data obtained from AA experiments, suggest that PKC plays a critical role in alpha-1 adrenergic receptor mediated PLA2 activation and subsequent AA release. Extracellular Ca2+ influx is a prerequisite for both PKC-alpha translocation and AA release. Whether Ca2+ acts directly upon the PLA2, or via PKC-alpha, to regulate AA generation is an intriguing question that remains to be clarified.

Animals↗
PubMed1995

Vitamin E enhances the lymphatic transport of beta-carotene and its conversion to vitamin A in the ferret.

BACKGROUND/AIMS: beta-Carotene and alpha-tocopherol may have either antagonistic or synergistic effects on each other's absorption and metabolism. The effects of both physiological and pharmacological concentrations of alpha-tocopherol on the absorption and metabolism of beta-carotene in ferret intestine were determined. METHODS: A high concentration of beta-carotene was perfused through the upper portion of the small intestine of ferrets in vivo with varying levels of alpha-tocopherol. The effluent of a mesenteric lymph duct cannulation, the intestinal mucosal scraping, and portal vein blood were sampled and analyzed by high-performance liquid chromatography. RESULTS: The lymphatic transport of beta-carotene was enhanced 4-fold by alpha-tocopherol at a physiological dose and 12-21-fold at a pharmacological dose. The lymphatic transport of alpha-tocopherol was linearly (r = 0.8; P < 0.05) related to the luminal alpha-tocopherol concentration even in the presence of a high concentration of beta-carotene. Furthermore, alpha-tocopherol increased the conversion of beta-carotene into retinol in the intestine in a dose-dependent manner. CONCLUSIONS: alpha-Tocopherol has a positive effect on the intestinal absorption of intact beta-carotene and may modulate the metabolic conversion of beta-carotene into retinoids.

Absorption↗
PubMed1995

Identification of protein kinase C and its multiple isoforms in FRTL-5 thyroid cells.

Protein kinase C (PKC) has been implicated as an important regulator of signal transduction in the FRTL-5 thyroid cell line, but little is known about its isoforms in this cell line. In the present investigation, we characterized the activation of PKC by measuring the enzyme activity and identifying its isoforms in both cytosol and membrane fractions. Phorbol 12-myristate 13-acetate (PMA) was used as a PKC activator in this study. PKC activity assay revealed that PMA (300 nM) induced a rapid translocation from cytosol to membrane within 1 min and led to an almost complete translocation within 15 min. Multiple PKC isoforms were examined by Western blot analysis with specific antibodies against alpha, beta, gamma, delta, epsilon, and zeta isoforms. PKC alpha, delta, epsilon, and zeta were identified in this cell line, but PKC beta and gamma were not. Exposure of the cells to PMA (300 nM) for 5 to 30 min led to the translocation of PKC alpha, delta, and epsilon from the cytosol to the membrane fraction, while PKC zeta was not affected. Treatment with PMA (300 nM) for 24 h resulted in the down-regulation of PKC alpha, delta, and epsilon, but not PKC zeta. This study demonstrates for the first time direct evidence for the activation of PKC, and expression and distribution of its isoforms in FRTL-5 thyroid cells.

Animals↗
PubMed1995

The role of oral administration of oatmeal fermented by Lactobacillus reuteri R2LC on bacterial translocation after acute liver failure induced by subtotal liver resection in the rat.

BACKGROUND: Previous experimental studies showed that a disturbed ecology of the enteric bacterial population might contribute to the occurrence of bacterial translocation from the gut in acute liver failure (ALF). METHODS: In the present study the effects of oral administration of exogenous Lactobacillus reuteri R2LC and oat fiber on bacterial overgrowth and translocation and on enterocyte protein contents were investigated in rats with ALF induced by subtotal liver resection. The oatmeal soup base was anaerobically inoculated with L. reuteri R2LC and fermented for 15 h. The animals were then fed with fermented or unfermented oatmeal or saline daily for 6 days before the experimental procedure. RESULTS: The incidence of bacterial translocation to the systemic circulation was nil and 17% in rats subjected to sham operation with saline or 90% hepatectomy with fermented oatmeal, respectively, and 80-90% and 34-50% in rats subjected to hepatectomy with saline or unfermented oatmeal. One rat treated with fermented oatmeal had positive bacterial growth in mesenteric lymph nodes (MLN), which was significantly lower than in hepatectomized rats with saline or unfermented oatmeal (80-100% and 50-67%). No significant differences was demonstrable between hepatectomized animals with oral administration of fermented or unfermented oatmeal as compared with sham-operated rats. The number of anaerobic bacteria, Gram-negative anaerobes, and Lactobacillus decreased significantly, and the number of Escherichia coli increased in the distal small intestine and colon in hepatectomized animals with saline or unfermented oatmeal, as compared with animals subjected to sham operation or hepatectomy with fermented oatmeal. CONCLUSIONS: The occurrence of bacterial translocation from the gut in 90% hepatectomy-induced ALF could be prevented by fermented oatmeal, which implies possibilities for biologically balancing the enteric bacterial ecology.

