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At least 595 records · Page 33Linked to original sources
PubMed1992

The relationship between biliary secretion of bilirubin and glutathione in the rat.

The relationship between biliary secretion of bilirubin and glutathione was investigated by infusing bilirubin solution (200 nmol/min/100 g body wt) into Sprague-Dawley rats and measuring bilirubin and glutathione in the bile. Hepatic glutathione level, when modified between the range of 1-10 mumols/g liver wt, did not affect biliary maximal secretory rate (Tm) of bilirubin (80 nmol/min/100 g body wt). However, when biliary secretion of bilirubin exceeded 10 mM or 30 nmol/min/100 g body wt, biliary secretion of glutathione was markedly impaired while the bile flow remained relatively constant. Thus, bilirubin impaired the biliary secretion of glutathione selectively compared to its effect on bile formation. The results indicate that the mechanisms of biliary secretion of the two physiological substances, bilirubin and glutathione, are closely related.

Animals↗
PubMed1988

Effect of atropine on feedback regulation of pancreatic enzyme secretion in rats.

The effect of atropine on the feedback regulatory mechanism of pancreatic enzyme secretion exerted by intraluminal trypsin was investigated in conscious rats. Intravenous atropine infusion (50 micrograms/kg/h) suppressed pancreatic enzyme secretion to the same extent in both the presence and the absence of pancreatic juice in the intestine. However, with or without atropine infusion, pancreatic secretory rate was higher throughout diversion of pancreatic juice than during intraduodenal return of the juice. Atropine also inhibited the stimulatory response to intraduodenal trypsin inhibitor and intravenous caerulein. The atropine-induced inhibitory effect was not significantly different between the two experimental conditions. Regardless of atropine administration, both trypsin inhibitor and caerulein caused a significant increase in pancreatic secretion. The results suggest that cholinergic mechanisms have little influence on the feedback regulation. Cholinergic mechanisms may play an important role in maintaining the physiologically basal secretion because the basal secretion is atropine-sensitive.

Amylases↗
PubMed1996

Effects of sub-chronic exposure to SO2 on lipid and carbohydrate metabolism in rats.

Sulfur dioxide (SO2) is a ubiquitous air pollutant, present in low concentrations in the urban air, and in higher concentrations in the working environment. While toxicological reports on SO2 have extensively dealt with the pulmonary system, essentially no data are available on the effects of chronic exposure to this pollutant on intermediary metabolism, although some biochemical changes in lipid metabolism have been detected. The present investigation was aimed at evaluating the effects of sub-chronic exposure to SO2 on concentrations of serum lipids/lipoproteins and on glucose metabolism, in animal models of hypercholesterolemia and diabetes. A specially designed control-inert atmosphere chamber was used, where male Sprague-Dawley rats fed on either standard or cholesterol enriched (HC) diets, as well as streptozotocin diabetics, were exposed to SO2 at 5 and 10 ppm, 24 h per day for 14 days. In rats, both on a standard diet and on a HC regimen, SO2 exposure determined a significant dose-dependent increase in plasma triglycerides, up to +363% in the 10 ppm HC exposed animals. This same gas concentration significantly reduced HDL cholesterol levels. In contrast, exposure of diabetic animals to 10 ppm SO2 resulted in a fall (-41%) of plasma and liver triglycerides and in a concomitant increase (+62%) of plasma HDL cholesterol. This discrepancy could apparently be related to diverging effects of SO2 exposure on plasma insulin levels in the different animal groups. Kinetic analyses of triglyceride synthesis carried out in rats on a standard diet revealed, in exposed animals, a significant reduction in the secretory rate, in spite of the concomitant hypertriglyceridemia. These findings suggest that SO2 exposure can markedly modify major lipid and glycemic indices, also indicating a differential response in normo/hyperlipidemic versus diabetic animals.

Animals↗
PubMed1996

A mathematical model of the pancreatic ductal epithelium.

