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Biomedical subjects

B Jeppsson

Publications and source records attributed to B Jeppsson.

At least 55 records · Page 3Linked to original sources
PubMed1996

Multiple-system organ damage resulting from prolonged hepatic inflow interruption.

BACKGROUND: It has been reported that patients undergoing major hepatectomy tolerated 90 and 127 minutes of continuous hepatic inflow interruption with no evidence of permanent damage to the liver. We questioned the safety and feasibility of the interruption beyond 90 minutes in normothermic human beings. We also postulated that, besides injury to the liver per se, extended continuous hepatic inflow interruption would cause extrahepatic multiple-system organ damage in subjects exposed to continuous hepatic inflow interruption for 90 or 120 minutes. DESIGN: Fifty Sprague-Dawley rats were divided into three groups. Group 1 served as controls that had only laparotomy. Group 2 underwent continuous hepatic inflow interruption for 90 minutes, and group 3 was subjected to continuous hepatic inflow interruption for 120 minutes. Scanning electron microscopy and transmission electron microscopy were used to evaluate ultrastructural alterations in the liver, lung, heart, and intestine. SETTING: Lund (Sweden) University Hospital and Top Cancer Institute, Lund. INTERVENTIONS: Intraoperative and postoperative infusion and blood transfusion were given in all experimental animals. MAIN OUTCOME MEASURES: Animal survival and manifestations of multiple-system organ failure. RESULTS: In rats with continuous hepatic inflow interruption for 90 or 120 minutes, scanning electron microscopy showed a necrotic surface of the liver cells together with fibrin exudation. Hepatic sinusoids and intrahepatic nerves also had severe injury. Destruction of pulmonary structures and breakdown of microcirculation in the lung were characterized by thinned and ruptured walls of alveoli and a greatly decreased number of capillaries in the damaged alveolar wall. Transmission electron microscopy showed four types of ultrastructural changes, ie, necrosis of epithelial cells, extremely swollen mitochondria in intestinal cells, death of mucosal cells, and increased permeability of vessels in the injured intestine. The affected heart manifested highly enlarged mitochondria in myocardial cells, thickened vascular walls, and scattered necrotic lesions in myocardial tissue. CONCLUSIONS: Multiple-system organ failure resulting from ischemia-reperfusion injury and obstacle of portal hemodynamics in a subject subjected to an extended continuous hepatic inflow interruption is an unrecognized new disorder that may cause a high mortality rate. Our preliminary results indicated that animals subjected to continuous hepatic inflow interruption for 90 or 120 minutes developed various injuries to the liver, lung, heart, and gut. Therefore, we believe that continuous hepatic inflow interruption exceeding 90 minutes could also be hazardous in human beings.

Animals↗
PubMed1996

Glutathione and phospholipid depletion of liver tumors after arterial ischemia.

Breakdown of membrane phospholipids is a causative event leading to irreversible cell injury after ischemia and reperfusion insults, which might be one mechanism leading to liver tumor cell death after repeated arterial ischemia as well. After 2 hr of hepatic dearterialization followed by 30 min of reperfusion tumor phospholipid was measured chromatographically, glutathione (GSH) analyzed by determining nonprotein sulfhydryl and activity of glutathione-S-transferase (GST) determined spectrophotometrically using 1-chloro-2,4-dinitrobenzene (CDNB) as the substrate. A transient, arterial ischemia for 2 hr induced a substantial decrease of phosphatidylserine (PS) and phosphatidylinosital (PI) compared with sham treatment (P < 0.01). Although phosphatidylcholine (PC) and phosphatidylethanolamine (PE) did not significantly decline after a single arterial ischemia for 2 hr, they dropped dramatically following repeated arterial ischemia for 2 hr during 5 days (P < 0.01 and P < 0.05 respectively). GSH was depleted in tumors after both a single (P < 0.01) and repeated arterial ischemia (P < 0.05) and GST was inactivated as well (P < 0.001). By contrast, neither liver phospholipid nor liver GSH or GST was significantly changed. Tumor growth was significantly retarded in rats subjected to repeated arterial ischemia compared with sham treatment (P < 0.01). Repeated arterial ischemia facilitated degradation of tumor membrane phospholipids and induced depletion of GSH and inactivation of GST without affecting the normal liver. Thus, ischemia/reperfusion induced depletion of membrane phospholipids and of GSH might represent two mechanisms by which repeated arterial ischemia led to tumor growth delay.

