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Biomedical subjects

S L Jensen

Publications and source records attributed to S L Jensen.

At least 37 records · Page 2Linked to original sources
PubMed1998

Sodium fusidate and the cytokine response in an experimental model of acute pancreatitis.

BACKGROUND: New therapies designed to downregulate the aberrant immune response associated with severe acute necrotizing pancreatitis (ANP) are being increasingly investigated in different experimental models of ANP. The aim of this study was to test the potential effects of sodium fusidate on the course of severe ANP in rabbits. METHODS: ANP was induced in 20 rabbits by retrograde injection of 5 per cent chenodeoxycholic acid into the pancreatic duct followed by duct ligation. The rabbits were allocated to pretreatment with intravenous physiological saline or sodium fusidate 80 mg/kg 30 min before the induction of ANP. Levels of serum amylase, lipase, tumour necrosis factor (TNF) alpha, interleukin (IL) 8, glucose and calcium, and leucocyte count were measured every 3 h for a total of 12 h. At the end of the experiment, ascitic fluid was collected and the pancreatic, lung and kidney tissues were obtained for histological examination. RESULTS: Pretreatment with sodium fusidate reduced the mortality rate from six of ten to three of ten (P < 005) and reduced the output of ascitic fluid from 5 2 to 2.0 ml/h (P < 0001). Serum levels of TNF-alpha and IL-8 were reduced significantly in the treated group from 5 min up to 9 h after induction of ANP. The leucopenia observed after 3 h in the untreated group was not significantly improved in the group treated with sodium fusidate (P = 0.055). By contrast, both treated and untreated rabbits had similar biochemical changes including levels of amylase, lipase, glucose and calcium as well as similar histological changes in the pancreas and lungs. CONCLUSION: Pretreatment with sodium fusidate resulted in a considerable reduction in mortality rate and ascitic fluid output in rabbits with bile-induced ANP, probably by lowering the TNF-alpha and IL-8 blood levels. However, pretreatment with sodium fusidate did not alter the local or systemic manifestations of ANP. Thus, cytokines other than TNF-alpha and IL-8 are likely to mediate the local and systemic symptoms of ANP.

Amylases↗
PubMed1998

A monoclonal anti-interleukin 8 antibody (WS-4) inhibits cytokine response and acute lung injury in experimental severe acute necrotising pancreatitis in rabbits.

BACKGROUND: Interleukin 8 (IL-8) has recently been proposed to have an important role in mediating the development of the systemic sequelae associated with severe acute pancreatitis. AIMS: To define the role of IL-8 in acute pancreatitis by neutralising its effects with a monoclonal anti-IL-8 antibody (WS-4), in a rabbit model of severe acute pancreatitis. METHODS: Acute pancreatitis was induced by retrograde injection of 5% chenodeoxycholic acid into the pancreatic duct and duct ligation. Twenty rabbits were divided equally into two groups: acute pancreatitis controls received physiological saline and the treated group received WS-4, 30 minutes before induction of acute pancreatitis. RESULTS: Pretreatment of animals with WS-4 resulted in significant down regulation of serum IL-8 and tumour necrosis factor alpha (TNF-alpha) from three to six hours after induction of acute pancreatitis (p = 0.011 and 0.047 for IL-8 and 0.033 and 0.022 for TNF-alpha, respectively). In addition, a significant reduction in the CD11b and CD18 positive cells and the amount of interstitial neutrophil infiltration in the lungs from WS-4 treated animals was seen. In contrast, WS-4 did not alter the amount of pancreatic necrosis and the serum concentrations of amylase, lipase, calcium, and glucose. CONCLUSION: WS-4 cannot change the amount of pancreatic necrosis induced by injection of 5% bile acid, but does reduce the acute lung injury, presumably through inhibition of circulating IL-8 and TNF-alpha, and CD11b/CD18 in lung tissue. Therefore, a role of IL-8 in the progression of acute pancreatitis and the development of its systemic complications is suggested.

Amylases↗
PubMed1998

Biliary parasites.

