Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “EXCRETION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 793 records · Page 44Linked to original sources
PubMed1989

[Urinary calcium and phosphorus excretion and their relationship in calcium-containing urinary stone formers].

Calcium-containing upper urinary stone formers (group SF-A, n = 116) and normal controls (group Normals, n = 10) were examined for urinary calcium (Ca) and phosphorus (P) excretion (mg/mg creatinine) on usual diet, on Ca-restricted diet and in basal period. As a result, urinary Ca and P excretion decreased significantly both in group SF-A and in normal controls, as the dietary intake was reduced. As compared with normal controls, group SF-A exhibited significant elevation in urinary Ca excretion and showed a slight, though not significant increase, in urinary P excretion. A significant positive correlation between urinary Ca and P excretion was observed in either mode of diet in group SF-A, while no correlation was seen in normal controls. To examine the legitimacy of the result above obtained, another 40 Ca-containing upper urinary stone formers (group SF-B) were studied on usual diet. Thus, better correlation was obtained between urinary Ca and P excretion. In conclusion, urinary Ca and P excretion will be strongly influenced by their dietary intake. Stone formers excrete more Ca and P than normal controls. Finally, a tendency was noted that stone formers excreted the more Ca, the more P.

Adult↗
PubMed1999

Canalicular membrane transport is primarily responsible for the difference in hepatobiliary excretion of triethylmethylammonium and tributylmethylammonium in rats.

Two structurally similar quaternary ammonium compounds, triethylmethylammonium (TEMA, M(r) 116) and tributylmethylammonium (TBuMA, M(r) 200) were used as model compounds to identify the unit process of hepatobiliary excretion that is responsible for markedly different biliary excretion of organic cations (OCs). Cumulative biliary excretion (in percentage of dose; i.v., 12 micromol/kg) was 0.17 for TEMA and 34.5 for TBuMA. In vivo uptake clearance into the liver was 0.686 +/- 0.020 ml/min for TEMA and 0.421 +/- 0.028 ml/min for TBuMA. When the uptake clearance was examined in an isolated hepatocyte system, comparable clearance between TEMA and TBuMA was obtained, consistent with the in vivo result. These observations suggest that uptake into the liver is not the major determinant for the difference in biliary excretion of the OCs. Coadministration of colchicine, an inhibitor of microtubule formation, had no effect on biliary excretion of the model compounds, and the primary site of subcellular distribution of the OCs appears to be the cytosol, suggesting that intracellular movement does not play a major role in the markedly different biliary excretion of the OCs. In contrast, in vivo excretion clearance across the canalicular membrane for TBuMA was 180-fold greater than that for TEMA, and in vitro efflux clearance of TBuMA was smaller than that of TEMA (p <.01), indicative of involvement of these processes in the markedly different biliary excretion of the OCs. Therefore, these data indicate that canalicular transport is primarily responsible for the markedly different biliary excretion of TEMA and TBuMA.

Algorithms↗
PubMed1975

Biliary excretion of colchicine.

After intravenous administration of 3H-colchicine (0.2 mg/kg) to rats, 68 percent was excreted in the feces in 48 hours suggesting bile might be the major route of excretion for colchicine. Rats with cannulated bile ducts excreted 50 percent of a 2 mg/kg dose into the bile within 2 hours; half of this was colchicine, and the rest was desmethylcolchicine and more polar metabolites. Colchicine was excreted into the bile of the rat against a bile/plasma concentration gradient of 800 which resulted from a liver/plasma ratio of 15 and a bile/liver ratio of 60. The biliary excretion of colchicine varied widely among the hamster, dog and rabbit. Of the administered colchicine, 32, 20 and 16 percent were excreted by the hamster, dog and rabbit, respectively, within 2 hours. There was also a species difference in the percentage of the radioactivity present in bile as the parent drug. In the hamster, dog and rabbit, the percentage of radioactivity excreted into the bile as colchicine was 45, 34 and 72 percent, respectively. These species excreted colchicine into the bile against a bile/plasma gradient ranging from 19 to 870. Partition of these gradients between liver/plasma and bile/liver ratios demonstrated that both ratios were greater than one, suggesting that colchicine is excreted by an active process. The liver/bile gradient was always the larger of the two ratios.

