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T Buanes

Publications and source records attributed to T Buanes.

At least 19 recordsLinked to original sources
PubMed1992

[Quality assurance in a surgical department].

The quality of a given service in a surgical department depends on many factors. Most important are adequate resources, training of the surgeons and nurses and time for follow-up and clinical research. Quality standards should be defined in accordance with the international literature and results should be continuously surveyed to ensure that the agreed goals are met. This article describes various general rules and routines which have been established in our department, as well as the specific systems used to measure the quality of our surgical service in three special fields: Care of patients with tumour mammae, care of patients with gallstone disease, and prospective registration of complications for all gastroenterological patients in our surgical department.

Norway↗
PubMed1992

[Necrosis of the small intestine. A diagnostic and therapeutic challenge].

The paper describes three patients with small intestinal necrosis from different causes: One patient had diabetes, and severe ketoacidosis, which may cause microthrombosis in small intestinal vessels. This patient died in septic shock during laparotomy, removing the necrotic gut. The second patient was laparotomized because of free air in the abdomen originating from a clostridial intestinal infection. The third patient caught a salmonella infection during a holiday in the Canaries, thereafter peritonitis due to small intestinal necrosis. These three patients illustrate principal aspects of the surgical management of patients with intestinal necrosis. Firstly, necrotic intestinal segments must be removed as soon as possible. Delay represents a threat to the patient's life in all situations when intestinal segments are devascularized. Secondly, relaparotomy may be mandatory in clostridial intra-abdominal infections. We report these patients to illustrate that well known surgical principles may be life-saving if effectuated without delay. This applies also in the case of patients with uncommon diseases and complications.

Aged↗
PubMed1991

Secretin dissipates red acridine orange fluorescence from pancreatic duct epithelium.

This study was undertaken to elucidate whether duct cells in the pancreas contain acidic cytoplasmic compartments regulated by secretin. Microdissected pancreatic ducts from pigs were examined by acridine orange (AO) and 2',7'-biscarboxyethyl-5(6)-carboxyfluorescein/tetraacetoxymethy l ester (BCECF/AM) epifluorescence microscopy. Estimated cytoplasmic pH using BCECF fluorescence was 7.43 +/- 0.04 and was not changed by altering CO2 tension in the incubation medium. The epithelium of acridine orange incubated peripheral interlobular pancreatic ducts exhibited green and red fluorescence; the colour depending on the experimental conditions. Red epithelial fluorescence was seen in resting pancreatic ducts and was greatly accentuated by raising CO2 in the incubation medium from 5.5 to 10 kPa. The red fluorescence was abolished by secretin, or following incubation with chloroquine or NH4Cl or the protonophores carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP) or carbonyl cyanide m-chlorophenylhydrazone (CCCP), leaving uniform green fluorescence. These findings suggest that pancreatic duct cells contain CO2-dependent acidic compartments which vanish during secretin stimulation and which may be cytoplasmic tubulovesicles.

Acridine Orange↗
PubMed1990

Colchicine inhibits the effects of secretin on pancreatic duct cell tubulovesicles and HCO3- secretion in the pig.

Secretin stimulation clears the cytoplasm of intralobular pancreatic duct cells in pigs of tubulovesicles and causes these cells to secrete HCO3- into the pancreatic juice. To determine whether the clearance of cytoplasmic tubulovesicles involves the microtubule system and is important for initiation of HCO3- secretion, the effect of the microtubule poison colchicine on duct cell morphology and pancreatic HCO3- secretion was measured in anaesthetized pigs. Before colchicine, secretin reduced the density of tubulovesicles in the cytoplasm of pancreatic duct cells from 92 +/- 8 U to 8 +/- 2 U and initiated pancreatic secretion of 176 +/- 21 mumols min-1 HCO3-. After colchicine, secretin failed to lower duct cell tubulovesicle density and caused the secretion of only 77 +/- 14 mumols min-1 HCO3-. By contrast, lumicolchicine, an isomer of colchicine that does not affect microtubules, did not inhibit pancreatic HCO3- secretion. Colchicine did not reduce carbonic anhydrase or Na,K-ATPase activities in in-vitro assays. The clearance of tubulovesicles from the cytoplasm of pancreatic duct cells therefore seems to be microtubule-dependent and important for the pancreatic HCO3- secretion.