Animals↗
PubMed1995

Antioxidant and calcium channel blockers counteract endothelial barrier injury induced by acute pancreatitis in rats.

BACKGROUND: Multiple organ failure is the major mortality-related complication in severe acute pancreatitis. Endothelial barrier injury may be involved in its pathophysiology. METHODS: The present study evaluated alterations in endothelial barrier integrity in different organs/tissues 12 h after induction of acute pancreatitis by intraductal infusions of bile. Potential effects of oxygen free radicals and calcium influx were evaluated by pretreatment with an antioxidant, N-acetyl-L-cysteine, and calcium channel antagonists, verapamil and diltiazem. RESULTS: Tissue edema, reflected by an increase in tissue water content, was noted in the stomach, proximal small intestine, cecum, spleen, pancreas, kidneys, liver, lungs, heart, and brain in rats with pancreatitis. Also, an increased endothelial barrier permeability, as evidenced by the leakage of radiolabeled human serum albumin from blood to tissues, occurred in the stomach, proximal small intestine, colon, peritoneum, spleen, pancreas, kidneys, liver, lungs, and heart, accompanied by altered liver functions, increased levels of pancreatic enzymes, compromised renal function, and delayed intestinal motility. N-acetyl-L-cysteine prevented tissue edema and endothelial permeability changes in most organs/tissues, whereas the effects of verapamil and diltiazem were less marked. The preventive effects occurred in an organ-dependent manner. CONCLUSIONS: Endothelial barrier injury is found in all investigated organs/tissues in acute experimental pancreatitis. Oxygen free radicals and calcium influx may play a role in the development of these changes.

Acetylcysteine↗
PubMed1995

Study on cerebrovascular disease of the elderly in China.

The average incidence, prevalence and mortality rates of cerebrovascular disease (CVD) in China were markedly increased with increase of age and were much higher in senile stage and males than those in presenile stage and females. The constituent ratio of CVD consisted cerebral infarction for 67.5% and cerebral hemorrhage about 24.8%. There was no difference between the characters of lesions confirmed by CT scan in senile and presenile groups. The majority of CT lesions in the two groups was lacunar infarction, being 76.3% and 85.9% respectively. There were more cases of lobar hemorrhage in the senile group. The most important risk factor for CVD was hypertension (65.8%). Heart disease and diabetes mellitus take second place, accounting 19.0% and 10.7% respectively. The incidence of mixed type of hypertension was high in CVD especially the isolated systolic hypertension. The incidence of cerebral stroke was obviously higher than myocardial infarction in China. The percentage of positive findings of atherosclerosis in extracranial portion of carotid artery system in elderly patients with thrombosis and transient ischemic attacks was 60-100% and 55-100%.

Adolescent↗
PubMed1995

Intestinal absorption and metabolism of 9-cis-beta-carotene in vivo: biosynthesis of 9-cis-retinoic acid.

This study was done to examine the intestinal absorption and cleavage of 9-cis-beta-carotene in vivo. A micellar solution, containing either no addition or 10 mumol of 9-cis- or all-trans-beta-carotene, was perfused for 2 h through the upper portion of the small intestine of ferrets. The effluent of a mesenteric lymph duct cannulation was collected, as well as intestinal mucosa scrapings, a portal blood sample, and a liver biopsy, both before and after perfusion. Carotenoids and retinoids were measured by reverse-phase, high performance liquid chromatography. 9-Cis- and all-trans-beta-carotene were transported equally well into mesenteric lymph, although the intestinal concentration of the corresponding isomer was tenfold higher after perfusion of the 9-cis- isomer than after perfusion of all-trans-beta-carotene. Regardless of which isomer was used, perfusion of beta-carotene resulted in the biosynthesis of similar amounts of retinoic acid in portal blood, liver, and intestine. However, after the perfusion of all-trans-beta-carotene, all the retinoic acid formed was in the all-trans- form, whereas the perfusion of 9-cis-beta-carotene resulted in the biosynthesis of about 50% of the total retinoic acid as the 9-cis-isomer. We conclude that in the in vivo ferret model, 9-cis-beta-carotene has a good bioavailability and is a precursor of 9-cis-retinoic acid.