Animals↗
PubMed2001

Clinical significance of the fractional excretion of anions in metabolic acidosis.

The fractional excretion of anions has been proposed as a new index for the differential diagnosis of metabolic acidosis, identifying the properties of the conjugate base by examining the renal handling of the anion. Here, we investigated clinical significance of the fractional excretion of anions in pathophysiologic diagnosis of metabolic acidosis by measuring urine ammonium (NH4+) excretion, the ratio of A plasma anion gap/delta plasma HCO3- concentration (deltaAG/deltaHCO3-), and fractional excretion of anions in three different groups of metabolic acidosis: acid overproduction (8 patients with lactic acidosis, 8 with diabetic ketoacidosis, 3 with hippuric acidosis following glue sniffing), acid underexcretion (10 patients with chronic renal failure) and normal controls (10 normal volunteers who underwent 3-day NH4Cl loading). As expected, urine NH4+ excretion was higher in overproduction acidosis than in acid-loaded normal controls (88.1 +/- 12.3 vs. 54.0 +/- 3.7 mmol/day, p < 0.05), and it was lower in chronic renal failure than in acid-loaded normal controls (12.8 +/- 1.7 vs. 54.0 +/- 3.7 mmol/day, p < 0.05). The fractional excretion of anions had no difference between overproduction acidosis and chronic renal failure (41.2 +/- 42.8% vs. 41.0 +/- 8.1%). However, the fractional excretion of anions showed significant differences between the subgroups in acid overproduction (lactic acidosis, 4.7 +/- 0.3%; diabetic ketoacidosis, 45.8 +/- 3.1%; hippuric acidosis, 126.0 +/- 14.4%; p < 0.05). The ratio of plasma deltaAG/deltaHCO3- also exhibited significant differences between the subgroups in acid overproduction (lactic acidosis, 1.5 +/- 0.1; diabetic ketoacidosis, 1.0 +/- 0.1; hippuric acidosis, 0.3 +/- 0.1; p < 0.05). There was an inverse linear correlation between the fractional excretion of anions and the ratio of plasma deltaAG/deltaHCO3- (r2 =-0.89, p < 0.05). In conclusion, determination of the fractional excretion of anions may provide a useful clue to the differential diagnosis of metabolic acidosis caused by acid overproduction.

Acidosis↗
PubMed1976

Significance of urinary excretion of fibrin degradation products during treatment of glomerulonephritis.

189 patients with various types of glomerular disease were studied. Creatinine clearance, protein excretion and urinary excretion of fibrin degradation products (FDPs) were measured before and at various intervals (up to 42 months) after starting treatment with indomethacin, alone or in combination with other drugs. The following observations were made: a. Patients with a urinary FDP in excess of 2 mg/24 hours before treatment had a significantly lower creatinine clearance and a significantly higher protein excretion than patients excreting less than 2 mg FDP/24 hours, indicating that FDP excretion reflects the severity of the renal disease. b. During treatment, the incidence of high FDP excretion decreases progressively, but remains high in patients who ultimately develop renal insufficiency. c. There is no correlation between the initial value of FDP excretion and the subsequent changes in creatinine clearance and proteinuria during treatment. This implies either that the initial FDP excretion has no prognostic value or, perhaps more likely, that disease activity is modified by treatment. d. The best correlation between FDP excretion and evolution is found in proliferative glomerulonephritis. There are reason to suppose that, in this group at least, the treatment influenced the evolution of the disease.

Creatinine↗
PubMedDate not supplied

[Local reference intervals for the excretion of creatinine in urine for an adult population].

