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Biomedical subjects

O Mathisen

Publications and source records attributed to O Mathisen.

At least 37 records · Page 2Linked to original sources
PubMed1990

Computed tomography after modified Whipple procedure with pancreatic duct occlusion.

Eighty-two CT examinations performed on 28 patients who had undergone a modified Whipple procedure including pancreatic duct occlusion were reviewed. Reduction of the antero-posterior diameter of the body and tail of the pancreatic remnant was observed on consecutive scans in 8 patients (29%). Decreasing liver attenuation was seen in 4 patients (14%) postoperatively, and pseudocysts in the pancreatic remnant in 6 (21%). In 10 examinations performed because of suspected intraabdominal abscess postoperatively, abscess was diagnosed in 2 patients. In 62 routine follow-up CT examinations, significant positive findings were diagnosed in 5 patients: tumor recurrence or metastases in 4, and a large pseudocyst in one. CT is of value in the early postoperative phase to reveal postoperative complications and in the follow-up of patients with specific symptoms indicating tumor recurrence or metastases.

Adult↗
PubMed1989

Amino acid- and glucose-induced cholestasis before and during secretin stimulation.

To identify the mechanisms of reduced bile flow after hypertonic amino acid and glucose infusion, acute experiments were performed on anesthetized pigs. When secretin was not administered, amino acids or glucose reduced bile acid-dependent bile secretion to 65 +/- 3% of control. During secretin stimulation amino acids or glucose diminished bile acid-independent bile secretion to 78 +/- 2% of control. No changes in serum bilirubin, alanine aminotransferase, and aspartate aminotransferase were observed. Amino acids and glucose attack different mechanisms responsible for bile formation, but the result is that when secretin is not administered, biliary secretion of bile acids is reduced, and, accordingly, bile acid-dependent bile flow diminished. During secretin stimulation biliary NaHCO3 secretion is depressed, accounting for a fall in bile acid-independent bile flow. Amino acids exert no effect on bile acid secretion or, as a result, on bile acid-dependent bile flow after secretin infusion.

Amino Acids↗
PubMed1986

Hypernatremia inhibits NaHCO3 reabsorption and associated NaCl reabsorption in dogs.

To examine the effect of selective rise of plasma NaCl concentration (hypernatremia) on NaHCO3 reabsorption and associated NaCl reabsorption remaining during continuous ethacrynic acid infusion, hypertonic NaCl solution was infused in three groups of anesthetized volume-expanded dogs. In six dogs examined at constant hematocrit and plasma pH, bicarbonate and water reabsorptions were inversely related to PNa and reduced by 37% and 39% respectively by raising PNa from 140 to 200 mM. Chloride reabsorption remained essentially constant until PNa exceeded 170 to 180 mM. At PNa 200 mM, sodium reabsorption was reduced by 22 +/- 6%. In six other dogs, mechanical variations of GFR showed that the inhibitory effects of hypernatremia (PNa 199 +/- 3 mM) were less pronounced at low GFR. After subsequent administration of acetazolamide (30 mg/kg body wt), only 20% of control bicarbonate reabsorption remained and glomerulo-tubular balance was completely abolished. Both hypernatremia and acetazolamide inhibited NaHCO3 and NaCl reabsorption in a molar ratio of about 1:2, as in normonatremic dogs. Finally, experiments in six dogs showed that the inhibitory effects of hypernatremia (PNa 213 +/- 4 mM) were not altered by varying PCO2 and plasma pH. We conclude that hypernatremia inhibits paracellular water and NaCl reabsorption in the proximal tubules by reducing the osmotic force caused by transcellular NaHCO3 reabsorption. A rise in PNa does not stimulate transcellular NaCl reabsorption during distal inhibition by ethacrynic acid.

Acetazolamide↗
PubMed1985

Dependency of renal potassium excretion on Na,K-ATPase transport rate.