Animals↗
PubMed1990

Colchicine blocks the effects of secretin on bile duct cell tubulovesicles and plasma membrane geometry and impairs ductular HCO3- secretion in the pig.

Secretin causes the bile duct cells to secrete HCO3-. To examine whether the transformation of duct cell ultrastructure that follows secretin stimulation depends on microtubules and is important for ductular HCO3- secretion, we examined the effect of colchicine on ductular HCO3- secretion and on the morphology of cells lining bile ductules of anaesthetized pigs. Colchicine blocked secretin-dependent cytoplasmic clearance of tubulovesicles and prevented expansion of the basolateral plasma membrane in duct cells and reduced the ductular HCO3- secretory response from 132 +/- 25 mumol min-1 to 97 +/- 14 mumol min-1. In contrast, lumicolchicine did not affect secretin-dependent tubulovesicle clearance or plasma membrane geometry or ductular HCO3- secretion. Accordingly, secretin-dependent cytoplasmic clearance of tubulovesicles in bile duct cells appears to depend on microtubules and to be important for ductular HCO3- secretion.

Animals↗
PubMed1990

Secretin-dependent HCO3- secretion from pancreas and liver.

Ultrastructural studies performed on pigs revealed that numerous cytoplasmic tubulovesicles were present in resting pancreatic duct cells. Elevation of systemic arterial PCO2 from 5.5 to 11 kPa increased the number of vesicles more than twofold. Following secretin administration, concurrent with the onset of HCO3- secretion (JHCO3), the cytoplasm became devoid of vesicles, and the basolateral plasma membrane surface area more than doubled. Similar phenomena were observed in bile duct cells. After pretreatment with the microtubules-inhibiting drug colchicine, secretin failed to reduce duct cell vesicle density, and JHCO3 was reduced by c. 50% compared to the control. These ultrastructural changes resemble those described in other H+/HCO3(-)-transporting organs such as the distal nephron and the urinary bladder. Our findings are compatible with the notion that cytoplasmic vesicles containing H(+)-ATPases are incorporated into the basolateral plasma membrane of secretory cells during secretin stimulation. Active transport of H+ into interstitial fluid might therefore be the driving force underlying JHCO3.

Animals↗
PubMed1989

[Duodenal injuries due to blunt trauma].

UNLABELLED: During the last ten years we have seen fourteen patients with duodenal injury after blunt trauma. Five patients with intramural hematomas received no treatment. Nine patients had a perforated duodenal wall, and in four of these the diagnosis was delayed for more than 24 hours. Revision and primary suture were carried out in seven patients, with no complications. In one patient, where the diagnosis was delayed for three days, the perforation was closed around a Pezzer catheter for external drainage. She developed an intraabdominal abscess which required reoperation. One patient died from liver injury with profuse bleeding; the others survived without sequelae from the duodenal injury. CONCLUSIONS: Duodenal injuries are rare and early diagnosis is difficult. We think that frequently repeated physical examinations, liberal use of diagnostic peritoneal lavage, and careful peroperative exploration of the entire duodenum when performing laparotomy after abdominal injuries, are important for early diagnosis and treatment.

Abdominal Injuries↗
PubMed1989

Effects of digitoxin and lithium, used as a marker of passive Na transport, on secretin-dependent bile flow in the pig.

