Effects of fasting on the diuretic response and disposition of furosemide in rats

1980 ◽  
Vol 58 (2) ◽  
pp. 205-211 ◽  
Author(s):  
Saroj K. Chakrabarti ◽  
Jules Brodeur
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Inhibitory Effect ◽  
Kidney Cortex ◽  
Control Mechanisms ◽  
Tissue Slices ◽  
Control Value ◽  
Renal Tubular Cells ◽  
Renal Tubular

The influence of fasting on the relationship between the disposition and diuretic effect of furosemide was studied in rats. Fasting consisted of withholding solid food, but not water, for a period of 16 h before administering furosemide (10 mg/kg, sc) or a saline vehicle. Normally fed animals also received furosemide or the vehicle. Fasting did not modify the diuretic or the natriuretic effect (per 100 g body weight) of furosemide. The distribution of total furosemide in plasma or tissues was not affected by fasting. On the other hand, fasting which produced increasing amounts of endogenous free fatty acids in plasma and kidneys increased the concentration of free furosemide in fasting plasma but not in fasting kidney or liver of rats. The in vitro binding constant of furosemide to physiological concentrations of plasma proteins was decreased from the control value by a factor of 6.5 as a result of fasting. Neither unchanged furosemide nor its metabolite in the urine was affected by fasting. Incubation of kidney cortex tissue slices with furosemide both in the presence and absence of free fatty acid indicated an inhibition of furosemide uptake in a manner closely parallel to inhibition by probenecid. Thus, failure to observe a more pronounced diuretic and saluretic effects of furosemide in fasted rats, in spite of higher concentration of free plasma furosemide, might be due to the inhibitory effect of endogenous free fatty acids and (or) other endogenous substances on the uptake of furosemide by renal tubular cells although some homeostatic control mechanisms related to fasting could also be involved.

Hexachlorocyclohexanes affect the arachidonic acid release from phosphatidylinositol but not from other phospholipid classes in tubular cell cultures

1995 ◽  
Vol 15 (4) ◽  
pp. 191-199 ◽  
Author(s):  
J. C. Puente-Fraga ◽  
P. López-Aparicio ◽  
S. Senar ◽  
M. N. Recio ◽  
M. A. Pérez-Albarsanz
Keyword(s):  
Fatty Acids ◽  
Phospholipase A2 ◽  
Free Fatty Acids ◽  
Arachidonic Acid Release ◽  
Phospholipase Activity ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Phospholipid Classes ◽  
Acid Release ◽  
Renal Tubular

Gamma- and delta-isomers of hexachlorocyclohexane caused marked decreases in the levels of radioactive phospholipids, and increases in the levels of [3H]arachidonate incorporated into free fatty acids in rat renal tubular cells. The increased radioactivity of free fatty acids arises from the decrease of [3H]arachidonate incorporated into phosphatidylinositol, but not into phosphatidylcholine, phosphatidylserine or phosphatidylethanolamine. This fact suggests that phosphatidylinositol can be broken down to the fatty acid from the sn-2 position and lysophospholipid by a phospholipase activity increased by hexachlorocyclohexanes. The observed specific toxicant action could be achieved in two ways: (a) operating upon a specific phospholipase A2 that acts on phosphatidylinositol, but not on other phospholipids as substrates and/or (b) involving substrate-phospholipase A2 interactions. Interestingly, the observed effect of the γ-isomer was more pronounced than that of the γ-one.

Free fatty acids and pancreatic function in the duck

1986 ◽  
Vol 112 (1) ◽  
pp. 100-104 ◽  
Author(s):  
R. Gross ◽  
P. Mialhe
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Inhibitory Effect ◽  
Feedback Mechanism ◽  
Pancreatic Function ◽  
Morphological Evidence ◽  
A Cell ◽  
Glucagon And Insulin

Abstract. The isolated perfused duck pancreas was used to study the effect of free fatty acids (FFA) on pancreatic function in vitro and to determine whether the FFA-glucagon negative feedback mechanism resulted from a direct inhibitory effect of FFA on the pancreatic A cell. Oleate, 2 mmol/l, increased the output rates of pancreatic somatostatin, glucagon and insulin. As there is poor morphological evidence in the duck for somatostatin to act as a paracrine intra-islet modulator, we reproduced in the pancreatico-duodenal artery, the rise in somatostatin level obtained in the pancreatic effluent after oleate. In these conditions the rises in glucagon and insulin secretions after oleate treatment were, respectively, reversed and suppressed, thereby reproducing observations previously made in vivo. Consequently, we may assume that the negative FFA-glucagon feedback mechanism that operates in vivo for physiological FFA variations does not result from a direct effect of FFA on the A cell, but may rather be mediated by an increase in pancreatic somatostatin secretion.