Animals↗
PubMed1996

Bacterial translocation in acute liver injury induced by D-galactosamine.

Acute liver injury is associated with a high rate of infectious and septic complications. Most of these infections are produced by gram negative enteric bacteria. We evaluated bacterial translocation, intestinal permeability, blood flow, portal pressure, and intestinal microflora after induction of liver injury and 70% liver resection in the rat. The rate of translocation to both portal and arterial blood was 100% at 24 hours and 50% at 48 hours after liver resection compared with 83% to portal vein and 50% to aortic blood at both time points after acute liver injury. Translocation to intraabdominal organs (liver, spleen, and mesenteric lymph nodes) was 100% in both groups at both 24 and 48 hours. The rate of translocation increased after liver injury at 48 hours with progression of the liver injury but was decreased in the 70% liver resection group with improvement of liver function. "Total aerobic" and "total anaerobic" bacterial counts in small intestine and cecum were not affected. Pulmonary, distal small intestine, and cecal blood flow were decreased in both groups, whereas blood flow in the proximal small intestine was unaffected. Portal pressure and flow were increased after 70% liver resection, but they were decreased in acute liver injury. After acute liver injury, permeability of both distal small intestine and cecum increased, but after liver resection only cecal permeability increased. The results of this experiment show that bacterial translocation occurs in experimental acute liver injury and that its dynamic, pattern and fate are different from that observed after liver resection, which is a reversible surgical model of liver insufficiency.

Analysis of Variance↗
PubMed1996

The effect of endotoxin and Lactobacillus pretreatment on peritoneal macrophage behavior in acute liver injury in rat.

The effect of endotoxin and Lactobacillus R2LC pretreatment in acute liver injury, induced by D-galactosamine was studied. Administration of D-galactosamine resulted in much higher luminescent activity than the control (49.24 mV vs 19.75 mV), while there was no change detected on the metabolic response to phorbol-12-myristate-13-acetate (PMA) stimulation in the calorimeter. Pretreatment of animals with intraperitoneal administration of heat-killed Lactobacillus resulted in higher oxygen free radical production (105.46 mV) and a much higher metabolic response to PMA in microcalorimeter (24.63 pW per cell vs 13.03 in the control). On the other hand pretreatment with endotoxin resulted in higher luminometric response to PMA compared to liver injury group (65.87 mV), and no response in the microcalorimeter at all. Phagocytic activity was decreased from 86 to 59% after administration of D-galactosamine, and was not significantly influenced by any of the pretreatment modalities. This experiment showed that pretreatment with Lactobacillus resulted in increased macrophage metabolic activity, while endotoxin pretreatment rendered the macrophages unresponsive to subsequent stimulation. These findings may explain why pretreatment with endotoxin is beneficial in acute liver injury induced by D-galactosamine, but not with gram-positive bacteria including Lactobacillus.

Animals↗
PubMed1996

Influence of colostomy on in vivo and in vitro permeability of the rat colon.

PURPOSE: Barrier properties of an isolated colon loop and the remnant colon in continuity with the gastrointestinal tract after colostomy were studied in the rat. METHODS: The in vivo absorption after colonic loop administration of the marker fluorescein sodium was measured as the urinary recovery. The in vitro permeability was measured in Ussing diffusion chambers as the transmucosal passage of [14C]mannitol and of human serum albumin in the isolated and the nonexcluded colonic segments and was compared with the corresponding colonic regions from sham-operated rats at 1 to 14 days after operation. RESULTS: Body weight gain of the rats decreased and diarrhea appeared from day 2 after colostomy. Histologic examination showed mucosal atrophy with decreased villus height in the isolated colonic loop and an increased villus height in the nonexcluded colon segment. Absorption of fluorescein sodium in the isolated loop was increased at 8 and 14 days. Moreover, permeability in the isolated loop was increased for both mannitol and human serum albumin from four days after colostomy compared with the corresponding colonic segments after the sham operation, whereas a decrease in the passage of mannitol was noted in the nonexcluded colon. CONCLUSIONS: Experimentally performed colostomy diversion in the rat induced alterations of the barrier function in both the isolated colonic loop and the nonexcluded colon in continuity with the fecal stream.

Animals↗
PubMed1996

The effects of Lactobacillus strains and oat fiber on methotrexate-induced enterocolitis in rats.