OBJECTIVE: To present the height- and sex-specific reference intervals for the urinary excretion of creatinine in cuban subjects with ages between 19-58 years. BACKGROUND: The standards advanced by Bistrian (1985) for anglosaxon subjects have been traditionally used for the construction of the Index of Creatinine Excretion (ICE). This practice could lead to diagnostic errors in the case of ICE calculation for non-anglosaxon populations differing in dietetic behaviour and body composition. METHODS: Values of urinary excretion of Creatinine measured in 103 men and 112 women with ages between 19 and 58 years, and preserved nutritional wellbeing (weight within the interquartile range for height; 18.5 < or = body mass index < or = 30.0 kg/m2) and renal function (serum Creatinine < or = 132 mumol/l) were drawn retrospectively from the databases of the Section of Urinalysis, Service of Clinical Laboratory, "Hermanos Ameijeiras" Hospital (La Habana, Cuba). For each sex, the regression line urinary-Excrecion-of-Creatinine = c + d. height, where c, d: parameters dependent on the subject's height, were constructed. The predicted values of the urinary excretion of Creatinine for the cuban subjects were derived from the 100 (1-alpha)% prediction intervals (PI) of the regression line. RESULTS: The urinary excretion of Creatinine for a 170 cm-height, 66.5 kg-weight, cuban male with age between 19-58 years, was 1216.19 mg/24 hours (95% Pl: 821.02-1611.36 mg/24 hours). The urinary excretion of Creatinine for a 160 cm-height, 59.7k Kg-weight, cuban female with age between 19-58 years, was 852.00 mg/24 hours (95% Pl: 420.15-1283.84 mg/24 hours). After taking into account the subject's weight, the urinary excretion of Creatinine for the cuban subjects was lower than that of their anglosaxon counterparts. There was not correlation between the age of the subject and the urinary excretion of Creatinine. CONCLUSIONS: We recommend the use of the values of the urinary excretion of Creatinine tabulated in this article in the conduction of studies of body composition and nutritional assessment.

Adult↗
PubMed2004

Biliary excretion of irinotecan and its metabolites.

PURPOSE: The aim of this study was to investigate the excretion of irinotecan hydrochloride (CPT-11) and its metabolites into the gastrointestinal lumen via the biliary route after intravenous administration of lactone and carboxylate forms of CPT-11. METHODS: Biliary excretions of CPT-11 and its metabolites, SN-38 and SN-38-glucuronide, were investigated by an in vivo administration study using rats. The biliary excretion profiles for both the lactone and carboxylate forms of CPT-11 and its metabolites were determined. RESULTS: After the i.v. injection of the lactone form of CPT-11, the cumulative biliary excretion of SN-38-glucuronide was much greater than that of CPT-11 and SN-38, and biliary excretion of SN-38 was less than that of CPT-11. Further, CPT-11 and SN-38 were mainly excreted into bile as carboxylate forms. After the administration of the CPT-11 carboxylate form, biliary excretion of SN-38-glucuronide was significantly smaller than that after the administration of CPT-11 lactone form. On the other hand, biliary excretion of CPT-11 and SN-38 was greater after dosing with the CPT-11 carboxylate form than that after the CPT-11 lactone form. CONCLUSIONS: The results suggest that the rate of conversion of lactone to carboxylate forms of CPT-11 and its metabolites plays a major role in the biliary excretion of these compounds.

Animals↗
PubMed2004

Benzene exposure assessed by metabolite excretion in Estonian oil shale mineworkers: influence of glutathione s-transferase polymorphisms.

Measurement of urinary excretion of the benzene metabolites S-phenylmercapturic acid (S-PMA) and trans,trans-muconic acid (t,t-MA) has been proposed for assessing benzene exposure, in workplaces with relatively high benzene concentrations. Excretion of S-PMA and t,t-MA in underground workers at an oil shale mine were compared with the excretion in workers engaged in various production assignments above ground. In addition, possible modifying effects of genetic polymorphisms in glutathione S-transferases T1 (GSTT1), M1 (GSTM1), and P1 (GSTP1) on the excretion of S-PMA and t,t-MA were investigated. Fifty underground workers and 50 surface workers participated. Blood samples and three urine samples were collected from each worker: (a) a preshift sample collected the morning after a weekend, (b) a postshift sample 1 collected after the first shift, and (c) a postshift sample 2 collected after the last shift of the week. Personal benzene exposure was 114 +/- 35 mug/m(3) in surface workers (n = 15) and 190 +/- 50 mug/m(3) in underground workers (n = 15) in measurements made prior to the study. We found t,t-MA excretion to be significantly higher in underground workers after the end of shifts 1 and 2 compared with the corresponding surface workers. The same picture, although not significant, was seen for S-PMA excretion. Excretion of S-PMA and t,t-MA was found to increase significantly during the working week in underground workers but not in those employed on the surface. Both t,t-MA and S-PMA excretion were significantly higher in smokers compared with nonsmokers. Subjects carrying the GSTT1 wild-type excreted higher concentrations of S-PMA than subjects carrying the null genotype, suggesting that it is a key enzyme in the glutathione conjugation that leads to S-PMA. The results support the use of benzene metabolites as biomarkers for assessment of exposure at modest levels and warrant for further investigations of health risks of occupational benzene exposure in shale oil mines.