Parasitic diseases of the biliary tract occur frequently in tropical and subtropical areas and cause high morbidity and mortality. In general, neither the clinical presentation nor the general laboratory findings are sufficiently unique to raise the possibility of a parasitic biliary infestation in the mind of the surgeon. Once considered, however, the presence of a parasitic biliary infestation is easily confirmed. Most commonly this is accomplished by the identification of the parasite in stools or duodenal contents. Ultrasonography, CT and MRI are not only important in the diagnosis of parasitic biliary diseases but also in the follow-up and surveillance. ERCP is an excellent diagnostic tool for demonstrating the presence of parasites in the biliary tree. Furthermore, ERCP is also used in the therapy of biliary parasitic infestations and carries less morbidity and mortality than the surgical approach. Surgery is only indicated in complicated cases. Mechanisms that may be effective against parasites include: antibodies; cytotoxic T cells; T-cell-induced activated macrophages; natural killer cells, and a variety of cells that mediate antibody-dependent cell-mediated cytotoxicity and modulators of the immune system such as cytokines. Future research has to focus on the importance of these mechanisms for the immune evasion by parasites.

Animals↗
PubMed1998

Epidemiology of ankle fractures. A prospective population-based study of 212 cases in Aalborg, Denmark.

We studied the epidemiology of ankle fractures prospectively during 1 year in a population of about 200,000. The overall incidence rate was 107 fractures per 10(5) person-years. Below the age of 50, ankle fractures were commonest in men. After this age, females became predominant and the age-specific incidence rates decreased in both sexes. The main cause of fracture was falls (87%), on the ground, on stairs or from a height. 137 fractures (55%) occurred in sports, play or other leisure activities. Most patients (64%) were walking, running or jumping at the time of injury. Alcohol and slippery surfaces were each involved in nearly a third of the cases. The distribution of the fractures according to both the Lauge-Hansen and the AO Weber classification systems were within the limits of previous series. Nearly half the patients were hospitalized and the fractures were operated on with osteosynthesis. Our findings indicate that ankle fractures are mainly caused by substantial trauma sustained during physical activity. Osteoporosis seems to be of minor importance.

Adolescent↗
PubMed1998

IT 9302, a synthetic interleukin-10 agonist, diminishes acute lung injury in rabbits with acute necrotizing pancreatitis.

BACKGROUND: Proinflammatory cytokines (eg, tumor necrosis factor [TNF]-alpha, interleukin [IL]-1 and Il- 8) are believed to play an important role in the pathogenesis of acute necrotizing pancreatitis (ANP) and its systemic complications. Recently, IL-10 has emerged as a major anti-inflammatory cytokine, inhibiting the secretion and activities of inflammatory cytokines. Further, a protective effect of IL-10 has recently been shown in experimental acute pancreatitis. The purpose of this study was to test the potential role of a newly developed IL-10 agonist, IT 9302, in a model of ANP in rabbits. METHODS: ANP was induced in 18 rabbits by retrograde injection of 5% chenodeoxycholic acid in the pancreatic duct, followed by duct ligation. The rabbits were allocated to pretreatment with intravenous physiologic saline solution or IT 9302 (200 micrograms/kg) 30 minutes before the induction of ANP. RESULTS: Injection of IT 9302 resulted in a significant reduction in the blood levels of TNF-alpha and IL-8 from 3 to 6 hours. IT 9302 also reduced the amount of ascitic fluid and significantly inhibited neutrophil infiltration and margination, as well as the number of CD11b- and CD18-positive cells in the lung tissues. By contrast, the local pancreatic necrosis, as well as the biochemical changes such as serum amylase, lipase, and calcium, was sever and similar in both groups. Survival was improved significantly after treatment with IT 9302. CONCLUSIONS: As expected, IT 9302 cannot change the degree of ANP induced by 5% bile acid but does reduce mortality rates and the development of acute lung injury, probably through the inhibition of circulating levels of TNF-alpha, IL-8, and the expression of the adhesion molecule complex CD11b/CD18.

Amylases↗
PubMed1997

Identification of functional domains on human interleukin 10.