Investigation of the Thermal and Injury Behavior During Microwave Thermal Therapy of Porcine Kidney

2002 ◽  
Author(s):  
Xiaoming He ◽  
Shawn Mcgee ◽  
James E. Coad ◽  
Paul A. Iaizzo ◽  
David J. Swanlund ◽  
...  
Keyword(s):  
Thermal Model ◽  
Histological Study ◽  
Kidney Cortex ◽  
Cellular Injury ◽  
Bioheat Equation ◽  
Tissue Slices ◽  
Thermal Histories ◽  
Microwave Probe

In this paper, we report on the characterization of microwave therapy of normal porcine kidneys both in vitro and in vivo. This technology is being developed for eventual use in the treatment of small renal cell carcinoma (RCC) by minimally invasive procedures. During experiments, microwave energy was applied through an interstitial microwave probe (Urologix, Plymouth, MN) to the kidney cortex with occasional involvement of the kidney medulla. The thermal histories at several locations were recorded. After treatment, the kidneys were bisected and small tissue slices were cut out at approximately the same depth as the thermal probes. The tissue slices were further processed for histological study. Both cellular injury and the area of microvascular stasis were quantitatively evaluated by histology. Absolute rate kinetic models of cellular injury and vascular stasis were developed and fit to this data. A 3-D finite element thermal model based on the Pennes Bioheat equation was developed and solved using a commercial software package (ANSYS, V5.7). The Specific Absorption Rate (SAR) of the microwave probe was measured experimentally in tissue equivalent gel-like solution. The thermal model was first validated by the measured in vitro thermal histories. It was then used to determine the blood perfusion term in vivo.

scholarly journals Inhibitory effect of propafenone derivatives on pseudomonas aeruginosa biofilm and pyocyanin production

2020 ◽  
Vol 148 (3-4) ◽  
pp. 196-202
Author(s):  
Snjezana Petrovic ◽  
Jasmina Basic ◽  
Zoran Mandinic ◽  
Dragana Bozic ◽  
Marina Milenkovic ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Biofilm Formation ◽  
Laboratory Strain ◽  
Inhibitory Effect ◽  
Negative Control ◽  
Clinical Strains ◽  
Control Value ◽  
Essential Components ◽  
Pyocyanin Production

Introduction/Objective. Biofilm and pyocyanin production are essential components of Pseudomonas aeruginosa virulence and antibiotic resistance. Our objective was to examine inhibitory effect of synthetized propafenone derivatives 3-(2-Fluorophenyl)- 1-(2- (2-hydroxy-3-propylamino-propoxy)-phenyl)-propan-1-one hydrochloride (5OF) and3-(2- Trifluoromethyl-phenyl)-1-(2-(2-hydroxy-3-propylamino-propoxy)-phenyl)-propan-1-one hydrochloride (5CF3) on biofilm and pyocyanin in Pseudomonas aeruginosa clinical strains. Methods. Effects were tested on nine clinical isolates and one control laboratory strain of P. aeruginosa. In vitro analysis of biofilm growing was performed by incubating bacteria (0.5 McFarland) with 5OF and 5CF3 (500?31.2 ?g/ml) and measuring optical density (OD) at 570 nm. Bacteria in medium without compounds were positive control. Blank medium (an uninoculated medium without test compounds) was used as negative control. Pyocyanin production was estimated by OD at 520 nm, after bacteria incubated with 5CF3 and 5OF (250 and 500 ?g/ml), treated with chloroform, and chloroform layer mixed with HCl. Results. A total of 500 ?g/ml of 5OF and 5CF3 completely inhibited biofilm formation in 10/10 and 4/10 strains, respectively. A total of 250 ?g/ml of 5OF and 5CF3 strongly inhibited biofilm formation in 7/10 strains, while inhibition with 125 ?g/ml of 5OF and 5CF3 was moderate. Lower concentrations had almost no effect on biofilm production. Pyocyanin production was reduced to less than 40% of the control value in 6/9, and less than 50% of the control in 7/9 strains with 500 ?g/ml of 5OF and 5CF3, respectively. At 250 ?g/ml 5OF and 5CF3, most strains had pyocyanin production above 50% of the control value. Conclusion. Synthetized propafenone derivatives, 5OF and 5CF3, inhibited biofilms and pyocyanin production of Pseudomonas aeruginosa clinical strains. Presented results suggest that propafenone derivatives are potential lead-compounds for synthesis of novel antipseudomonal drugs.