BACKGROUND & AIMS: Administration of methotrexate to rats on an elemental diet results in severe enterocolitis and death. Lactobacilli, an integral part of the healthy gastrointestinal microecology, may provide therapeutic benefits to help the recovery from enterocolitis. The purpose of this study was to evaluate the effects of lactobacilli and oatbase on methotrexate-induced enterocolitis in rats. METHODS: Rats received continuous intragastric infusion of elemental diet or with supplementation of oatbase, Lactobacillus reuteri R2LC, and Lactobacillus plantarum DSM 9843, with and without fermentation, from the beginning of the study. Methotrexate (20 mg/kg) was injected intraperitoneally on day 3, and the sampling was performed on day 6. RESULTS: Lactobacilli and oatbase decreased body weight loss and intestinal permeability and increased bowel mucosal mass in enterocolitic rats. Administration of lactobacilli, but not oatbase, decreased the intestinal myeloperoxidase level, reestablished intestinal microecology, and reduced bacterial translocation to extraintestinal sites. Both lactobacilli and oatbase reduced plasma endotoxin levels. The effects of lactobacilli were greater with fermentation than without fermentation or oatbase alone, and L. plantarum was more effective in reducing intestinal pathogens than L. reuteri. CONCLUSIONS: Exogenous administration of lactobacilli, especially L. plantarum with fermentation, is helpful in reducing the severity of enterocolitis in rats.

Animals↗
PubMed1996

Dynamics of bacterial translocation in acute liver injury induced by D-galactosamine in rat.

Bacterial translocation may play a role in acute liver injuries as high rates of infectious and septic complications are observed in these clinical conditions. Increased passage of endotoxin and translocating bacteria not only potentiates the extent of liver injury, but may also play a determining role in its final outcome. In this paper the incidence of bacteria] translocation in acute liver injury in rats is evaluated with other important pathological changes observed at different time points after liver injury induced by intraperitoneal administration of D-galactosamine. The bacterial translocation to the blood and other extraintestinal sites starts 3 h after induction of liver injury and is not found to be related to light microscopic changes in the liver or ileal or cecal mucosa, detectable levels of endotoxin in the portal blood, or DNA changes in the small and large intestinal mucosa, but corresponds to the release of liver enzymes in the serum.

Analysis of Variance↗
PubMed1996

Pectin-supplemented enteral diet reduces the severity of methotrexate induced enterocolitis in rats.

BACKGROUND: Administration of methotrexate (MTX) to rats fed an elemental diet results in a high mortality from severe enterocolitis. Previous studies have shown that pectin is an important precursor of substrates for intestinal structure and function and may facilitate intestinal recovery after enterocolitis. The aim of this study is to evaluate the effect of pectin on MTX-induced enterocolitis in rats. METHODS: Rats received intragastric infusion of either 1% pectin-supplemented or pectin-free elemental diet from the beginning of the study via a gastrostomy. On the 4th day animals received either MTX, 20 mg/kg intraperitoneally, or saline injection and were killed on the 7th day for sampling. RESULTS: Pectin supplementation significantly decreased body weight loss, organ water content, and intestinal myeloperoxidase levels and increased mucosal protein, DNA, and RNA content in enterocolitis rats. The intestinal permeability was increased by administration of MTX, and pectin supplementation significantly reversed the increased permeability in the distal small bowel and colon. Pectin supplementation also lowered the magnitude of bacterial translocation, decreased plasma endotoxin levels, and restored bowel microecology. CONCLUSIONS: Pectin significantly decreased MTX-induced intestinal injury and improved bowel integrity.

Animals↗
PubMed1996

The effect of pretreatment with endotoxin and lactobacillus on bacterial translocation in acute liver injury.

OBJECTIVE: To evaluate the effect of pretreatment with endotoxin or Lactobacillus reuteri pretreatment on bacterial translocation after acute liver injury. DESIGN: Experimental study. SETTING: University department, Sweden. SUBJECTS: 96 Sprague-Dawley rats were divided into four groups of 24 each. Three of them received intraperitoneal D-galactosamine, the fourth received pyrogen free water and was used as the normal control. Twenty-four hours later the study was terminated and samples collected. INTERVENTIONS: Endotoxin and L reuteri R2LC were injected intraperitoneally three days, one week, and two weeks before induction of liver injury. MAIN OUTCOME MEASURES: Extent of liver injury and bacterial translocation to mesenteric lymph nodes, liver, and systemic blood. RESULTS: The extent of liver injury and rate of bacterial translocation were lower three days after pretreatment with endotoxin, than after pretreatment with L reuteri. There was no other difference among the other groups. High concentrations of serum endotoxin were detected three days after pretreatment with endotoxin. There were no significant changes in small intestinal and caecal bacterial counts. CONCLUSION: Pretreatment with endotoxin effectively prevented liver injury by D-galactosamine and subsequent bacterial translocation. Pretreatment with L reuteri had no beneficial effect.