The present study was performed in anaesthetized pigs, and the first aim was to assess the role of Na,K-ATPase in secretin-dependent biliary HCO3 secretion (JbHCO3). Intra-arterial administration of the cardiac glycoside digitoxin (0.2 mg/kg-1) reduced hepatic Na K-ATPase activity, JbHCO3 and secretin-dependent bile flow by 24, 55 and 34% respectively. In the second part of this study lithium (Li) was used as a marker of passive Na transport to assess the electrochemical gradient for Na flux into bile duct lumen during secretin-stimulated bile flow and impeded biliary osmotic water flow by i.v. infusion of glucose. At plasma glucose 85 (73-96) mmol l-1, bile [Na] and [Li] exceeded their concentrations in plasma by 57 and 47% respectively. By using the Nernst equation, transepithelial potential difference (PD) during hyperglycaemia was estimated to be -6.2 (0 to -10.8) mV (ductal lumen negative), which corresponds to a [Li]bile/[Li]plasma ratio of 1.3 (1.0-1.5). The ratio was not significantly different from the observed [Li]bile/[Li]plasma ratio of 1.4 (1.3-1.5). It is concluded (1) that Na, K-ATPase is necessary for JbHCO3, probably by sustaining the cell membrane PD (cell interior negative) which is a driving force for apical electrogenic HCO3 secretion, and (2) transepithelial Li (and hence Na) flux is driven solely by the negative transcellular PD during secretin-stimulated bile flow in the pig.

Animals↗
PubMed1988

Secretin empties bile duct cell cytoplasm of vesicles when it initiates ductular HCO3- secretion in the pig.

To determine whether secretin has any effect on bile duct cell ultrastructure, bile duct cells from liver biopsy specimens of pigs were analyzed morphometrically. During secretory rest, bile duct cell cytoplasmic vesicles totaled 96 (84-103) arbitrary units per cell volume (U). Secretin increased bile HCO3- secretion from 9 mumol/min (range 6-15) to 131 mumol/min (range 118-200) and lowered the bile duct cell vesicles to 5 U (range 3-9). Acute elevation of arterial PCO2 to 10.9 kPa (range 10.2-11.1) doubled vesicle number in resting duct cells and augmented the secretory response to secretin. At high arterial PCO2, secretin cleared the duct cell cytoplasm of vesicles and more than doubled the basolateral plasma membrane surface area. Taurocholate-induced canalicular choleresis, in contrast, did not alter duct cell morphology. It is concluded that secretin clears the bile duct cell cytoplasm of vesicles as it initiates ductular HCO3- secretion, possibly through causing exocytotic insertion of vesicle material into the basolateral plasma membrane.

Animals↗
PubMed1988

Effects of arterial pH and carbon dioxide on pancreatic exocrine H+/HCO3- secretion and secretin-dependent translocation of cytoplasmic vesicles in pancreatic duct cells.

To elucidate why arterial pH and carbon dioxide (PaCO2) modify the pancreatic H+/HCO3- secretory response to secretin stimulation, experiments were performed on anaesthetized pigs, recording the effects of arterial pH and PaCO2 on exocrine H+/HCO3- secretion and on morphology of pancreatic duct cells. Duct cells contained numerous cytoplasmic vesicles at secretory rest. Their number more than doubled during elevation of PaCO2 from 5.5 to 11.0 kPa. At arterial pH 7.40, maximal secretin stimulation cleared the cytoplasm of duct cells of more than 90% of the vesicles. At high PaCO2, this was accompanied by doubling the basolateral plasma membrane area and a 30% higher secretion rate than at PaCO2 5.5 kPa. Lowering arterial pH to 7.0 more than halved the secretin-induced vesicle clearance of duct-cell cytoplasm as well as exocrine H+/HCO3- secretion and abolished the secretin-dependent basolateral membrane area changes. Supramaximal secretin stimulation did not reverse the inhibitory effect of severe metabolic acidosis on secretion. It is concluded that PaCO2 and arterial pH may modify the secretory response to secretin through determining the incorporation of cytoplasmic vesicle material into the basolateral plasma membrane of duct cells.

Animals↗
PubMed1988

Effects of bumetanide on bile flow in the pig.

