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T Buanes

Publications and source records attributed to T Buanes.

At least 73 records · Page 4Linked to original sources
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

Ultrastructure of pancreatic duct cells at secretory rest and during secretin-dependent NaHCO3 secretion.

The study was undertaken to identify possible ultrastructural changes occurring in pancreatic duct cells in relation to secretin-dependent NaHCO3 secretion, Pancreatic biopsies were obtained for examination, following in situ glutaraldehyde fixation from four groups of anaesthetized, young pigs. In the resting state, pancreatic duct cell cytoplasm was found to contain multiple vesicles of approximately 0.2 micron diameter. Elevation of systemic arterial PCO2 to 11.1 (10.6-11.6) kPa increased the number of vesicles per unit volume of resting cells by approximately 250%. During secretin-dependent NaHCO3 secretion, the duct cell cytoplasm was devoid of vesicles. Following cessation of secretin-dependent NaHCO3 secretion, cytoplasmic vesicles reappeared. The observed changes in the population of cytoplasmic vesicles in pancreatic duct cells may be causally related to the exocrine secretion of NaHCO3.

Animals↗
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↗
PubMed1987

DCCD (N,N'-dicyclohexylcarbodiimide) inhibits biliary secretion of HCO-3.

To study whether a proton pump is an integral part of the mechanism responsible for secretin-dependent biliary secretion of HCO-3 ions, the proton pump inhibitor N,N'-dicyclohexylcarbodiimide (DCCD) was systemically administered to six anesthetized, secretin-infused pigs. Because biliary HCO-3 secretion varies with arterial pH, secretion rate was measured at several different arterial pH values, before and after DCCD (25 mumol/kg). At arterial pH 7.45, bile flow was 2.1 (1.6-2.9) ml/min, and HCO-3 secretion was 224 (157-311) mumol/min. DCCD reduced bile flow and HCO-3 secretion by 30% and 40%, respectively, independent of arterial pH. In contrast, bile acid secretion, 46 (41-59) mumol/min, was not changed by DCCD. The hepatic adenosine triphosphatase (ATP) level, 2.0 (1.8-2.1) mumol/g wet tissue, was not changed by DCCD. DCCD (10(-4) mol/l) affected neither Na,K-ATPase nor carbonic anhydrase activities in separate in vitro assay systems. The reduction in biliary HCO-3 secretion induced by the proton pump inhibitor DCCD may indicate that a proton pump is integrated into the mechanism responsible for secretin-dependent biliary secretion of HCO-3.

Adenosine Triphosphate↗
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↗
PubMed1986

Histochemical localization of carbonic anhydrase in the pig's exocrine pancreas.

Carbonic anhydrase is essential for the pancreatic secretion of NaHCO3. To localize the distribution of carbonic anhydrase in the exocrine gland and, hence, identify the potential cellular source of secreted NaHCO3, histochemical staining of carbonic anhydrase was carried out on pancreatic biopsies obtained from six pigs at both supramaximal intravenous secretin stimulation and at secretory rest. Tissue staining, using Hansson's technique, revealed a strong staining both in membranes and cytoplasm in the duct cells and a weaker cytoplasmic staining in the acinar cells. Staining reaction was abolished by 10(-5) mol l-1 acetazolamide. Duct cells, accordingly, seem to be responsible for NaHCO3 secretion, while acinar cells appear unlikely to contribute substantially to NaHCO3 secretion.

Acetazolamide↗
PubMed1986

NN'-dicyclohexylcarbodiimide (DCCD) reduces pancreatic NaHCO3 secretion without changing pancreatic tissue ATP levels.

To study the mechanism responsible for pancreatic NaHCO3 secretion, the inhibitor NN'-dicyclohexylcarbodiimide (DCCD) was administered to six secretin-infused, anaesthetized pigs. Pancreatic juice was collected from a catheter in the main pancreatic duct. Secretion rate was measured at several arterial pH values in each animal, both before and after DCCD. 15 (14-30) mumol kg-1 body wt DCCD, intra-arterially, reduced pancreatic NaHCO3 secretion from 296 (234-398) to 181 (134-237) mumol min-1 at arterial pH 7.43 (7.42-7.47). Similar fractional reductions of secretion occurred at lower arterial pH. Pancreatic tissue ATP concentration, 1.8 (1.4-2.0) mumol g-1 wet wt, was not changed by DCCD. DCCD, less than or equal to 10(-4) mol l-1, did not change Na,K-ATPase nor carbonic anhydrase activities in separate in vitro assay systems. It is concluded that DCCD reduced pancreatic NaHCO3 secretion by a mechanism not involving ATP depletion nor inhibition of Na,K-ATPase nor carbonic anhydrase activities in pancreatic cells. Because DCCD inhibits proton pumps, DCCD may have reduced NaHCO3 secretion through interfering with a proton pump involved in extruding H+ from HCO-3 secreting cells to interstitial fluid in the pancreas.

Adenosine Triphosphate↗
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↗
PubMed1983

[Chylothorax].

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Adult↗