Acetylcysteine↗
PubMedDate not supplied

Peritoneal albumin excretion is a strong predictor of cardiovascular events in peritoneal dialysis patients: a prospective cohort study.

BACKGROUND: Microalbuminuria is a marker of systemic endothelial dysfunction. We hypothesize that peritoneal albumin excretion in peritoneal dialysis (PD) patients, which is conceptually analogous to microalbuminuria in non-uremic patients, can predict cardiovascular disease in new PD patients. METHOD: We studied peritoneal albumin excretion in 43 new PD patients. They were then followed prospectively for the development of cardiovascular events. All-cause mortality and duration of hospitalization for cardiovascular diseases were also recorded. RESULT: The average duration of follow-up was 26.5 +/- 17.6 months. During the follow-up period, 15 patients developed cardiovascular events. Event-free survival at 36 months was 81.4% and 53.6% for low (< 300 mg/L) and high (> 300 mg/L) peritoneal albumin excretion groups respectively (log rank test, p = 0.042). By Cox regression analysis, the only independent factors for event-free survival were diabetic status and peritoneal albumin excretion rate. For every 100 mg/L increase in peritoneal albumin excretion, the adjusted hazard ratio of developing a cardiovascular event was 1.83 [95% confidence interval (CI) 1.11 - 3.02, p = 0.018]. Actuarial patient survival at 36 months was 85.7% and 59.1% for low and high peritoneal albumin excretion groups respectively (log rank test, p = 0.10). After adjusting for the duration of follow-up for individual patients, the average duration of hospitalization was 9.1 +/- 16.2 and 21.7 +/- 25.7 days per year of follow-up for low and high peritoneal albumin excretion groups respectively (Mann-Whitney U test, p = 0.012). CONCLUSION: Although the sample size of our present study is small and does not have adequate statistical power, we conclude that peritoneal albumin excretion may be an important predictor of cardiovascular disease. Further studies are needed to examine the role of dialysate albumin excretion as a means of cardiovascular risk stratification in PD patients.

Adult↗
PubMed1991

[The mechanisms of exercise-induced proteinuria--relationship between urinary excretion of proteins and lactate after exhaustive exercise].

Exercise-induced proteinuria is of the mixed glomerular-tubular type and has been thought to be due to increased glomerular permeability to macromolecular proteins in response to activation of the renin-angiotensin system and catecholamines and a reduction in renal hemodynamics. The excretion of the tubular type of proteins, however, can't be explained by the above mechanism. Two groups, consisting of subjects with the highest (H-alb, n = 20) and the lowest (L-alb, n = 20) excretion of albumin 30 min after exhaustive exercise were selected from a total of 69 normal male participants. No differences in VO2max, maxHR, changes in plasma angiotensin II, catecholamines, urine volume, or Ccr following exercise were observed between the two groups. The increase in blood lactate concentration immediately after exercise, increases in urinary excretion of lactate, pyruvate, alpha 1 M, beta 2 M, albumin and decrease in Cl- excretion 30 min after exercise in the H-alb group were significantly greater than in the L-alb group. The greater the urinary excretion of lactate and pyruvate, the greater the excretion of albumin, alpha 1M and beta 2M, and the less the urinary excretion of Cl-. The coefficient of correlation between the urinary excretion of lactate and beta 2M was 0.757, and between urinary excretion of albumin and beta 2M, 0.756 (p less than 0.001). These results suggest that exercise-induced organic acids and/or decrease in renal circulatory pH caused by organic acids may alter renal glomerular permeability and inhibit renal tubular reabsorption of low molecular weight proteins (alpha 1M, beta 2M). The permeability of the glomerular basement membrane (GBM) to macromolecular proteins may be altered by a reduction in the charge barrier of the GBM, which may be caused by the over-production of organic acids and a lower pH.