Potassium secretion may depend on the transport rate of Na, K-ATPase in basolateral cell membranes of distal tubular cells. To examine this hypothesis experiments were performed in anaesthetized dogs during inhibition of proximal potassium reabsorption by acetazolamide or mannitol (fractional potassium excretion 1.2 - 1.4) or additional stimulation of potassium secretion by ethacrynic acid (fractional potassium excretion 2.1). Ouabain in a dose which inhibits 70-80% of the Na, K-ATPase activity reduced fractional potassium excretion to 0.8 - 0.9 by an effect on distal tubular secretion since potassium transport in the proximal tubules was not affected. Ouabain-sensitive potassium excretion varied in proportion to ouabain-sensitive sodium reabsorption during variation in glomerular filtration rate, even at urinary sodium concentrations exceeding 80 mmol X 1(-1). In experiments without ouabain, saline infusion raised potassium excretion and sodium reabsorption until maximal Na,K-ATPase transport rate was reached, as judged from heat production measurements, but not during further increments in urine flow. After inhibition of Na,K-ATPase activity by hypokalaemia, potassium excretion and cortical heat production remained constant over a wide range of urine flow and sodium excretion. We conclude that potassium secretion is dependent on intact Na,K-ATPase activity and is stimulated by sodium delivery to the distal nephron until maximal transport rate of the enzyme is reached.

Animals↗
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↗
PubMed1985

Role of osmosis in biliary NaCl secretion and bile formation.

To challenge the osmotic hypothesis of biliary NaCl secretion and bile formation, experiments were performed in anaesthetized pigs. An increase in plasma osmolality of 7 +/- 1 mosm/kg H2O induced by intravenous sucrose infusion decreased NaCl secretion, NaHCO3 secretion, and bile flow by 36 +/- 3%, 34 +/- 2%, and 34 +/- 3%, respectively. There was no change in the biliary concentration of NaCl and NaHCO3. When bile acids were infused intravenously, the secretion of 1 mmol bile acids caused an osmotic flow of 12.0 ml bile containing 0.92 mmol NaCl and 0.30 mmol NaHCO3 in an isotonic solution. Bile acids are therefore much stronger choleretic substances than NaHCO3. When the plasma sodium concentration was increased to 200 mM, bile flow increased by 31 +/- 5% and the secretion of bile acids, NaHCO3, and NaCl was increased by 63 +/- 3%, 96 +/- 4%, and 93 +/- 4%, respectively. These data are consistent with osmotic transport as the main mode of bile formation, but diffusion could be responsible for a small fraction. A raised plasma sodium concentration stimulates osmotic formation of bile by increasing both the bile acid-dependent and -independent secretion through stimulation of biliary bile acid and NaHCO3 secretion.

Animals↗
PubMed1983

Mechanism of hepatic bicarbonate secretion and bile acid independent bile secretion.

To examine hepatic bicarbonate transport and bile acid independent bile secretion, bile was sampled via a T-tube inserted into the common bile duct of anaesthetized pigs. Secretin was infused intravenously at a rate of 2.7 C.U./kg body weight h-1 (large dose) or 0.45 C.U./kg body weight h-1 (small dose). Hepatic water and electrolyte secretion were studied during systemic acid-base disturbances while secretin was continuously administered. Systemic acidosis reduced the rate of NaHCO3 secretion which fell in proportion to changes in plasma pH, by 9% and 2% per 0.1 pH unit for the large and small dose of secretin, respectively. Plasma pCO2 and bicarbonate concentration had little influence on NaHCO3 secretion. Consequently, plasma pH appeared to be the main determinant of hepatic NaHCO3 secretion during acid-base changes. Secretion of 1 mol NaHCO3 was accompanied by an isotonic solution containing water and 0.25 mol NaCl. After secretin infusion, 14C-erythritol clearance increased in proportion to bile flow. Bicarbonate secretion is determined by a gradient limited H+-pump at the contraluminal cell. During secretin stimulation bile acid independent bile secretion is osmotically driven by bile NaHCO3 flux.

Acid-Base Equilibrium↗
PubMed1983

Role of sodium, bicarbonate, and plasma osmolality in biliary secretion.