Interleukin 10 (IL-10) is a recently described natural endogenous immunosuppressive cytokine that has been identified in human, murine, and other organisms. Human IL-10 (hIL-10) has high homology with murine IL-10 (mIL-10) as well as with an Epstein-Barr virus genome product BCRFI. This viral IL-10 (vIL-10) shares a number of activities with hIL-10. IL-10 significantly affects chemokine biology, because human IL-10 inhibits chemokine production and is a specific chemotactic factor for CD8+ T cells. It suppresses the ability of CD4+ T cells, but not CD8+ T cells, to migrate in response to IL-8. A nonapeptide (IT9302) with complete homology to a sequence of hIL-10 located in the C-terminal portion (residues 152-160) of the cytokine was found to possess activities that mimic some of those of hIL-10. These are: (i) inhibition of IL-1beta-induced IL-8 production by peripheral blood mononuclear cell, (ii) inhibition of spontaneous IL-8 production by cultured human monocytes, (iii) induction of IL-1 receptor antagonistic protein production by human monocytes, (iv) induction of chemotactic migration of CD8+ human T lymphocytes in vitro, (v) desensitization of human CD8+ T cells resulting in an unresponsiveness toward rhIL-10-induced chemotaxis, (vi) suppression of the chemotactic response of CD4+ T human lymphocytes toward IL-8, (vii) induction of IL-4 production by cultured normal human CD4+ T cells, (viii) down-regulation of tumor necrosis factor-alpha production by CD8+ T cells, and (ix) inhibition of class II major histocompatibility complex antigen expression on IFN-gamma-stimulated human monocytes. Another nonapeptide (IT9403) close to the NH2-terminal part of hIL-10 did not reveal cytokine synthesis inhibitory properties, but proved to be a regulator of mast cell proliferation. In conclusion, we have identified two functional domains of IL-10 exerting different IL-10 like activities, an observation that suggests that relatively small segments of these signal proteins are responsible for particular biological functions.

Animals↗
PubMed1997

Monocyte chemotactic and activating factor (MCAF/MCP-1) has an autoinductive effect in monocytes, a process regulated by IL-10.

MCAF (MCP-1) a member of the chemokine-beta-family known to be chemotactic for monocytes is believed to play a significant role in several inflammatory processes, both immuno-pathological disorders, such as atherosclerosis, psoriasis, chronic inflammatory diseases of the liver and lungs, and during the normal immune response against microorganisms. This chemokine is produced spontaneously by monocytes, and in the present article we also demonstrate that MCAF induces its own production in monocytes. The methods used are two dimensional SDS-PAGE gel electrophoresis. Western-blotting and ELISA quantification of supernatant from monocyte cultures stimulated with MCAF (1, 10, 100 ng ml). Also, we found that this process is regulated by IL-10 (100 ng ml). Our results suggest that monocytes migrating to a site of inflammation due to the local production of the chemokine MCAF/MCP-1 further enhance the focal accumulation of monocytes by producing and releasing bioactive MCAF MCP-1.

Blotting, Western↗
PubMed1997

Compartment syndrome and fasciotomy in vascular surgery. A review of 57 cases.

OBJECTIVE: To investigate the occurrence of compartment syndrome and the results of fasciotomy in vascular surgical patients. DESIGN: Retrospective study of case records from 1980-1994. MATERIALS: Fifty-seven limbs in 53 patients had fasciotomies following surgical revascularisation. Fifty-three (93%) limbs were acutely ischaemic, while four (7%) had undergone elective vascular surgery. Forty-four (77%) limbs had signs of compartment syndrome, while 13 (23%) fasciotomies were prophylactic. METHODS: The fasciotomies were done as subcutaneous procedures (n = 40), as double-incision fasciotomies (n = 11), or by an unknown method (n = 6). The skin incisions were closed primarily in 26 (46%) cases, delayed primarily in 11 (19%) cases, and by skin grafting in eight cases (14%). RESULTS: Five (13%) subcutaneous fasciotomies required revision. Surgical debridement was required in four (7%) limbs. At discharge, 36 (68%) patients had kept their limbs, 11 (21%) patients were amputated, and six (11%) had died. No complications relating to the fasciotomies were observed. CONCLUSIONS: Compartment syndrome is usually related to acute ischaemia and rarely following elective vascular surgery. Subcutaneous fasciotomy does not always ensure sufficient decompression of all four lower leg compartments. Complications related to fasciotomy are rare.

Adolescent↗
PubMed1997

Double gloving as self protection in abdominal surgery.

OBJECTIVE: To investigate if double gloving can reduce the rate of perforation of glove barriers during abdominal surgery. DESIGN: Randomised controlled trial. SETTING: County hospital, Denmark. SUBJECTS: 400 glove barriers from principal surgeons and first assistants used at consecutive abdominal operations. INTERVENTION: Each participant was randomised to wear either a pair of single or double gloves. MAIN OUTCOME MEASURES: The number of perforated glove barriers in the two study groups. RESULTS: 40 single glove barriers perforated (20%) and in 8 of the double glove group both gloves perforated (4%) (p < 0.001). Glove barriers on non-dominant hands were more often perforated than those on dominant hands, and both the duration of the operation and the seniority of the doctor were associated with increased rates of perforation. CONCLUSION: Double gloving reduces the rate of perforation of glove barriers during abdominal surgery and thereby the number of episodes in which transmission of disease from patient to surgeon would be possible.