Adult↗
PubMedDate not supplied

Effect of microsomal enzyme inducers on biliary and urinary excretion of acetaminophen metabolites in rats. Decreased hepatobiliary and increased hepatovascular transport of acetaminophen-glucuronide after microsomal enzyme induction.

Treatment of rats with phenobarbital (PB), 3-methylcholanthrene, and pregnenolone-16 alpha-carbonitrile increased the total (biliary plus urinary) excretion of thioether and glucuronic acid conjugates of acetaminophen (AA) without influencing AA-sulfate excretion, suggesting that these microsomal enzyme inducers enhance both cytochrome P-450-mediated toxication and UDP-glucuronosyltransferase-mediated detoxication of AA. However, induction with transstilbene oxide (TSO) did not increase the total excretion of AA-thioethers or AA-glucuronide and decreased AA-sulfate excretion. In addition, all inducers increased the ratio of AA metabolites excreted into urine over that excreted into bile. The extent of this shift from biliary to urinary excretion was dependent on both the AA metabolite and the inducer. The largest shift in the excretory route was seen with AA-glucuronide and induction with PB and TSO as inducers. Specifically, PB and TSO treatments decreased biliary excretion of AA-glucuronide by 70 and 89%, respectively, and increased its blood concentration up to 6- and 11-fold and urinary excretion 3- and 3.6-fold, respectively. Galactosamine depletes UDP-glucuronic acid from the liver only, thereby inhibiting hepatic but not extrahepatic glucuronidation. Galactosamine treatment prevented the PB-induced increase in AA-glucuronide in blood and urine. This suggests that the PB-induced increases in AA-glucuronide in blood and urine originated from the liver. Thus, microsomal enzyme inducers not only influence xenobiotic biotransformation, but may also after the contribution of the excretory routes (i.e. bile and urine) in the elimination of xenobiotic metabolites by changing the direction of hepatic transport.

Acetaminophen↗
PubMed1987

Factors affecting the urinary excretion of albumin in insulin-dependent diabetes.

To determine the specificity of the urine excretion of albumin as a measure of glomerular permeability in early insulin-dependent diabetic nephropathy, the effect of variable glomerular filtration and urine flow rates on albumin, beta 2-microglobulin excretion, and the fractional renal clearance of neutral dextran (Stokes Einstein Radius 24-46 A) was examined. Five insulin-dependent diabetic subjects with normal glomerular permeability (albumin excretion less than 30 micrograms/min) and one with elevated albumin excretion (195 micrograms/min) were studied pre and post strict glucose control with constant subcutaneous insulin infusion for 7 days. The albumin excretion in the 5 subjects never exceeded 30 micrograms/min during wide variations in glomerular filtration and urine flow rates. A positive correlation between beta 2-microglobulin excretion and urine flow (r = 0.81), and glomerular filtration (r = 0.77) rates was observed. In contrast, albumin excretion showed no correlation, indicating different factors affect the excretion rate of albumin and beta 2-microglobulin. Therefore, elevated albumin excretion (greater than 30 micrograms/min) in insulin-dependent diabetes is due to increased glomerular permeability and not changes in glomerular filtration and urine flow rates, and the albumin/ beta 2-microglobulin ratio may not be a valid indicator of changing glomerular permeability. The fractional neutral dextran clearances remained unchanged with variation in glomerular filtration and urine flow rates. The sieving curve was identical in all subjects for neutral dextran 40 A, the size of albumin, suggesting that reduced glomerular charge selectivity may contribute to increased albuminuria in progressive diabetic glomerulosclerosis.

Adult↗
PubMed1989

Effect of vitamin K deficiency on urinary gamma-carboxyglutamic acid excretion in rats.