To examine the effect of changes in biliary sodium and bicarbonate secretion on bile formation, experiments were performed on fasted, pentobarbital-anesthetized pigs. During continuous intravenous secretin infusion (2.7 CU X kg body wt-1 X h-1) sodium secretion was altered by increasing or reducing plasma sodium concentration. Bicarbonate secretion was altered by varying arterial plasma pH. At increased biliary sodium secretion, bile formation was depressed, but changes in bicarbonate secretion were accompanied by parallel alterations in bile formation. Bile acid secretion was increased during elevated plasma sodium concentration, whereas reduced plasma sodium concentration depressed bile acid secretion. To distinguish between the effect of changes in plasma osmolality and sodium concentration, bile formation was also studied during intravenous sucrose infusion at normal plasma sodium concentration. About 50% of the effect on bile formation of changing plasma sodium concentration is solely caused by the changes in plasma osmolality. During secretin stimulation bile formation is mainly determined by bicarbonate. Changes in plasma osmolality affect bile secretion through alterations in the net osmotic force across the hepatocellular membrane. Sodium has an impact on the bile-acid-dependent fraction, whereas bicarbonate is the mediator of the bile-acid-independent fraction of bile secretion.

Animals↗
PubMed1982

Abolished relationship between pancreatic HCO-3 secretion and arterial pH during carbonic anhydrase inhibition.

After acetazolamide administration, CO2 hydration in pancreatic cells would be slow and might become a rate-limiting factor to pancreatic HCO-3 secretion. Correspondingly, pancreatic HCO-3 secretion-normally pH dependent-would become slow and pH-independent. However, acetazolamide would not be expected to interfere with the capacity of the secretory mechanism to generate a proton potential gradient between pancreatic cells and interstitial fluid. These predictions were examined in 5 anesthetized, secretion infused (2.7 C. U./kg b.wt. h-1) pigs. Pancreatic juice was collected from a catheter in the pancreatic duct. Arterial pH was varied through i.v. HCl and NaHCO3 infusions and CO2 addition to inspired air. Before acetazolamide, HCO-3 secretion varied with plasma pH and averaged 298 +/- 30 mumol/min at control arterial pH. Acetazolamide (150 mg/kg, i.v.) reduced HCO3 secretion to 84 +/- 12 mumol/min and rendered secretion independent of arterial pH between pH 7.6 and pH 7.0. It is concluded that acetazolamide imposes a pH-independent transport maximum on pancreatic HCO-3 secretion, but does not reduce the capacity of the secretory mechanism to sustain a proton potential gradient between cells and interstitial fluid.

Acetazolamide↗
PubMed1982

Effect of intravenous infusion of hypertonic glucose solutions on pancreatic HCO3(-) secretion.

To examine why intravenous infusion of hypertonic non-electrolyte solutions inhibit pancreatic HCO3(-) secretion, the relationship between pancreatic HCO3(-) secretion and plasma pH was examined before and following intravenous infusion of hypertonic glucose to 5 anesthetized, secretin infused (2.7 C.U./kg b.wt.h-1) pigs. Hyperglycemia (plasma glucose 103 +/- 6 mmol/l) did not significantly change plasma pH, Na+, K+, Cl- and HCO3(-) concentrations. Hyperglycemia reduced pancreatic water flux by 48 +/- 5% and raised pancreatic juice HCO3(-) concentration by 43 +/- 4 mmol/l. Concurrently, HCO3(-) secretion fell by 34 +/- 5%. Acidosis, produced through intravenous HCl infusion and CO2 addition to inspired air, reduced HCO3(-) secretion by 40 +/- 6 mumol/min and 30 +/- 5 mumol/min per 0.1 pH unit reduction in plasma pH before and during hyperglycemia, respectively, and abolished HCO3(-) secretion at an estimated plasma pH of 6.51 +/- 0.06 before and a pH of 6.63 +/- 0.05 during hyperglycemia. We conclude that hypertonic glucose infusions inhibit pancreatic water flux and cause an increase in pancreatic juice HCO3(-) concentration which may inhibit HCO3(-) secretion through an effect on acid-base balance in secretory cells.

Acid-Base Equilibrium↗
PubMed1981

Filtered bicarbonate and plasma pH as determinants of renal bicarbonate reabsorption.