A mathematical model of the HCO-3-secreting pancreatic ductal epithelium was developed using network thermodynamics. With a minimal set of assumptions, the model accurately reproduced the experimentally measured membrane potentials, voltage divider ratio, transepithelial resistance and short-circuit current of nonstimulated ducts that were microperfused and bathed with a CO2/HCO-3-free, HEPES-buffered solution, and also the intracellular pH of duct cells bathed in a CO2/HCO-3-buffered solution. The model also accurately simulated: (i) the effect of step changes in basolateral K+ concentration, and the effect of K+ channel blockers on basolateral membrane potential; (ii) the intracellular acidification caused by a Na+-free extracellular solution and the effect of amiloride on this acidification; and (iii) the intracellular alkalinization caused by a Cl--free extracellular solution and the effect of DIDS on this alkalinization. In addition, the model predicted that the luminal Cl- conductance plays a key role in controlling both the HCO-3 secretory rate and intracellular pH during HCO-3 secretion. We believe that the model will be helpful in the analysis of experimental data and improve our understanding of HCO-3-transporting mechanisms in pancreatic duct cells.

Animals↗
PubMed2000

Control of salt gland activity in the hatchling green sea turtle, Chelonia mydas.

We studied the control of salt gland secretion in hatchling Chelonia mydas. The threshold salt load to activate salt secretion was between 400 mumol NaCl 100 g bodymass (BM)-1 and 600 mumol NaCl 100 g BM-1, which caused an increase in plasma sodium concentration of 13% to 19%. Following a salt load of 2700 mumol NaCl 100 g BM-1, salt gland secretion commenced in 12 +/- 1.3 min and reached maximal secretory concentration within 2-7 min. Maximal secretory rate of a single gland averaged 415 mumol Na 100 g BM-1 h-1. Plasma sodium concentration and total osmotic concentration after salt loading were significantly higher than pretreatment values within 2 min. Adrenalin (25 micrograms kg BM-1) and the cholinergic agonist methacholine (1 mg kg BM-1) inhibited salt gland activity. Atropine (10 mg kg BM-1) reversed methacholine inhibition and stimulated salt gland secretion when administered with a subthreshold salt load. Arginine vasotocin produced a transient reduction in sodium secretion by the active gland, while atrial natriuretic factor, vasoactive intestinal peptide and neuropeptide Y had no measurable effect on any aspect of salt gland secretion. Our results demonstrated that secretion of the salt gland in C. mydas can be modified by neural and hormonal chemicals in vivo and that the cholinergic and adrenergic stimulation of an exocrine gland do not appear to have the typical, antagonist actions on the chelonian salt gland.

Animals↗
PubMed1986

Characterization of the in vivo and in vitro inhibition of gastrin secretion from gastrinoma by a somatostatin analogue (SMS 201-995).

Earlier experiments characterized the effect of SMS 201-995 on gastrin secretion from gastrinoma in vivo. The results showed that the somatostatin analogue inhibits basal as well as secretin- and calcium-stimulated gastrin secretion. The current study examined the effect of SMS 201-995 on gastrin secretion from gastrinoma in vitro. Gastrinoma cells were prepared in cell culture or acute cell dispersion to study basal gastrin release. In cell culture, SMS 201-995 at 10(-9) M, 10(-8) M, and 10(-7) M significantly stimulated gastrin secretion (basal medium gastrin, 157 +/- 7.9 pg/ml; with SMS 201-995 10(-9) M, 786 +/- 62 pg/ml; with SMS 201-995 10(-8) M, 569 +/- 72 pg/ml; and with SMS 201-995 10(-7) M, 258 +/- 26 pg/ml). In contrast, in acute cell dispersion, the somatostatin analogue inhibited gastrin secretion (basal medium gastrin, 12.8 +/- 1.3 ng/ml; with SMS 201-995 10(-9) M, 9.0 +/- 0.1 ng/ml; with SMS 201-995 10(-8) M, 8.4 +/- 1.5 ng/ml; and with SMS 201-995 10(-7) M, 7.9 +/- 0.2 ng/ml). Gastrinoma cells were prepared in cell culture to study the effect of SMS 201-995 on gastrin secretion stimulated by secretin and by post-receptor increases in adenosine cyclic nucleotide. The somatostatin analogue inhibited gastrin secretion stimulated by secretin (10(-6) M) (797 +/- 48 pg/ml for secretin alone, compared with 396 +/- 9.4 pg/ml for secretin plus SMS 201-995). SMS 201-995 did not inhibit gastrin secretion stimulated by dibutyryl cyclic AMP (10(-7) M) (617 +/- 62 pg/ml for dibutyryl cyclic AMP alone, compared with 778 +/- 55 pg/ml for the two together). In vitro, SMS 201-995 inhibits basal gastrin secretion from gastrinoma prepared in acute cell dispersion, but not gastrinoma in cell culture, probably due to differences in basal secretory rates. The effect in vitro is less than that in vivo. SMS 201-995 does not inhibit postreceptor increases in adenosine nucleotide. This indirectly supports the hypothesis that SMS 201-995 acts in gastrinoma cells to inhibit gastrin secretion by inhibition of adenylate cyclase activity.