Since gamma-carboxyglutamic acid (Gla) in Gla-containing proteins is stoichiometrically excreted into urine as free Gla, urinary Gla excretion is believed to reflect the rate of synthesis and degradation of vitamin K-dependent proteins and the utilization of vitamin K in body. We studied the daily changes in urinary Gla excretion and plasma vitamin K-dependent clotting factor levels in rats fed vitamin K-deficient diets followed by subcutaneous injection of vitamin K1 or after the oral administration of Warfarin. Urinary Gla excretion in normal rats fed a standard diet that contained about 500 ng of vitamin K1 per gram of diet was 2.35 +/- 0.25 mumoles/day, but the level in rats fed a markedly vitamin K-deficient diet (less than 5 ng/g) decreased to 1.40 +/- 0.14 mumoles/day. When rats were fed a moderately vitamin K-deficient diet (20-50 ng/g), plasma vitamin K-dependent clotting factor levels decreased significantly, but urinary Gla excretion did not decrease. Warfarin, a vitamin K antagonist, caused a significant decrease in urinary Gla excretion and plasma clotting factor levels. When vitamin K, (200 micrograms/kg) was injected subcutaneously in rats fed a markedly vitamin K-deficient diet, the plasma vitamin K-dependent clotting factor levels recovered quickly to normal, but urinary Gla excretion showed only a partial recovery to 1.74 +/- 0.15 mumoles/day. These results indicate that urinary Gla excretion decreases in vitamin K deficiency, but changes in urinary Gla excretion do not reflect vitamin K deficiency in rats as sensitively as changes in the prothrombin time and plasma K-dependent clotting factor levels.

1-Carboxyglutamic Acid↗
PubMed1988

Excretion of endogenous digoxin-like immunoreactive factors in human urine is a function of urine flow rate.

We studied the effect of varying water and salt intake on the renal excretion of endogenous digoxin-like immunoreactive factors (DLIF). DLIF were measured in human urine and serum by competitive displacement of 125I-labeled digoxin from anti-digoxin antibodies. Diuresis was selectively induced in normal healthy humans by acute water ingestion, and natriuresis was preferentially induced by acute saline ingestion. We found the amount of endogenous immunoreactivity excreted in urine to be correlated with urine flow rate but not with urinary sodium excretion. Urinary excretion of DLIF, normalized to creatinine, was 3.6-fold greater at a urine flow rate of 5.5 mL/min than at 0.5 mL/min. On the other hand, saline intake increased urine flow rate 1.9-fold and increased sodium excretion threefold, but did not affect urinary excretion of DLIF. Fractional excretion of DLIF was linearly related to fractional excretion of water. This study demonstrates that normalization of DLIF values to urinary creatinine does not make DLIF excretion independent of urine flow rate and underscores the need for information on urine flow rate when DLIF measurements in urine are being interpreted.

Blood Proteins↗
PubMed1988

Effect of cyclosporine on urinary kallikrein excretion in patients with rheumatoid arthritis.

The effect of cyclosporine (6 to 8 mg/kg/day) on urinary kallikrein excretion was examined in 10 patients with rheumatoid arthritis by using a radioimmunoassay for kallikrein, a product of renal tubular biosynthesis. All patients had baseline values of serum creatinine and blood urea nitrogen (BUN) within the normal range. The group had a mean baseline kallikrein excretion of 98.30 +/- 29.98 micrograms/24 hours (mean +/- SEM), and 3 and 6 months after therapy was initiated, kallikrein excretion was 44% and 46% of baseline, respectively (p less than 0.01). The five patients who had a normal mean baseline kallikrein excretion rate (106.60 +/- 15.21 micrograms/24 hr) excreted significantly less (p less than 0.05) kallikrein 3 and 6 months after therapy was initiated (56.60 +/- 3.98 micrograms/24 hr and 34.50 +/- 11.02 micrograms/24 hr, respectively), as did one patient with an elevated baseline kallikrein. All six of these individuals completed the protocol. In a subgroup of four patients with low baseline levels (28.25 +/- 5.06 micrograms/24 hr), two individuals experienced elevations of BUN such that cyclosporine was discontinued; in the two who completed the protocol, there was some further decrement in kallikrein excretion. Kallikrein excretion increased in all patients after a 3-month washout period. During a low-dose (3 mg/kg/day) open extension study that followed the initial trial, kallikrein excretion was determined monthly. Seven episodes in which kallikrein excretion decreased in six patients by 44% +/- 18% over a 1-month interval preceded any increase in serum creatinine by 1 to 4 months.(ABSTRACT TRUNCATED AT 250 WORDS)

Arthritis, Rheumatoid↗
PubMed1986

Influence of insulin on urinary eicosanoid excretion in rats with experimental diabetes mellitus.