Free fatty acids normalize a rosiglitazone-induced visfatin release

2006 ◽  
Vol 291 (5) ◽  
pp. E885-E890 ◽  
Author(s):  
Dominik G. Haider ◽  
Friedrich Mittermayer ◽  
Georg Schaller ◽  
Michaela Artwohl ◽  
Sabina M. Baumgartner-Parzer ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Term Treatment ◽  
Double Blind ◽  
Lipid Infusion ◽  
Major Mechanism ◽  
Insulin Mimetic ◽  
Long Term Treatment ◽  
Plasma Ffa

The detrimental effect of elevated free fatty acids (FFAs) on insulin sensitivity can be improved by thiazolidinediones (TZDs) in patients with type 2 diabetes mellitus. It is unknown whether this salutary action of TZD is associated with altered release of the insulin-mimetic adipocytokine visfatin. In this study, we investigated whether visfatin concentrations are altered by FFA and TZD treatment. In a randomized, double-blind, placebo-controlled, parallel-group study 16 healthy volunteers received an infusion of triglycerides/heparin to increase plasma FFA after 3 wk of treatment with rosiglitazone (8 mg/day, n = 8) or placebo ( n = 8), and circulating plasma visfatin was measured. As a corollary, human adipocytes were incubated with synthetic fatty acids and rosiglitazone to assess visfatin release in vitro. The results were that rosiglitazone treatment increased systemic plasma visfatin concentrations from 0.6 ± 0.1 to 1.7 ± 0.2 ng/ml ( P < 0.01). Lipid infusion caused a marked elevation of plasma FFA but had no effect on circulating visfatin in controls. In contrast, elevated visfatin concentrations in subjects receiving rosiglitazone were normalized by lipid infusion. In isolated adipocytes, visfatin was released into supernatant medium by acute addition and long-term treatment of rosiglitazone. This secretion was blocked by synthetic fatty acids and by inhibition of phosphatidylinositol 3-kinase or Akt. In conclusion, release of the insulin-mimetic visfatin may represent a major mechanism of metabolic TZD action. The presence of FFA antagonizes this action, which may have implications for visfatin bioactivity.

Lipid Labelling in Intact Chloroplasts from Exogenous Nucleotide Precursors

1981 ◽  
Vol 36 (1-2) ◽  
pp. 62-70 ◽  
Author(s):  
Margrit Bertrams ◽  
Käthe Wrage ◽  
Ernst Heinz
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
De Novo ◽  
Membrane System ◽  
Chloroplast Envelope ◽  
Label Free ◽  
Intact Chloroplasts ◽  
Time Required

Abstract De novo-synthesis of glycerolipids in chloroplasts is initiated by a stroma enzyme which catalyzes the formation of lyso-phosphatidic acid from glycerophosphate and acyl-CoA. When these substrates are added to isolated, intact chloroplasts, only glycerophosphate can readily pass through the chloroplast envelope which represents a permeation barrier for acyl-CoA, although higher thioester concentrations destroy this membrane system. At low concentrations of acyl-CoA, which do not impair the envelope, intact chloroplasts metabolize exogenous acyl-CoA in two ways to give free fatty acids and labelled phosphatidyl choline. This indicates that the envelope thioesterase can use exogenous substrates. Isolated, intact chloroplasts fixing radioactive CO2 label free fatty acids and acylglycerols but not galactolipids, since they cannot convert 3-phosphoglycerate into UDP-galactose which in vivo is supplied by the cytoplasm. This cooperation was simulated in vitro by adding all enzymes and cofactors necessary for conversion of 3-phosphoglycerate into UDP-galactose to intact chloro­plasts which then formed labelled monogalactosyl diacylglycerol from labelled CO2. The time required to transfer envelope-made galactolipids from the envelope into thylakoids was studied by incubating intact chloroplasts with radioactive UDP-galactose, subsequent osmotic disruption of organelles with concomitant enzymatic degradation of UDP-galactose followed by separation of envelopes and thylakoids. Only after short times (< 1min) appreciable proportions 920-30%) of radioactive galactolipid export from envelopes into thylakoids.

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