Adult↗
PubMed1978

Short circuit current in tight and leaky epithelia.

The effect of short circuit current on the unidirectional fluxes of ions transported across tight and leaky epithelia was investigated. It was found that short circuiting of the frog gastric mucosa (classified as a tight epithelium) caused a decease of the passive JClms and a significant increase of the net Cl- secretion. However, no significant change of H+ secretory rate was observed. On the other hand, short circuiting of the mouse intestine (a known leaky membrane) caused a simultaneous increase of both Jms and Jsm fluxes of Na+ while the net fluxes of Na+ and Cl- remained unchanged. Also, short circuiting did not change the water permeability of the mouse intestine. To explain some of these results a theoretical model is presented to demonstrate that while short circuiting can block the passive ionic movement, it will cause an increase in the energy consumption of the system and introduce certain important changes in the ionic barriers and e.m.fs. The simultaneous increase in the unidirectional fluxes of Na+ under short circuit conditions can best be explained by a decrease in the polarized nature of the transepithelial shunt, thereby increasing the diffusion coefficient of the ion(s). Such an increase is specially favorable to the Na+ rather than an anion.

Animals↗
PubMed1987

Secretion of alpha-tocopherol from cultured rat hepatocytes.

Primary cultures of rat hepatocytes and rat liver perfusions were used to study hepatic secretion of alpha-tocopherol. The secretion of alpha-tocopherol from hepatocytes in culture was linear with time for 4 h. Ultracentrifugation of the medium revealed that 89.4 +/- 2.1% of alpha-tocopherol secreted during 4 h incubation was associated with the very-low density lipoprotein fraction (VLDL, d less than 1.006 g/ml). Oleic acid had no significant effect on the secretory rate of alpha-tocopherol, whereas eicosapentaenoic acid reduced the amount of alpha-tocopherol secreted to 48.4 +/- 12.7% of the control value after 20 h incubation (P less than 0.01). Monensin, a known inhibitor of VLDL secretion, reduced the secretion of alpha-tocopherol to 14.1 +/- 4.3% of the control value (P less than 0.02). Colchicine and chloroquine inhibited the secretion of alpha-tocopherol in the same order of magnitude as monensin. Hepatic perfusion after intravenous injection of in vivo labeled alpha-[3H]tocopherol lymph, showed that about 75% of the secreted radioactivity was in the VLDL fraction. From these results we conclude that most alpha-tocopherol is secreted from the liver associated with nascent VLDL in rats.

Animals↗
PubMed1989

Stimulation of surfactant secretion by vasopressin in primary cultures of adult rat type II pneumocytes.