Urinary prostaglandin (PG) and thromboxane (Tx) excretion, measured by radioimmunoassay, were examined in two groups of male Wistar rats made diabetic with streptozotocin, 70 mg/kg, one of which received daily insulin beginning on the 7th day after administration of streptozotocin. In addition, urinary kallikrein excretion and blood pressure were monitored. After the induction of diabetes the profile of urinary eicosanoid excretion was altered. 6-keto-PGF1 alpha and TxB2 excretion increased markedly within 24 to 48 hr and remained elevated for the duration of the study, up to 58 days. PGF2 alpha excretion also increased, the change being apparent after 6 days whereas PGE2 excretion was reduced at this time. Urinary kallikrein excretion was unchanged but blood pressure became elevated above control levels 2 weeks after the induction of diabetes. Insulin treatment, to maintain mean blood glucose levels below 200 mg/dl, resulted in decreased excretion of TxB2, PGF2 alpha and 6-keto-PGF1 alpha. However, excretion of PGE2 and kallikrein were increased after insulin treatment which also prevented the elevation in blood pressure. These studies indicate that insulin treatment of experimental diabetes corrects alterations in renal arachidonic acid metabolism and prevents the associated increase in blood pressure.

Animals↗
PubMed1986

Urinary excretion of nitrosodimethylamine and nitrosoproline in humans: interindividual and intraindividual differences and the effect of administered ascorbic acid and alpha-tocopherol.

Gas chromatography-high resolution mass spectrometry methods were developed for quantifying nitrosodimethylamine (NDMA) and nitrosoproline (NPRO) in human urine. The limits of quantitation of these methods, which utilize stable isotope analogues of NDMA and NPRO as internal standards, were 5 pg per ml for NDMA and 0.14 ng per ml for NPRO. The assays were used to quantify NDMA and NPRO in urine samples collected 4 times a wk for 5 wk from 24 healthy volunteers. The mean urinary excretion of NDMA during this time was found to be 38.2 ng per day, and the mean urinary excretion of NPRO was found to be 3.26 micrograms per day. Treatment of the volunteers with 600 mg of ascorbic acid and 100 IU of alpha-tocopherol 4 times a day for the final 3 wk of the study did not influence the urinary excretion of NDMA or NPRO. Considerable person-to-person and day-to-day variations were observed for the urinary excretion of both nitrosamines, but the urinary excretion of NDMA was not correlated with the urinary excretion of NPRO. Person-to-person and day-to-day differences in the urinary excretion were greater for NPRO than for NDMA. The mean urinary excretion of NDMA by the 24 subjects was as much as 5-fold higher on some days than on other days, but this was not observed for NPRO. Day-to-day differences in the mean urinary excretion of NDMA were correlated with the concentrations of nitrogen dioxide in the air.

Adult↗
PubMed1985

Relationship between urine flow rate and prostaglandin E excretion in human beings.

Although an increase in urine flow rate has been shown to augment urinary prostaglandin E (PGE) excretion, the relationship between these two variables has not been quantitated. Because we have previously shown that water immersion to the neck induces diuresis and augmentation of PGE excretion, we utilized water immersion to the neck to assess kinetically the relationship between changes in flow rate and PGE excretion. Fourteen normal male subjects were studied twice during 4 hours of water immersion to the neck, once after 11 hours of fluid deprivation and again during moderate hydration. PGE excretion as determined by radioreceptor assay was measured each hour. When subjects deprived of fluids underwent immersion to the neck, flow rate increased from 0.5 ml/min (control) to 1.5 ml/min, and PGE excretion rose from 1.4 to 2.6 ng/min (both p less than 0.01). In contrast, when subjects were studied during hydration, flow rate increased from 4.1 to 7.2 ml/min and PGE excretion increased from 8.1 to 13.0 ng/min at the same time intervals (both p less than 0.01). There was a significant positive correlation between flow rate and PGE excretion during both fluid deprivation and hydration. Were there an effect, independent of flow rate, of hydration on PGE, the slope of these two regression lines would differ. When the regression line slopes of these relationships were analyzed by the F test, there was a statistically significant (p less than 0.01) difference between the two regression coefficients. Our data suggest that, in addition to the previously characterized relationship between flow rate and PGE excretion, there is also a direct effect of hydration on PGE excretion.

Adult↗