Animals↗
PubMed1994

Biosynthesis of 9-cis-retinoic acid from 9-cis-beta-carotene in human intestinal mucosa in vitro.

The role of 9-cis-beta-carotene (9-cis-beta-C) as a potential precursor of 9-cis-retinoic acid (9-cis-RA) has been examined in human intestinal mucosa in vitro. By using HPLC, uv spectra, and chemical derivatization analysis, both 9-cis-RA and all-trans-retinoic acid (all-trans-RA) have been identified in the postnuclear fraction of human intestinal mucosa after incubation with 9-cis-beta-C at 37 degrees C. The biosynthesis of both 9-cis-RA and all-trans-RA from 9-cis-beta-C was linear with increasing concentrations of 9-cis-beta-C (2-30 microM) and was linear with respect to tissue protein concentration up to 0.75 mg/ml. Retinoic acid was not detected when a boiled incubation mixture was incubated in the presence of 9-cis-beta-C. The rate of synthesis of 9-cis- and all-trans-RA from 4 microM 9-cis-beta-C were 16 +/- 1 and 18 +/- 2 pmol/hr/mg of protein, respectively. However, when 2 microM all-trans-beta-C was added to the 4 microM 9-cis-beta-C, the rate of all-trans-RA synthesis was increased to 38 +/- 6 pmol/hr/mg of protein, whereas the rate of 9-cis-RA synthesis remained the same. These results suggest that 9-cis-RA is produced directly from 9-cis-beta-C. Furthermore, incubations of either 0.1 microM 9-cis- or all-trans-retinal under the same incubation conditions showed that 9-cis-RA could also arise through oxidative conversion of 9-cis-retinal. Although only 9-cis-RA was detected when 9-cis-RA was used as the substrate, the isomerization of the all-trans-RA to 9-cis-RA cannot be ruled out, since both all-trans-RA and trace amounts of 9-cis-RA were detected when all-trans-retinal was incubated as the substrate. These data indicate that 9-cis-beta-C can be a source of 9-cis-RA in the human. This conversion may have a significance in the anticarcinogenic action of beta-C.

Carotenoids↗
PubMed1994

A phospholipase C inhibitor, U-73122, blocks TSH-induced inositol trisphosphate production, Ca2+ increase and arachidonic acid release in FRTL-5 thyroid cells.

To characterize the role of phospholipase C (PLC)-mediated intrathyroid signal transduction by thyrotropin, we studied the effect of U-73122, an aminosteroid inhibitor of PLC-dependent activity, on TSH-activated PLC-Ca2+ and arachidonic acid (AA) signalling systems in cultured FRTL-5 rat thyroid cells. In the presence of extracellular Ca2+, TSH (0.1 microM) increased intracellular free calcium concentration ([Ca2+]i) by 63 +/- 6% with a sustained plateau phase, and AA release by 160 +/- 16%. By deletion of extracellular Ca2+, TSH induced a similar maximal [Ca2+]i increase, but the plateau phase and AA release were entirely suppressed. U-73122 (5 microM) inhibited TSH stimulation of 3H-labelled inositol trisphosphates (IP3) production by 73 +/- 3% (P < 0.01) in one study, and completely in another. U-73122 concentration-dependently blocked the TSH-induced Ca2+ increase in either the presence or absence of external Ca2+. U-73122 also showed a similar concentration-response inhibition of TSH-induced AA release. These results provide direct evidence of PLC mediation of TSH-stimulated signal transduction in FRTL-5 thyroid cells. TSH-induced external Ca2+ entry, as well as intracellular Ca2+ mobilization, is probably a PLC-mediated process. From an IP3-sensitive intracellular pool, TSH induces intracellular Ca2+ mobilization. External Ca2+ entry seems to be a prerequisite for TSH-induced AA release. U-73122 inhibition of both cytosolic Ca2+ increase and AA release further confirms [Ca2+]i dependence for TSH stimulation of AA release.

Animals↗
PubMed1994

Bacterial translocation, intestinal ultrastructure and cell membrane permeability early after major liver resection in the rat.