Animals↗
PubMed1995

Reticuloendothelial system function in acute liver injury induced by D-galactosamine.

AIMS/METHODS: Reticuloendothelial system function, as assessed by clearance of radiolabelled bacteria, was evaluated in acute liver injury induced by D-galactosamine in rats, and compared with that after 70% liver resection model. RESULTS: Reticuloendothelial system function was significantly impaired in both instances, but the extent and the pattern of reticuloendothelial system impairment differed in the two models. While the elimination rate of the radiolabelled bacteria (k-value) decreased in both the liver resection and D-galactosamine groups (19% and 52%, respectively), the corrected phagocytic index (alpha) increased in 70% liver resection (247%), indicatine increased activity among the remaining reticuloendothelial system cells of the liver. Estimation of subserosal organ blood flow showed decreased flow to the cecum and distal small intestine (correction of intesting) in both groups, whereas it was significantly increased (477%) in the remaining parts of the liver in the liver resection group. CONCLUSIONS: These findings show that reticuloendothelial system activity is deranged in both these groups, which may explain the increased occurrence of bacterial complications observed in corresponding clinical conditions.

Animals↗
PubMed1995

Mesocaval shunt or repeated sclerotherapy: effects on rebleeding and encephalopathy--a randomized trial.

BACKGROUND: Sclerotherapy is usually effective in controlling acutely bleeding esophageal varices. It may not be as effective as shunt surgery for prevention of rebleeding; therefore we undertook a prospective study comparing interposition mesocaval shunt (MCS) and repeated sclerotherapy. METHODS: Forty-five patients (mean age, 52.6 +/- 9.8 years) with variceal bleeding were randomized after emergency endoscopic sclerotherapy either to repeat variceal obliteration followed by regular check endoscopy (n = 21) or to elective interposition mesocaval shunting by use of 14 mm polytetrafluoroethylene graft (n = 24). There was an equal distribution of Child's classes in the two groups. RESULTS: In the sclerotherapy group 12 patients had recurrent hemorrhages causing five deaths compared with the shunt group, in which four patients had postoperative bleeding but without associated death. No difference was noted in the incidence of encephalopathy despite the development of total shunting 1 year after MCS. The median hospital stay was similar; 34.5 days (MCS) and 33 days (sclerotherapy). The number of intensive care unit days was also similar in the two groups. No difference was noted in survival in patients with Child's A and Child's B disease in the treatment groups. In patients with Child's C cirrhosis there was a statistically significant longer survival in patients undergoing MCS compared with patients undergoing sclerotherapy. CONCLUSIONS: The results of the study show that the rate of rebleeding is significantly higher after sclerotherapy than after mesocaval shunting. In patients with Child's C cirrhosis MCS may be an alternative to sclerotherapy for the prevention of rebleeding from esophageal varices in patients not suitable for transplantation.

Adult↗
PubMed1995

Small intestinal absorption of polyethylene glycol 400 to 1,000 in the portacaval shunted rat.

Functional changes of the intestinal barrier that may occur after the creation of a portacaval shunt (PCS) were investigated. After chronic PCS in the rat, the intestinal absorption of and the jejunal permeability to the inert polymer marker polyethylene glycol (PEG) with molecular weight (Mw) ranging from 400 to 1,000 g/mol were investigated. The PEG mixture was orally fed to PCS and sham-operated rats, and urine was collected for 24 hours to obtain the urinary recovery of the different PEG polymers as a measure of intestinal absorption. To study the intestinal permeability, segments from the proximal small intestine were incubated in diffusion chambers with the PEG mixture on the mucosal side, and samples were withdrawn from the serosal side for analysis. The urinary recovery for the PEGs increased (P < .01) while the tissue permeability decreased (P < .001) in the PCS group rats in comparison with Sham-operated rats. The increased absorption in vivo was caused neither by altered renal clearance, nor by changed portal blood pressure. The decreased jejunal permeability in the PCS rats could be explained by a reduction of the mucosal area by shortening of the microvilli. This discrepancy indicates that changes in permeability and absorption may not be parallel during PCS. It is possible that these changes also may be affected by nutritional factors, drug therapy, as well as toxic substances.

Animals↗