Abdomen↗
PubMed1996

Pancreas autotransplantation in pig with systemic or portal venous drainage. Effect on the endocrine pancreatic function after transplantation.

The effect of the type of venous drainage of the graft on its endocrine function was studied in two groups of pigs after segmental pancrease autotransplantation. Group 1 comprised 10 pigs with portal venous drainage (PVD) and group 2 comprised 10 pigs with systemic venous drainage (SVD). The graft consisted of body and tail of the pancreas. The pigs were totally pancreatectomized. The pancreatic duct was occluded by neoprene injected into the duct. One week before and 1 and 3 months after transplantation, intravenous glucose tolerance (IVGTT) and meal stimulation tests (MST) were performed. Plasma glucose (PG), insulin (INS), C-peptide, glucagon (GLU),and pancreatic polypeptide (PP) were measured during the tests. All pigs had normal fasting PG, 1 and 3 months after PanTx, although MST disclosed significantly higher PG (P<0.05) during the test after transplantation. In the PVD group, a decrease in INS level during both test was recorded after PanTx (P<0.05), while in the SVD group a nonsignificant rise in INS level was recorded compared with before transplant. A significant difference (P<0.05) in INS levels were present both 1 and 3 mon. after PanTx between the two groups. Pigs with PVD showed a higher (P<0.05) C-peptide level than pigs with SVD during IVGTT. The initial significant rise in PP during MST and the initial fall in PP during IVGTT recorded in all pigs before transplantation were totally lost after transplantation in both groups. During the tests, PP remained steady and significantly lower than the pretransplantation levels in both groups. A significantly higher GLU level during both IVGTT and MST was observed in SVD compared with PVD 1 month after PanTx (P<0.05), being more pronounced during MST. This accentuated GLU concentration decreased by 3 months after transplantation, although it was still significantly greater than pretransplantation levels. We concluded that the unnatural mode of delivery of pancreas endocrine secretion to systemic rather than to portal circulation leads to derangements in pancreatic endocrine function in order to maintain glucose homeostasis. This may cause earlier exhaustion of islet cells. Segmental rather than whole organ and duct occlusion rather than exocrine drainage may further contribute to this, shortening the effective life of the graft.

Animals↗
PubMed1996

Effects of brain death and glucose infusion on hepatic glycogen and blood hormones in the pig.

We wished to study the effects of intravenous glucose/ insulin infusion to brain-dead pigs on the hepatic glycogen content. Four groups of 40-kg pigs were studied: brain-dead and control pigs given isotonic saline or glucose/insulin (7.5 mg glucose/kg/min, 1.25 mU insulin/kg/ min) (n = 5 to 10 in each group). Brain death was induced by inflating a balloon placed in the epidural space. In brain-dead pigs given saline, liver glycogen decreased from 45 +/- 11 mmol/g DNA (mean +/- SEM) to 7 +/- 3 mmol/ g DNA after 6 hours. Thereafter, it increased to 28 +/- 9 mmol/g DNA after 9 hours (P = .05 compared with the 6-hour measurement). These changes were accompanied by transient increases in plasma adrenaline, glucose, free fatty acids (FFA), and glucagon. Following glucose/ insulin infusion, hepatic glycogen increased steadily and was approximately double after 12 hours (P < .01) in both brain-dead and in non-brain-dead pigs. In brain-dead pigs, the increases in the aforementioned blood measurements were smaller following glucose/insulin infusion than following saline infusion. However, studies of longer duration will be needed to examine these effects on a time scale that is relevant to human organ donors. In conclusion, the decrease in hepatic glycogen content after brain death could be prevented by intravenous glucose/insulin infusion probably because of a reduction of the adrenaline response to the induction of brain death.

Animals↗
PubMed1996

IL-8 induces T cell chemotaxis, suppresses IL-4, and up-regulates IL-8 production by CD4+ T cells.

