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T Buanes

Publications and source records attributed to T Buanes.

16 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

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↗
PubMed1987

Localization of K-NPPase and Li+ secretion in the exocrine pancreas of the pig.

To study the mode of transepithelial Na+ transport into pancreatic ducts during secretin-dependent NaHCO3 secretion, Na, K-ATPase was first localized within the exocrine pancreas of the pig using a cytochemical reaction for K-dependent p-nitrophenylphosphatase (K-NPPase). K-NPPase staining was confined to the lateral cell membrane bordering the intercellular spaces between ductal cells, negating the possibility of primary active, transcellular Na+ transport into pancreatic ducts. To assess how transepithelial Na+ transport may be coupled to HCO-3 secretion, net flux of Li+ into pancreatic juice was measured following intravenous systemic Li+ loading of 12 secretin infused, anaesthetized pigs. At plasma Li+ 32 (23-35) mmol l-1, Li+ displaced Na+ as accompanying cation to secreted HCO-3, and Li+/Na+ in pancreatic juice matched Li+/Na+ in arterial plasma. During superimposed inhibition of pancreatic water flux by hyperglycaemia, Li+ and Na+ were both transported against a transepithelial concentration gradient. Li+ reduced pancreatic HCO-3 secretion rate by 14 (-2 to -20)%, as well as Na,K-ATPase activity in a separate in vitro assay. The finding that Li+ substituted for Na+ in the secretion even during reduced osmotic water flow suggests that Na+ and Li+ are transported together with secreted HCO-3 into pancreatic juice by an electrogenic mechanism in addition to solvent drag and diffusion.

4-Nitrophenylphosphatase↗
PubMed1987

Effect of arterial pH and PCO2 on biliary HCO3- secretion in the pig.

The purpose of the present study was to examine the effect of changes in arterial pH and PCO2 on biliary HCO3- secretion. This was done in order to further characterize the various ion transport mechanisms considered responsible for biliary HCO3- secretion in the pig. Experiments were performed on two groups of six pigs. In both groups arterial pH was varied in steps from pH 7.40 to 7.00, both at PCO2 5.5 kPa and PCO2 10 kPa. In group I (n = 6), data were obtained on the effect of arterial pH and PCO2 on ductular HCO3- secretion in bile acid depleted (cholestyramine pretreated), secretin-infused pigs. In group II (n = 6), the effect of pH and PCO2 on canalicular HCO3- secretion was studied in ursodeoxycholic acid (UDCA)-infused pigs (3 mumol min-1 kg-1 body wt). In group I, biliary HCO3- secretion exhibited PCO2-dependent, positive straight line relationships to arterial pH. An increment in biliary HCO3- secretion of 17 (11-24)% was seen during high PCO2 at pH 7.40. In group II, biliary HCO3- secretion exhibited PCO2-dependent, positive curvilinear relationships to arterial pH. A median increment in HCO3- secretion of 37 (20-62)% was seen during elevated PCO2 at arterial pH 7.40. The linear dependence of ductular HCO3- secretion on arterial pH and the effect of elevated PCO2 on HCO3- secretion fit well with findings in other epithelia, where proton transport is thought be driven by a proton pump. A computer simulation provided evidence suggesting that secretin-dependent HCO3- secretion does not involve the action of a Na+/H+ ion exchanger--in contrast to UDCA-dependent HCO3- secretion. It is concluded that ductular and canalicular HCO3- secretion could be mediated by a proton pump and a Na+/H+ ion exchanger in addition to canalicular HCO3- secretion due to solvent drag and diffusion, respectively.

Animals↗
PubMed1986

Lack of effect of amiloride, furosemide, bumetanide and triamterene on pancreatic NaHCO3 secretion in pigs.

This study examines the effects of the Na entry blockers amiloride, furosemide, bumetanide and triamterene on pancreatic NaHCO3 secretion. The purpose of the study was to elucidate whether Na flux through a Na-H-antiport, a Na,K,Cl-symport or a Na-K(H)-antiport respectively, may be rate limiting for pancreatic NaHCO3 secretion. The effect of each drug on secretion was tested in four groups of six anaesthetized pigs (20-25 kg body wt) during supramaximal, intravenous secretin infusion (3.0 CU kg-1 body wt. h-1), following laparotomy and cannulation of the pancreatic duct. Secretion was measured over a wide range of arterial pH values, both before and after drug administration in each animal. Pancreatic NaHCO3 secretion averaged 268 (219-308) mumol min-1 at physiological arterial pH 7.40 in the control period. Neither amiloride (90 mg kg-1 body wt), furosemide (10 mg kg-1 body wt), bumetanide (0.6 mg kg-1 body wt) nor triamterene (25 mg kg-1 body wt) affected the rate of secretin-dependent NaHCO3 secretion or the relation between NaHCO3 secretion and arterial pH. It is concluded that Na flux through neither a Na-H-antiport, a Na,K,Cl-symport nor a Na-K(H)-antiport appears to be rate limiting for pancreatic secretion of NaHCO3.

Amiloride↗
PubMed1985

Effects of digitoxin and hypokalaemia on pancreatic NaHCO3 secretion and pancreatic Na,K-ATPase activity.

To study the role played by Na,K-ATPase in the pancreatic secretion of NaHCO3, experiments were performed in 20 anaesthetized, secretin-infused pigs (3.0 clinical units X kg b. wt. X h-I). The relationship between pancreatic NaHCO3 secretion and arterial pH was obtained before and during Na,K-ATPase inhibition by digitoxin and hypokalaemia. Na,K-ATPase activity in pancreatic tissue homogenate averaged 5.45 (5.02-6.68) mumol Pi X mg X protein X h-I. Retrograde injection of 0.5 ml 1.4 X 10(-4) mol X l-I digitoxin into pancreatic ducts reduced pancreatic Na,K-ATPase activity by 3I(I8-47)%, while intra-arterial injection of 0.2 mg X kg b. wt-I digitoxin reduced pancreatic Na,K-ATPase activity by 50(45-56)%. Digitoxin and hypokalaemia reduced the rate of pancreatic NaHCO3 and shifted the normal, proportional relationship between NaHCO3 secretion and arterial pH towards higher pH. Hypokalaemia reduced Na,K-ATPase activity and NaHCO3 secretion in proportion. These effects indicate that Na,K-ATPase helps to sustain the requisite electrochemical potential gradients for driving H+ ions, and hence HCO-3 ions, out of secretory cells.

Animals↗