The current study examined the effect of vasopressin on the secretion of phosphatidylcholine, the principal component of pulmonary surfactant, from adult rat alveolar type II pneumocytes in primary culture. Vasopressin stimulated secretion in a time- and dose-dependent manner. At a concentration of 10 nM, vasopressin stimulated release by 6-fold over the basal secretory rate. The concentration producing half the maximal response for vasopressin-induced secretion was 0.4 nM. The stimulation of phosphatidylcholine release by vasopressin was duplicated by the vasopressin fragment, amino acids 4 through 9. [Lys8]vasopressin and the selective vasopressin-2 agonist [deamino-8-D-Arg]vasopressin did not stimulate surfactant secretion effectively. The vasopressin- and fragment-induced secretion was inhibited by the vasopressin-1 receptor antagonist d(CH2)5TDAVP and the protein kinase C inhibitor, tetracaine, but not by the beta-adrenergic antagonist alprenolol. Vasopressin did not activate adenylate cyclase, which suggests that stimulation by vasopressin was independent of cyclic AMP. When vasopressin and isoproterenol were added concomitantly, the effects on phosphatidylcholine secretion were additive. This suggests that these two secretagogues operate via separate mechanisms.

Adenylyl Cyclases↗
PubMed1995

Effect of Escherichia coli lipopolysaccharide on surfactant secretion in primary cultures of rat type II pneumocytes.

The purpose of this study is to evaluate the effect of the Escherichia coli lipopolysaccharide on the secretion of phosphatidylcholine, the principal component of pulmonary surfactant, in primary cultures of rat alveolar type II pneumocytes. Lipopolysaccharide stimulated phosphatidylcholine secretion in a time- and dose-dependent manner. At a concentration of 200 micrograms/ml, lipopolysaccharide stimulated the release of phosphatidylcholine 4-fold over the basal secretory rate, and the concentration producing half the maximal response was 20 micrograms/ml. The stimulatory effect of lipopolysaccharide on phosphatidylcholine secretion was additive to that of the protein kinase C activator TPA, which is a potent stimulator of surfactant secretion. Lipopolysaccharide did not activate protein kinase C, which suggests that stimulation of phosphatidylcholine secretion by the endotoxin was through a mechanism independent of protein kinase C activation.

Animals↗
PubMed1996

The pattern of apolipoprotein B100 containing lipoprotein subclasses produced by the isolated visceral rat yolk sac depends on developmental stage and fatty acid availability.

Explants of visceral rat yolk sacs from gestational days 16, 18 and 22 were used for studying developmental changes of secretion and density distribution of lipoproteins, particularly of those containing apoB. Moreover, the influence of fatty acid supply on the amount and density distribution of secreted apolipoproteins was studied on day 18 of gestation. Active lipoprotein production was observed in yolk sacs taken on days 16 and 18 of gestation. It declined considerably on day 22 of gestation in parallel with the production of total protein, triacylglycerols and cholesterol. On all gestational days, apoB floated mainly in the LDL range ( > or = 70%) with differences in the distribution pattern of LDL subclasses. The lowest density of secreted LDL was found on day 18 of gestation (peak at d = 1.025 g/ml) followed by day 16 (peak at d = 1.035 g/ml) and day 22 of gestation (peak at d = 1.045 g/ml). ApoAIV, apoE and apoAI floated exclusively in the HDL range with a peak at d = 1.089 g/ml independently of the gestational day. After incubation of yolk sacs from the 18th day of gestation with 0.4 mM or 0.8 mM oleate, the density of secreted apoB containing particles was decreased (peaks in the VLDL and IDL density range), whereas palmitate in the same concentrations caused a redistribution of secreted apoB toward higher densities (peaks at d > or = 1.032 g/ml). Taken together, the data provide evidence that the density of LDL subclasses produced by isolated yolk sacs between days 16 and 22 of gestation depended on the gestational stage. Moreover, addition of unsaturated or saturated fatty acids to the organ culture differently affected the secretory rate and the density of lipoproteins delivered by yolk sacs on day 18 of gestation.

Animals↗
PubMed1986

Defective bile acid transport in an animal model of defective debrisoquine hydroxylation.