Interleukin-8 (IL-8), a neutrophil-activating cytokine, also activates certain T cell functions such as chemotaxis. We additionally find (n = 6) that recombinant (rIL-8; 1-100 ng/ml), when added to 24 h culture of human CD4+ T cells, suppressed the spontaneous production of IL-4 (50-85%). Steady state production of Il-4 was typically around 30 pg/ml, determined by use of a solid- phase immunoabsorbant assay. De novo synthesis of IL-4 from CD4+ T cells cultured for 3 days was also evaluated by use of detection of [35S]methionine incorporation, as visualized by autoradiography of 2-D gels, and showed that IL-8 suppressed IL-4 production. This suppression of IL-4 production was confirmed in the cytosol fraction by use of Western blotting. The effect of IL-8 (100 ng/ml) was comparable to that of 10 ng/ml recombinant interferon-gamma, both strongly suppressing IL-4 production. The regulatory effect of IL-8 on IL-4 production was also indicated by the fact that addition of a neutralizing monoclonal anti-IL-8 antibody (WS.4) enhanced the spontaneous IL-4 production when added to the culture of CD4+ T cells, thereby probably inactivating the effect of IL-8 originating from the cultured T cells. Also, we observed that IL-4 mRNA expression was down-regulated when the CD4+ T cells were cultured for 12 h in the presence of 100 ng/ml IL-8. The suppression of IL-4 mRNA expression could be prevented by adding anti-IL-8 (20 microgram/ml) or IL-10 (100 ng/ml) l h before adding rIL-8. Thus, IL-8 may be an important regulator of CD4+ T cell-derived IL-4, thereby possibly regulating the balance between humoral and cellular T cell-dependent responses.

CD4-Positive T-Lymphocytes↗
PubMed1996

Increased levels of nm23 H1/nucleoside diphosphate kinase A mRNA associated with adenocarcinoma of the prostate.

Overexpression of the nm23H1 gene has been associated with the suppression of metastasis in several solid tumors. However, in colorectal carcinoma and neuroblastoma, increased levels of nm23 H1 nucleoside diphosphate kinase A (NDPKA) mRNA are associated with tumorigenesis. To determine the role of nm23 H1/NDPKA in the prostate, normal and/or malignant tissue samples from 29 consecutive patients were studied. Levels of nm23 H1/NDPKA mRNA and nm23 H1/NDPKA mRNA protein were determined in tissue from 18 and 27 patients, respectively. In all, 16 of the 18 tumor samples expressed increased levels of nm23 H1/NDPKA mRNA as compared with those measured in normal tissue. The level of nm23 H1/NDPKA mRNA was > 10-fold higher in a metastatic lymph node than in normal prostate tissue. All cancer specimens and areas of prostatic intraepithelial neoplasia showed immunoreactivity with the nm23 H1/NDPKA antibody; however, normal prostatic tissue was unreactive. These findings suggest that overexpression of the nm23 H1/NDPKA gene occurs frequently in adeno-carcinomas of the prostate and may be an early event in prostate cancer tumorigenesis.

Adenocarcinoma↗
PubMed1995

Interleukin-8 induces its own production in CD4+ T lymphocytes: a process regulated by interleukin 10.

The neutrophil and T cell chemotactic factor interleukin 8 (IL-8) is believed to play a pathophysiological role in the development of various inflammatory disorders. So far no other effects of IL-8 on T cells have been observed. We observed that purified CD4+ T cells in particular, but also CD8+ T cells, spontaneously synthesize IL-8 mRNA and secrete IL-8 protein. The culture supernatants of CD4+ T cells contained T cell chemotactic activity as well as IL-8 protein. In addition, we confirmed the ability of CD4+ T cells to produce IL-8 by double immunofluorescence staining and by the demonstration of IL-8 mRNA expression. Further, IL-8 induced its own production in CD4+ T cells, while its synthesis by CD8+ T cells was low and not always auto-stimulatory. Both the spontaneous, as well as the IL-8 induced IL-8 production, could be inhibited in the presence of human interleukin 10 (100 ng/ml). This observation suggests that IL-10 plays a homeostatic role in regulating the IL-8 circuit in CD4+ T cells.

Autoradiography↗
PubMed1995

Passive elastic wall properties in isolated guinea pig small intestine.