To examine if bicarbonate reabsorption varies with filtered bicarbonate and plasma pH, we infused anesthetized dogs i.v. with sodium chloride and sodium bicarbonate to alter plasma bicarbonate concentration (PHCO3) without changing hematocrit. Examinations in five dogs over a wide range of glomerular filtration rates (GFR) during ethacrynic acid infusion showed that bicarbonate reabsorption at equal filtered load and equal plasma pH of 7.5 was not significantly changed by increasing PHCO3 from 30.2 +/- 0.4 to 55.2 +/- 0.6 mM and PCO2 from 33.8 +/- 0.7 to 74.1 +/- 2.1 mm Hg. Examinations during respiratory and metabolic alkalosis in five dogs at plasma pH of 7.8 showed that bicarbonate reabsorption at equal filtered load was not significantly different at a PCO2 of 20.2 +/- 0.8 and 36.8 +/- 0.8 mm Hg. Finally, in five dogs that did not receive ethacrynic acid, plasma pH was lowered by inducing respiratory acidosis at a PHCO3 of 30 mM and raised during progressive respiratory and metabolic alkalosis, Bicarbonate reabsorption was linearly related to plasma pH within the range 7.1 to 7.85 (r = 0.92). By altering plasma pH by 0.1 unit, bicarbonate reabsorption was altered by 10 +/- 1%. Thus, filtered bicarbonate rather than GFR and plasma pH rather than PCO2 are important acute regulators of bicarbonate reabsorption. This regulation may be achieved by determining pH and bicarbonate concentration in the luminal fluid along the proximal tubules.

Alkalosis↗
PubMed1981

Mechanism of osmotic diuresis.

Mannitol might inhibit paracellular reabsorption of water and sodium chloride in the proximal tubules by reducing the osmotic driving force. We examined this hypothesis in anesthetized dogs. Bicarbonate reabsorption was kept constant by sodium bicarbonate infusion, and transcellular sodium chloride reabsorption was inhibited by ethacrynic acid. The glomerular filtration rate (GFR) was varied by altering renal perfusion pressure. Mannitol infusion reduced sodium chloride reabsorption from 62 +/- 5% to 33 +/- 5% of the filtered load. The calculated increase in reabsorbate osmolality, averaging 82 +/- 6 mOsm/kg H2O, was due to sodium bicarbonate and equalled the increase in plasma osmolality. Mannitol concentration averaged 81 +/- 7 mM in plasma and 101 +/- 12 mM in urine. A linear relationship between reabsorption and GFR (glomerulo-tubular balance) was maintained over the same range of GFR before and after mannitol infusion. Mannitol infusion reduced sodium chloride reabsorption from 2.6 to 1.4 moles for each mole of sodium bicarbonate reabsorbed. During mannitol infusion, acetazolamide inhibited sodium bicarbonate reabsorption as in control experiments, but reduced sodium chloride reabsorption less. We conclude that reduced water reabsorption increases sodium bicarbonate concentration in the paracellular fluid as much as mannitol concentration is raised in the plasma and glomerular filtrate. Along the proximal tubules, net osmotic force is progressively reduced as mannitol concentration rises, accounting for reduced water and sodium chloride reabsorption.

Acetazolamide↗
PubMed1981

Plasma Na+-iron concentration or pH as regulator of pancreatic HCO-3 secretion.

Pancreatic HCO-3 secretion is caused by proton flux from pancreatic cells to interstitial fluid which, hypothetically, may be derived by a Na-pump or a proton pump. A Na-pump would reabsorb protons from pancreatic duct in proportion with plasma Na+ concentration (PNa+). A proton pump would cause passive HCO-3 flux into pancreatic ducts that would vary with pancreatic jice HCO-3 concentration (CHCO-3). Because pancreatic ducts are water-permeable, CHCO-3 varies with plasma osmolarity. This phenomenon allows testing of the two hypotheses. Intravenous infusion of hypotonic salt solution to 5 anesthetized, secretin infused pigs (2.7 C.U./kg b. wt. H-1) lowered PNa+ by 20 +/- 2 mmol/l and CHCO-3 by 20 +/- 4 mmol/l and increased pancreatic HCO-3 secretion by 71 +/- 5 mumol/min. Intravenous infusion of hypertonic salt solutions to 5 other pigs raised PNa+ by 52 +/- 3 mmol/l and CHCO-3 by 54 +/- 3 mmol/l and reduced HCO-3 secretion by 86 +/0 26 mumol/min. Isotonic glucose infusion lowered PNa+ by 27 +/- 2 mmol/l and did not change CHCO-3 nor HCO-3 secretion rate in 5 pigs. These findings comply with the proton pump hypothesis and are at variance with the Na-pump hypothesis of pancreatic HCO-3 secretion.