This study was performed on 12 anaesthetized pigs in order to examine the effect of the 'loop' diuretic bumetanide (inhibitor of Na,K,Cl-co-transport) on ductular bile secretion. It has previously been shown that administration of furosemide (a less potent 'loop' diuretic) to dogs and rats increases bile flow due to inhibition of ductular reabsorption of electrolytes and water. In group I (n = 6) bumetanide (median biliary concentration: 8.4 x 10(-3) mol l-1) increased bile flow and biliary concentration of HCO3 by 200% (116-320) and 50% (26-96), respectively. Biliary concentration of Cl was significantly decreased by 6% (2-12) following administration of bumetanide. In group II (n = 6) bile secretion was measured during secretin infusion (3 CU kg b. wt h-1) in the arterial pH range of 7.40-7.00, both before and after bumetanide administration in each animal. Bumetanide (median biliary concentration: 2.7 x 10(-3) mol I-1) did not significantly alter biliary secretion of water, HCO3, Na, K or Cl. Bile acid secretion was reduced by 30% from 43 (28-55) to 30 (17-41) mumol min-1 (P less than 0.05) while hepatic venous concentration of bile acids was raised by 90% (54-126) from 184 (113-309) to 350 (229-502) mumol l-1 (P less than 0.05) at slightly increased hepatic blood flow. Hepatic venous serum concentration of bumetanide was 4.8 (2.1-7.4) x 10(-4) mol l-1 (unbound fraction).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Importance of carbonic anhydrase for canalicular and ductular choleresis in the pig.

To assess the importance of carbonic anhydrase (CA) for canalicular and ductular choleresis, the effect of acetazolamide on bile secretion was measured in three experimental groups of anaesthetized pigs. CA activity in liver homogenate was 46 (43-54) U g-1 wet weight, 150 mg kg-1 b.w. acetazolamide completely abolished the CA activity. Acetazolamide reduced bile HCO3- secretion in six secretin infused, bile-acid depleted pigs by 67 (58-71)% at arterial pH 7.41 (7.38-7.46). By contrast, acetazolamide did not affect HCO3- secretion in six Na-taurocholate (TCA) infused pigs in the absence of secretin stimulation. Acetazolamide reduced ursodeoxycholic-acid- (UDCA) dependent HCO3- secretion by 24 (11-38)% in six other pigs in the absence of secretin stimulation. Histochemical examination using modifications of Hansson's method showed strong reaction in bile ductules and weaker reaction in peripheral zones of liver lobules. Because acetazolamide impairs HCO3- secretion from cells sustaining high rates of H+/HCO3- transport, it is suggested that high rates of H+/HCO3- transport are confined to bile ductules under conditions of secretin- and UDCA-induced choleresis.

Acetazolamide↗
PubMed1987

The effect of amiloride on biliary HCO3- secretion in the anaesthetized pig.

The present study was performed on 29 anaesthetized pigs and shows that the bile acid ursodeoxycholic acid (UDCA) produces a flow of bile rich in HCO3- compared with taurocholic acid (TCA). The slope relating biliary HCO3- secretion to bile acid secretion was 0.59 (0.44-0.82) and 0.33 (0.29-0.38) during venous infusion of UDCA and TCA, respectively. We next wanted to evaluate the importance of Na+/H+ ion exchange for biliary HCO3- secretion. High doses of amiloride were employed in order to impair the hepatic Na+/H+ ion exchanger. It was reasoned that any reduction in H+ efflux through the hepatic Na+/H+ ion exchanger involved in causing biliary HCO3- secretion would be translated into an equimolar fall in biliary HCO3- secretion. We found that amiloride (2.0 X 10(-4) mol l-1 plasma) reduced UDCA-dependent canalicular HCO3- secretion by 26 (14-35)% without concurrently reducing bile acid secretion. Amiloride (2.9 X 10(-4) mol l-1 plasma) did not significantly reduce secretin-dependent ductular HCO3- secretion. In this group of animals amiloride reduced bile acid secretion by 13 (5-22)%. It is concluded that Na+/H+ ion exchanger is essential for UDCA-dependent canalicular HCO3- secretion, but not for secretin-dependent ductular HCO3- secretion.

Amiloride↗