scholarly journals The Metabolic Fate of Pentylenetetrazol in the Rat

1971 ◽  
Vol 49 (4) ◽  
pp. 356-365 ◽  
Author(s):  
G. K. W. Ko ◽  
E. A. Hosein
Keyword(s):  
Elemental Analysis ◽  
Intraperitoneal Injection ◽  
Mobile Phase ◽  
Phase Distribution ◽  
Liver Perfusion ◽  
Metabolic Fate ◽  
Isolated Rat Liver ◽  
Water Saturated ◽  
Sulfur Containing ◽  
Isolated Rat

Pentylenetetrazol administered to rats was metabolized to a derivative which was excreted in the urine along with unchanged pentylenetetrazol. Pentylenetetrazol and its metabolite can be separated on paper chromatograms developed in water-saturated isobutanol. The substances, however, are chromatographically inseparable with water as the mobile phase. Distribution of tritium-labelled pentylenetetrazol in the rat after intraperitoneal injection indicated that it was readily taken up by the liver. Perfusion of the isolated rat liver with citrated blood containing tritiated pentylenetetrazol demonstrated that the metabolite was formed in the intact liver. Formation of the metabolite was inhibited by SKF 525A. The metabolite was isolated from the urine of rats treated with pentylenetetrazol on an Amberlite XAD-2 column and elemental analysis showed it to be a sulfur-containing derivative.

scholarly journals The metabolism of dipotassium 2-hydroxy-5-nitrophenyl [35S]sulphate, a substrate for lysosomal arylsulphatases A and B

1967 ◽  
Vol 105 (3) ◽  
pp. 1003-1012 ◽  
Author(s):  
T. G. Flynn ◽  
K S Dodgson ◽  
G M Powell ◽  
F A Rose
Keyword(s):  
Bile Duct ◽  
Kidney Function ◽  
Intraperitoneal Injection ◽  
Chromogenic Substrate ◽  
Metabolic Fate ◽  
Isolated Rat Liver ◽  
Anaesthetized Rats ◽  
Free Ranging ◽  
Rat Livers ◽  
Isolated Rat

The metabolic fate of dipotassium 2-hydroxy-5-nitrophenyl [35S]sulphate ([35S]NCS), a chromogenic substrate for lysosomal arylsulphatases A and B, has been studied in rats. Intraperitoneal injection of [35S]NCS into free-ranging animals is followed by excretion of the bulk of the radioactivity in the urine within 24hr., less than 13% being eliminated as inorganic [35S]sulphate. Most of the urinary radioactivity can be accounted for as [35S]NCS, but small amounts of a labelled metabolite are also present. Experiments in which [35S]NCS was injected intravenously into anaesthetized rats with bile-duct and bladder cannulae confirm that the ester is rapidly excreted in the urine. However, small amounts of radioactivity appear in bile, mainly in the form of the metabolite detected in urine. When [35S]NCS is perfused through the isolated rat liver, about 35% of the dose is hydrolysed within 3hr. Similar results are obtained if [35S]NCS is injected into anaesthetized rats in which kidney function has been eliminated by ligature of the renal pedicles. The labelled metabolite has been isolated from bile obtained by perfusing several rat livers with blood containing a total of 100mg. of [35S]NCS. It has been identified as 2-β-glucuronosido-5-nitrophenyl [35S]sulphate. The implications of the various findings are discussed. The Appendix describes the preparation of [35S]NCS.

Uridine regulation by the isolated rat liver: perfusion with an artificial oxygen carrier

1982 ◽  
Vol 242 (5) ◽  
pp. R465-R470 ◽  
Author(s):  
A. Monks ◽  
R. L. Cysyk
Keyword(s):  
Rat Liver ◽  
Oxygen Carrier ◽  
Liver Perfusion ◽  
Blood Substitute ◽  
Rat Plasma ◽  
Perfusion Medium ◽  
Artificial Oxygen Carrier ◽  
Isolated Rat Liver ◽  
Rat Liver Perfusion ◽  
Isolated Rat

The isolated rat liver was used to investigate the role of the liver in the regulation of circulating uridine concentrations. A synthetic blood substitute (Fluosol-43) was utilized as an alternative oxygen-carrying perfusion medium to a simplified blood preparation and produced no apparent hepatotoxicity within the perfusion period. The isolated rat liver excreted uridine into a circulating perfusion medium achieving concentrations similar to those found in rat plasma (1.4 +/- 0.6 microM). The mean output of uridine over 2 h was 107 nmol.h-1.g liver-1, but if the perfusate was recirculated the net output of uridine was reduced to 12.7 nmol.h-1.g-1. The rate of depletion of nonphysiological concentrations of circulating uridine was found to be concentration dependent up to 25 microM. At a steady state of circulating uridine, a radioactive uridine spike was cleared with a half-life of 7.4 min and an elimination constant of 0.094 min-1; 30% of the radioactivity appeared in the perfusate as metabolites of uridine within 40 min. Thus the perfused rat liver acts to maintain circulating uridine concentrations similar to those measured in plasma.

The Protective Effects of Antioxidants and Propranolol on Hepatotoxicity of TCDD During Isolated Rat Liver Perfusion

2005 ◽  
Vol 1 (4) ◽  
pp. 336-341 ◽  
Author(s):  
M. Ghazi-Khan ◽  
M. Karami . ◽  
M. Rezayat . ◽  
M. Abdollahi . ◽  
B. Minaie . ◽  
...  
Keyword(s):  
Rat Liver ◽  
Liver Perfusion ◽  
Protective Effects ◽  
Isolated Rat Liver ◽  
Rat Liver Perfusion ◽  
Isolated Rat

EFFECTS OF INSULIN AND GLUCAGON ON PRODUCTION OF RENIN SUBSTRATE BY THE ISOLATED RAT LIVER

1980 ◽  
Vol 85 (1) ◽  
pp. 151-153 ◽  
Author(s):  
EIKI MURAKAMI ◽  
KUNIO HIWADA ◽  
TATSUO KOKUBU
Keyword(s):  
Normal Control ◽  
Rat Liver ◽  
Liver Perfusion ◽  
Perfusion System ◽  
Angiotensin I ◽  
Renin Substrate ◽  
Isolated Rat Liver ◽  
Rat Liver Perfusion ◽  
Isolated Rat

SUMMARY An isolated rat liver perfusion system was used to study the effects of insulin and glucagon on renin substrate production. Normal livers synthesized renin substrate at a rate of 28·3 ± 3·8 (s.e.m.) ng angiotensin I equiv./g liver each h (n = 8). The addition of insulin (more than 0·1 i.u.) to the perfusion significantly enhanced the production of renin substrate which was about twofold higher than normal control values (P< 0·001). However, glucagon (20 μg) did not affect the synthesis of renin substrate. These results indicated that insulin promoted the synthesis of renin substrate by the isolated rat liver.

Sign in / Sign up

Export Citation Format

Share Document