Animals↗
PubMed1980

Renal bicarbonate reabsorption during bicarbonate loading.

To examine bicarbonate reabsorption at different GFR's, we varied the renal perfusion pressure in anesthetized dogs after inhibiting autoregulation by expanding extracellular volume and infusing ethacrynic acid. At a plasma bicarbonate concentration (PHCO3) of 28 +/- 1 mM, bicarbonate reabsorption varied in proportion to GFR (glomerulotubular balance). When PHCO3 was raised to 52 +/- 2 mM at constant PCO2 and hematocrit, bicarbonate reabsorption was reduced at all levels of filtered load. When plotted against GFR, different results were obtained dependent on the GFR level examined. At the control GFR,. bicarbonate loading reduced bicarbonate reabsorption by 30 +/- 5%. At a GFR level about 50% below the control GFR, bicarbonate loading increased reabsorption by about one third because the inhibitory effect of raising PHCO3 and extracellular pH was not sufficient to counteract the stimulatory effect of a higher filtered load. At intermediate levels of GFR, a rise in PHCO3 did not alter bicarbonate reabsorption. The finding that acetazolamide (30 mg/kg of body wt) at high PHCO3 failed to reduce bicarbonate reabsorption supports the hypothesis that the depressive effect of high extracellular pH on bicarbonate reabsorption may be attributed to reduced net tubular hydrogen ion secretion.

Absorption↗
PubMed1980

Relationship between plasma pH and pancreatic HCO3- secretion at different intravenous secretin infusion rates.

The relationship between pancreatic HCO3- secretion and plasma pH during acute systemic acid-base changes was investigated in 6 anesthetized, artificially ventilated pigs (20-25 kg) at 2 different, i.v. secretion infusion rates. At 0.45 C.U./kg b. wt. h-1 secretin infusion and plasma pH 7.40 +/- 0.01 pancreatic HCO3- secretion averaged 61+/- 12 mumol/min. Stepwise lowering of plasma pH through i.v. infusion of HCl and CO2 administration to inspired air proportionately reduced secretion rate; estimated zero HCO3- secretion occurring at plasma pH 7.01. Subsequent i.v. secretin infusion at 2.70 C.U./kg b. wt. h-1 increased HCO3- secretion to 249 +/- 42 mumol/min at plasma pH 7.33 + 0.04; stepwise lowering of plasma pH proportionately reduced HCO3- secretion to estimated zero at plasma pH 6.71. A reduction of plasma pH by 0.1 pH unit reduced HCO3- secretion during low and high rate of i.v. secretin infusion by 18 +/- 3 mumol/min and 35 +/- 8 mumol/min, respectively. Secretin infusion rate did not affect pancreatic chloride excretion. These findings support the view that secretin increases HCO3- secretion, and hence proton transport to the interstitial fluid, by augmenting the proton motive force developed by HCO3- secreting cells.

Animals↗
PubMed1980

Oxygen requirement of bicarbonate-dependent sodium reabsorption in the dog kidney.

The ratio between changes in sodium reabsorption and renal oxygen consumption (Na/O2) was measured in anesthetized dogs at high plasma bicarbonate concentration (32 +/- 1 mM); ethacrynic acid was infused continuously to prevent variations in transcellular NaCl reabsorption when sodium reabsorption was altered by varying plasma PCO2 and glomerular filtration rate (GFR). At high plasma PCO2 (110 mmHg) sodium reabsorption varied in proportion to GRF between 50 and 125% of control GFR (glomerulotubular balance). By reducing PCO2 to 20 mmHg, sodium reabsorption was reduced by 50-60% at constant GFR. The Na/O2 ratio was not significantly different during the two procedures and averaged 48 +/- 2. The ratio between changes in NaHCO3 reabsorption and oxygen consumption averaged 17 +/- 1, which is not significantly different from the Na/O2 ratio of Na-K-ATPase-dependent sodium transport. We propose that NaHCO3 is admitted to the cell by Na+/H+ exchange and that sodium is actively transported by Na-K-ATPase across the peritubular cell membrane; NaHCO3 provides the osmotic force for paracellular reabsorption of water and NaCl (bicarbonate-dependent reabsorption) without additional energy requirement.

Absorption↗