Bile acid transport in female DA (dark Aguti) rats, a model for debrisoquine hydroxylation deficiency in man, was investigated. Compared to hydroxylation competent male DA and Sprague-Dawley rats of either sex, the female DA rat had a significantly lower taurocholate maximal secretory rate in vivo. Studies in the perfused liver showed this to be due to a decreased extraction efficiency during exogenous taurocholate loading. To characterize further the defect, taurocholate uptake velocity into isolated hepatocytes was studied. This showed a decreased maximal uptake velocity in the female DA rat (P less than 0.02). Whether this defect in bile acid uptake is related to the defective debrisoquine hydroxylation, remains to be established.

Animals↗
PubMed1988

The effect of methimazole on bile flow and bile acid secretion in the rat.

The effect of methimazole on bile flow and composition was studied in male Wistar rats. Administration of methimazole as a single bolus (175-700 mumol/kg body wt) or infusion over three hours (1 mumol/100 g body wt/min) significantly increased bile flow and the biliary output of bile acids and inorganic electrolytes. Choleresis was a transient phenomenon and at the end of the experiments bile flow had returned to control values, although bile acid output was significantly lowered. When the amounts of bile acids arriving into the liver were increased by taurocholate infusion or decreased by cholestyramine pretreatment, a transitory enhancement was also found in bile flow and bile acid output, but the amounts of bile acid secreted and the choleretic effect induced were different according to the bile acid secretory rate found before methimazole administration. The bile acid content in the liver of taurocholate-infused rats was reduced during methimazole-induced choleresis. Our data indicate that the higher bile flow in methimazole-treated rats is related to an enhanced biliary secretion of bile acids probably due to a transitory stimulating effect on the transport into bile of the intrahepatocytary bile acid pool. The choleretic effect is not apparently shared by other thiocarbamide compounds.

Animals↗
PubMed1988

Hepatic transport of bile acids in the isolated perfused rat liver. Structure-kinetic relationship.

We studied the transport kinetics of a series of bile acids from blood to bile in the isolated perfused rat liver in order to define better the relationship between chemical structure of bile acid molecules and efficiency of the overall hepatic transport process. BA studied were taurocholate (TC), glycocholate (GC), cholate (C), tauroursodeoxycholate (TUDC), ursodeoxycholate (UDC) and hyodeoxycholate (HDC). Estimates of intrinsic hepatic clearance (Cl(int)), maximal secretory rate (Vmax) were provided from the analysis of the relationship between bile acid removal rates and sinusoidal concentration under steady-state conditions. TC and TUDC had the highest Cl(int) (about 5 ml/min/g liver) and Vmax (about 800 nmol/min/g liver) followed in order by GC (1.71 ml/min/g liver; 442 nmol/min/g liver); C (1.25 ml/min/g liver; 252 nmol/min/g liver); HDC (0.86 ml/min/g liver; 238 nmol/min/g liver); UDC (0.72 ml/min/g liver; 176 nmol/min/g liver). The findings suggest that the efficiency of the overall hepatic transport of bile acids is highly dependent on their molecular structure and that conjugation has a more important effect on both Cl(int) and Vmax that the number or position of hydroxyl groups.

Animals↗
PubMed1979

Interpretive reporting of laboratory data. Gastric analysis.

The reporting of gastric analysis data requires clearly formatted and documented analytic results, accurately calculated secretory rates, appropriate normal values based on age, sex and weight of the patient, and interpretive review of the data based on well-documented personal experience or comprehensive studies reported in the medical literature. We report here a technique using inexpensive and flexible data processing equipment suitable to most community hospital laboratories.

Clinical Laboratory Techniques↗
PubMed1989

Effects of endothelin on renal function and renin secretion in anesthetized rats.

The infusion of endothelin into the renal artery of anesthetized rats at 1 ng/kg per min, a dose with no influence on renal function, had no effect on the basal levels of plasma renin activity (PRA) and renin secretory rate (RSR), but significantly inhibited the isoproterenol-induced increases in PRA and RSR. Endothelin, 2 ng/kg per min, elicited significant decreases in renal hemodynamics and in urine formation but the mean arterial pressure was not affected. The possibility that endothelin may participate in controlling renal function and renin secretion in vivo warrants further attention.

Anesthesia↗