The aim was to study and compare the passive biomechanical wall properties in the isolated duodenum and distal ileum of the guinea pig in vitro. The organ bath contained a Krebs-Ringer solution with 10(-2) M MgCl2 to abolish smooth muscle contractile activity. Stepwise inflation of an intraluminal balloon, in which the cross-sectional area (CSA) was measured, provided the distension stimulus. The circumferential wall tension-strain distributions and wall stiffness-strain relations were computed from steady-state values of these measurements in order to evaluate the passive elastic properties. The CSA always reached equilibrium within the 2-min distension period. The CSAs obtained in the distal ileum were higher than those in the duodenum (P < 0.001). The basal CSA was 17.31 +/- 1.14 mm2 and 12.96 +/- 0.42 mm2 for the distal ileum and the duodenum, respectively (P < 0.01). At a maximum pressure of 6 kPa, the CSA of the ileum was 56.63 +/- 1.81 mm2 and 36.86 +/- 1.76 mm2 for the duodenum (P < 0.01). The circumferential wall tension-strain distributions showed an exponential behavior that accorded well with the equation Y = exp(a+bX) with determination coefficients of 0.96 +/- 0.01 and 0.99 +/- 0.00 in the duodenal segments in the distal ileal segments, respectively. The values of a (intercept with the y-axis) were 0.54 +/- 0.11 and -0.35 +/- 0.19 for the duodenal and ileal segments, respectively (P < 0.001). The slope of the curves (b values) were 4.34 +/- 0.35 in the duodenal and 5.23 +/- 0.37 in the ileal segments (0.1 > P > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

A new combined high-frequency ultrasound-impedance planimetry measuring system for the quantification of organ wall biomechanics in vivo.

The aim was to develop a method for the quantification of the stress-strain distribution of tubular organs in vivo using the porcine duodenum as an experimental model. We placed four electrodes for impedance planimetry and a 20 MHz ultrasound transducer inside an inflatable balloon mounted on a 6 mm-diameter probe for intraluminal use. By means of the ultrasound transducer and the impedance planimetric system, we measured the wall thickness and luminal cross-sectional area of the duodenum. We calculated the luminal radius on the basis of the latter. We validated ultrasonic measurements of wall thicknesses by comparing the former to microscopic measurements of the wall thickness of unstrained duodenal specimens in vitro. Also, we tested whether the magnitude of the applied balloon pressure affected ultrasonic measurements in vitro. The luminal and the outer radius increased non-linearly by a factor of three, rising steeply at low balloon pressures, moderately at higher pressures. The wall thickness decreased as an almost linear function of the applied balloon pressure, resulting in a 50% decrease. The stress-strain distribution calculated on the basis of the balloon pressures, the wall thicknesses and the luminal radii were non-linear. The wall reached a maximum circumferential strain of 1.71 at 6 kPa, corresponding to a stress of 64.8 kPa. Our system enabled us to quantify the stress-strain distribution of the porcine duodenum in vivo, and it may become a valuable tool for future biomechanical investigations of tubular organs in health and disease.

Animals↗
PubMed1995

Elective laparoscopic cholecystectomy nearly abolishes the postoperative hepatic catabolic stress response.

OBJECTIVE: Surgery results in a catabolic state of postoperative stress, where the efficiency of the liver to convert amino acids to urea is increased. This study measured the metabolic consequences of the less traumatic laparoscopic surgery in elective cholecystectomy compared with traditional open surgery technique. SUMMARY BACKGROUND DATA: The authors previously have shown that open cholecystectomy doubles the urea synthesis measured by the means of the functional hepatic nitrogen clearance. Glucagon and cortisol increased by 50% (p < 0.05) and 75% (p < 0.05), respectively, after open cholecystectomy. METHODS: Patients undergoing uncomplicated elective laparoscopic cholecystectomies were included. Preoperatively and on the first postoperative day, blood and urine samples were drawn every hour under basal conditions and during amino acid infusion. The urea synthesis rate was calculated from the urea excreted in urine and accumulated in total body water. Functional hepatic nitrogen clearance was quantified as the slope of the linear relation between blood amino-N concentration and the urea synthesis rate. The results were compared with an historic matched group of patients who underwent open cholecystectomies and were studied by the same protocol. RESULTS: The laparoscopic cholecystectomy increased the functional hepatic nitrogen clearance by only 25% (from 8.7 +/- 0.9 to 11.1 +/- 1.5 mL/sec [mean +/- SEM; p < 0.05]), compared with a doubling after open cholecystectomy (from 9.4 +/- 0.9 to 17.6 +/- 3.3 mL/sec [p < 0.05]). The difference between the groups was significant (p < 0.05). Neither glucagon nor cortisol increased significantly after laparoscopic cholecystectomy. CONCLUSIONS: The laparoscopic technique results in a much smaller postoperative hepatic catabolic stress response and probably reduced tissue loss of amino-N. This may be important for the more rapid convalescence and reduced postoperative fatigue.

Adult↗