The process and route of bacterial translocation from the gut after major liver resection remain unclear. In the present study enteric bacterial translocation, enterocyte ultrastructure in the ileum and colon, the process and route of bacterial invasion and the permeability of the cell membrane system and blood-tissue barrier were evaluated in rats receiving sham operation, and 70 or 90 per cent hepatectomy. The incidence of bacterial translocation to mesenteric lymph nodes was 80-100 per cent in rats 6 h after 70 per cent and 2-4 h after 90 per cent hepatectomy, and 80-100 per cent to the systemic circulation 2-4 h after 90 per cent hepatectomy but only 20 per cent to the portal vein. An increase in bacterial adherence to the intestinal surface, damage to the permeability of the cell membrane system and blood-tissue barrier, and pathological alterations in the ileum and colon developed, correlating with the extent of liver removed and the time that had passed after hepatectomy. Most translocating bacteria appeared in morphologically intact enterocytes with increased membrane permeability, in antigen-presenting cells and in submucosal lymphatics, but some bacteria were also seen within damaged enterocytes 4h after 90 per cent hepatectomy. These results indicate that altered permeability of the cell membrane system may be one of the earliest characteristics of challenged enterocytes, and that enteric bacteria translocate through both morphologically normal and abnormal enterocytes. Translocation occurred mainly into the lymphatics, bacteria either being 'carried' by antigen-presenting cells or entering by active invasion.

Animals↗
PubMed1994

Review: absorption and metabolism of beta-carotene.

To better understand the potential function of beta-carotene (beta-C) in the prevention of cancer, greater knowledge of beta-C metabolism and a suitable animal model to mimic human beta-C metabolism are necessary. The small intestinal mucosa contains beta-C cleavage enzyme(s), thereby playing an important role in both the provitamin A activity and anti-cancer properties of beta-C. The ability of the ferret (Mustela putorius furo) to absorb intact beta-C makes it an appropriate model for studying human beta-C absorption. This article reviews the absorption and cleavage mechanisms of beta-C in both the human and the ferret. The biosynthesis of retinoic acid (RA) from beta-C via central and eccentric cleavage pathways is reviewed. The possible significance of the conversion of beta-C to RA as an anticancer mechanism is discussed.

Animals↗
PubMed1994

Phospholipids prevent enteric bacterial translocation in the early stage of experimental acute liver failure in the rat.

BACKGROUND: Bacterial infections and bacteremia in acute liver failure may at least partly be attributed to translocation of enteric bacteria. Attempts to prevent or treat such infections by the use of antibiotics may instead result in overgrowth of surviving microbes. METHODS: In the present study, normal saline (1.5 ml/100 g body weight), phosphatidylcholine (1.5 ml/100 g body weight), and phosphatidylinositol (1.5 ml/100 g body weight) were orally administered by means of a gastric tube both 12 h and 30 min before operation. Effects of enteric administration of phospholipids on the prevention of enteric bacterial translocation, intestinal and mucosal mass, and enterocyte protein contents in acute liver failure induced by subtotal liver resection in the rat were evaluated. RESULTS: The incidence of bacterial translocation increased significantly 2 and 4 h after 90% hepatectomy as compared with sham-operated animals. Enteric administration of phospholipids, however, significantly reduced the incidence of bacterial translocation after 90% hepatectomy. Phospholipid treatment prevented the postoperative decrease in intestinal mucosal mass and enterocyte protein content. CONCLUSIONS: Enteral administration of phospholipids thus seems to protect against translocation of enteric bacteria and prevent against a decrease in intestinal mucosal mass and enterocyte protein content after subtotal hepatectomy in the rat.

Animals↗
PubMed1994

The association between enteric bacterial overgrowth and gastrointestinal motility after subtotal liver resection or portal vein obstruction in rats.

OBJECTIVE: To test the hypothesis that intestinal motility is delayed after hepatectomy, which alters the ecology of the enteric microflora and contributes to the development of bacterial translocation from the gut. DESIGN: Open experimental study. SETTING: University department of surgery. MATERIAL: Adult male Sprague-Dawley rats (n = 6 in each group at each time point). INTERVENTIONS: Sham operation, 90% hepatectomy, and portal venous obstruction. MAIN OUTCOME MEASURES: Intestinal morphology, immunocytochemistry of the enteric nervous system, enteric bacterial growth in the small intestine and colon, and intestinal transit time. RESULTS: Intestinal transit was already delayed one hour after 90% hepatectomy, and histopathological alterations and overgrowth by Escherichia Coli had developed after two hours. There were significant differences in intestinal transit time between sham operated rats and those subjected to portal venous obstruction on the one hand, and those that underwent 90% hepatectomy on the other. There was no difference in intestinal transit time between rats with portal venous obstruction and the sham operated animals. CONCLUSION: Delayed intestinal transit after 90% hepatectomy may contribute to enteric bacterial overgrowth and thereby contribute to the development of bacterial translocation from the gut.

Animals↗