Increment In Excretion Research Articles

Yield of microbial protein in sheep fed diets differing in protein degradability

Modern protein systems for ruminants require estimates of microbial protein yield relative to the amount of energy fermented in the rumen. In the Metabolizable Protein (MP) System (Webster 1992) this is expressed by the ratio of microbial nitrogen to fermented metabolizable energy (MiN:FME). However uncertainty as to the estimation of MiN yield both in absolute terms and relative to rumen degradable N (RDN) generates further uncertainty as to the efficiency of capture of quickly and slowly degraded N (QDN and SDN). Moreover the MP system assumes no capacity to recapture recycled undegraded N (UDN). This experiment measures increments in excretion of purine derivatives by sheep to explore the effects of varying relative and absolute supply of QDN, SDN and UDN on relationships between FME utilisation and yield of microbial N from the rumen.

8-Epi PGF2 alpha: specific analysis of an isoeicosanoid as an index of oxidant stress in vivo.

1. Excessive free radical generation is thought to contribute to tissue injury in a broad spectrum of diseases. A particular constraint in addressing this hypothesis has been the inability to assess free radical generation in vivo and the lack of information on drugs or vitamins which act as effective antioxidants in vivo. 2. Traditional approaches have relied upon measures of substrate oxidizability or spin trapping of free radical adducts ex vivo. It is unknown how these measurements might relate, in a quantitative fashion, to the generation of reactive oxygen species in vivo. Isoeicosanoids are free radical catalyzed products of arachidonic acid. One of these compounds, 8-epi prostaglandin F2 alpha (8-epi PGF2 alpha) exhibits biological activity and may function as an autacoid. Specific analysis of this 8-epi PGF2 alpha isomer indicates that it is elevated in certain syndromes thought to be associated with oxidant stress. These include vascular reperfusion, paracetamol poisoning and liver cirrhosis. Apparently healthy individuals who smoke cigarettes or consume alcohol exhibit dose dependent increments in excretion of 8-epi PGF2 alpha. Excretion is depressed by antioxidant vitamins, although not by the nonspecific cyclooxygenase (COX) inhibitor, aspirin, even though 8-epi PGF2 alpha may be formed by either COX-1 or COX-2. 3. Specific analysis of this and other isoeicosanoids may afford an opportunity to evaluate the effects of antioxidant interventions in human diseases characterized by excessive lipid peroxidation in vivo.

Increased formation and degradation of malondialdehyde-modified proteins under conditions of peroxidative stress.

The effect of increased in vivo lipid peroxidation on excretion of the main urinary metabolites of malondialdehyde (MDA) was investigated. peroxidative stress in the form of vitamin E deficiency or the administration of iron nitrilotriacetate or carbon tetrachloride was imposed on rats fed an MDA-free diet. Significant increases were observed in excretion of the lysine-MDA adduct epsilon-propenal lysine, its N-acetyl ester, and free MDA. Under the conditions imposed, the increments in excretion of the lysine adducts reflect increased peroxidative modification of tissue proteins in vivo. These adducts also were found to be the main forms of MDA excreted in human urine. Reacting 14C-bovine serum albumin (BSA) with MDA resulted in its accelerated proteolysis in vitro by soluble enzyme preparations derived from human erythrocytes and rat liver mitochondria. The increments observed were similar to those reported for the hydrolysis of BSA following its exposure to hydroxyl radicals. The results show that lipid peroxidation in vivo results in peroxidative damage to tissue proteins and indicate that such proteins are subject to an accelerated rate of proteolysis.

Circadian rhythms and time course of adaptive sodium and potassium excretion in rats after uninephrectomy

The relationship between renal circadian cyclic excretion and renal compensatory adaptation after uninephrectomy for K, Na, and water was studied. Rats in a 12:12-h light-dark environment were given a liquid diet, and urine was collected for 16 days with consecutive 90-min periods. Days 1-4 were control, 5-10 followed a sham operation, and 11-16 followed uninephrectomy. The major findings were 1) the circadian cycles in excretion were virtually unchanged after sham and uninephrectomy; 2) an adaptive increase in excretion of Na, K, and water by the remaining kidney occurred within 90 min after uninephrectomy; 3) after uninephrectomy the distribution of the 24-h increment in excretion for the remaining kidney closely followed the preexisting pattern of circadian excretion for Na but was evenly distributed between light and dark phases for K; and 4) after uninephrectomy the ratio of excretion to intake was unchanged. This is the first study to document the time course of adaptation to uninephrectomy using consecutive brief collections over several days in unanesthetized and undisturbed rats. Adaptation after uninephrectomy occurred essentially immediately; was maintained unchanged; and preserved Na, K, and water homeostasis. Uninephrectomy did not alter the circadian control of excretion.

Effects of indomethacin on furosemide-stimulated urinary PGE 2 excretion in man

We studied the effects of furosemide on urinary excretion of PGE 2 and sodium and the effects of inhibition of prostaglandin (PG) synthesis with indomethacin or furosemide-induced PGE 2 excretion and natriuresis in normal man. Furosemide (20 mg i.v.) increased the urinary excretion of PGE 2 from 71.2 ± 17.2 to 255.9 ± 41.0 ng/4 h. Sodium excretion increased in parallel. Indomethacin, in a dose sufficient to decrease basal urinary PGE 2 excretion by >90%, significantly decreased both urinary PGE 2 and sodium excretion under furosemide without affecting delivery of furosemide into the urine. The urinary excretion of furosemide was 9.4 ± 0.4 and 9.3 ± 1.4 mg/24 h with and without indomethacin, respectively. However, the furosemide-induced encrement in PGE 2 excretion and sodium excretion over baseline was not changed. Furosemide-stimulated urinaary PGE 2 excretion correlated significantly with sodium excretion rate with and without indomethacin. Indomethacin changed the relationship between absolute amounts of furosemide in urine and PGE 2 excretion but did not affect the increment in excretion over baseline or the significant correlation of urinary PGE 2 with sodium excretion.

PARTIAL 11− AND 21-HYDROXYLASE DEFICIENCIES IN HIRSUTE WOMEN

NEWMARK, STEPHEN; DLUHY, ROBERT G.; WILLIAMS, GORDON H.; POCHI, PETER; ROSE, LESLIE I. Author Information

Partial 11- and 21-hydroxylase deficiencies in hirsute women

Thirty-one women with idiopathic hirsutism were evaluated for partial 11- and 21-hydroxylase adrenocortical enzyme deficiencies. Twenty-four hour urine collections for 17-ketosteroids, 17-hydroxycorticoids, tetrahydro compound S (THS), and pregnanetriol were obtained basally and following a continuous 24 hour infusion of α 1–24 ACTH (cosyntropin). The results were compared to those in eight normal, nonhirsute women studied under identical conditions. Normal control subjects and 18 of 31 hirsute female patients (Group I) showed similar small increments in the excretion of THS and pregnanetriol following the infusion of cosyntropin. Thirteen hirsute women (Group II) showed cosyntropin-stimulated increments in either THS and/or pregnanetriol that were significantly greater than the mean response of the control group. The cosyntropin-stimulated increments in 17-ketosteroid excretion and basal sebum production rates were also significantly greater in Group II. The results are consistent with partial 11- and/or 21-adrenocortical hydroxylase deficiencies in some hirsute women whose condition would have previously been designated as “idiopathic”. Thus, prolonged ACTH stimulation testing may identify patients who might benefit from glucocorticoid suppression therapy.

The effect of furosemide on residual nephrons of the chronically diseased kidney in man.

Clearance studies were performed in 50 patients with varying degrees of stable chronic renal disease and 13 normal subjects in order to determine the effect of intravenous furosemide on residual nephrons of the chronically diseased kidney compared to nephrons within normal kidneys. Expression of data in terms of fractional excretion and excretion rate factored by GFR allows an analysis of furosemide effect as related to nephron population, in addition to an assessment of the absolute effect of this drug in producing a negative sodium, water, and potassium balance. A 0.25 mg/kg dose of furosemide produced virtually the same increment in the excretion rate per 100 ml GFR of sodium, water and potassium in diseased kidneys as in those of normal subjects until the GFR approached 15 ml/min. Thereafter, increments in sodium and water excretion were reduced out of proportion to the reduction in nephron mass, but were restored to a range comparable to normal by a 1 mg/kg dose. Studies in transplant donors before and after nephrectomy suggested that the increase in absolute sodium reabsorption which accompanies an increase in GFR per nephron does not explain the decreased responsiveness to the 0.25 mg/kg dose of furosemide observed in advanced azotemia. Thus, until severe disease supervenes with associated advanced azotemia, residual nephrons of the chronically diseased kidney retain responsiveness to a moderate dose of furosemide. The decrease in responsiveness per nephron observed in the presence of severe disease can be restored to normal levels by a 1 mg/kg dose of furosemide and appears to be more closely related to the presence of advanced azotemia rather than to other variables studied.

Excretion of testosterone and epitestosterone glucuronides in pre-school, pre-adolescent and adolescent children

Urinary excretions of testosterone and epitestosterone glucuronides were longitudinally studied in 42 pre-school, pre-adolescent and adolescent children aged 3 to 14 years. Differences between individual boys in the excretion of testosterone were marked but reduced when the results were plotted against skeletal maturity score. With the girls the increment in excretion was slow and gradual. In epitestosterone excretion there was no marked difference between boys and girls, nor was any association with skeletal maturity score observed. Boys with advanced sexual maturation excreted more testosterone than less developed subjects irrespective of chronological age. With epitestosterone no such association was found.

Studies on the characteristics of the control system governing sodium excretion in uremic man.

Sodium excretion was studied in a group of patients with chronic renal disease, (a) on constant salt intakes of varying amounts with and without mineralocorticoid hormone administration and, (b) after acute extracellular fluid volume expansion. The lower the steady-state glomerular filtration rate (GFR), the greater was the fraction of filtered sodium excreted on both a 3.5 and 7.0 g salt diet; and the lower the GFR, the greater was the change in fractional excretion in the transition from the 3.5 to the 7.0 g salt diet. This regulatory capacity did not appear to be influenced by mineralocorticoid hormone administration. After acute expansion of extracellular fluid (ECF) volume, the increment in sodium excretion exceeded the concomitant increment in filtered sodium in six of nine studies and in the remaining three studies, the increment in excretion averaged 59% of the Delta filtered load (i.e., only 41% of the increase in filtered sodium was reabsorbed). During saline loading, the decrease in fractional reabsorption of sodium tended to vary inversely with the steady-state GFR, although all patients received approximately the same loading volume. When an edema-forming stimulus was applied during saline infusion, the natriuretic response was aborted and the lag time was relatively short. When GFR and the filtered load of sodium were increased without volume expansion, the Delta sodium excretion averaged only 19% of the Delta filtered load; moreover, changes in fractional sodium reabsorption were considerably smaller than those observed during saline loading. The data implicate the presence of a factor other than GFR and mineralocorticoid changes in the modulation of sodium excretion in uremic man.