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PubMed1987

Dissociation and diurnal variation of prostaglandin E2 6-keto-prostaglandin-F1-alpha, and thromboxane B2 excretion in healthy females.

The existence of diurnal variation in renal function is well described. Prostaglandins are intimately involved with renal physiology, yet a diurnal variation in their excretion is not well documented. We collected 12 consecutive 2 hour urine specimens from 10 young healthy females and measured prostaglandin E2 [PGE2], thromboxane B2 [TXB2], and 6-keto-prostaglandin-F1-alpha by radioimmunoassay for each specimen. We also measured urine volume, urine sodium, and urine creatinine levels. Regression analysis was used to determine the best sine curve for time versus each set of mean values. Only the urinary excretion of PGE2 and TXB2, as well as water were found to significantly fit the generated sine curves. The curves for PGE2 and TXB2 showed a temporal dissociation in their peak and trough values. The excretion of PGE2 between 0800 hours and 2000 hours was significantly higher than during the hours of 2000 and 0800. The opposite was true for the TXB2 excretion. This data suggests that these two prostaglandins and water are excreted in a sine wave pattern. It also suggests that the excretion of PGE2 and TXB2 may respond to different time associated stimuli. We also showed a significant correlation between PGE2 excretion and both the excretion of water and sodium.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Investigation of factors influencing urinary porphyrin excretion in rats: strain, gender, and age.

Urinary porphyrin excretion rates were evaluated in male rats of the Sprague-Dawley, Fischer 344, and Osborne-Mendel strains, and in female Fischer 344 rats, in order to identify an appropriate rat model for long-term studies of chemical-induced porphyria. Sprague-Dawley rats displayed a wide interanimal range in total 24-hr porphyrin excretion rates, from 0.9 to 59.6 nmol/24 hr (64-fold). Additionally, individual Sprague-Dawley rats varied by up to 5-fold in total porphyrins excreted from week to week over a 4-week period. Osborne-Mendel rats displayed a 12-fold interanimal difference in 24-hr total porphyrin excretion rates (ranging from 6.2 to 71.1 nmol/24 hr) and up to 4-fold individual variation from 1 week to another. In contrast, rats of the Fischer 344 strain displayed no significant differences in porphyrin excretion rates either among different animals or for individuals from week to week. Determination of individual porphyrin concentrations in the urine demonstrated that inconsistencies in total porphyrin concentration were attributable principally to differences in coproporphyrin concentrations. Frequency analysis of 24-hr coproporphyrin excretion levels among Sprague-Dawley rats demonstrated a widespread range encompassing low levels comparable to those of Fischer rats, high levels similar to those of most Osborne-Mendel rats, as well as intermediate levels. The mean total porphyrin excretion rate among female Fischer 344 rats was 1.2 +/- 0.51 nmol/24 hr, compared to 2.1 +/- 0.50 nmol/24 hr among male Fischer rats. Maturation and aging were found to have little influence on porphyrin excretion rates in male Fischer 344 rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1990

Modernization and catecholamine excretion of young Samoan adults.

Urinary catecholamine excretion rates have been used as a cross-culturally valid measure of generalized stress. The purposes of this paper are to examine group differences in catecholamine excretion rates in three Samoan groups who differ in degree of modernization and to compare these findings to rates of norepinephrine and epinephrine excretion in other populations. In 1986-1987, 24-hr urine samples were collected from 18-37-year-old Samoans; 46 rural Western Samoan villagers, 53 American Samoans, and 49 Samoans residing in Honolulu. The results show that norepinephrine excretion is significantly higher in more modernized Samoan groups (P less than 0.05), while epinephrine excretion is not significantly different in the three groups. The higher norepinephrine excretion rate in the more modernized Samoan groups may be related to differences in relative work load associated with changes in body weight, work capacity, and work patterns which accompany modernization. Samoan epinephrine excretion rates are relatively high compared to the results of other population studies, while norepinephrine excretion in three Samoan samples ranged from among the lowest rates observed worldwide to among the highest.

Adult↗
PubMed1987

The absorption, tissue distribution and excretion of di-n-octyltin dichloride in rats.

In this study the absorption, tissue distribution and excretion of 14C-labeled di-n-octyltin dichloride ([14C]DOTC) in rats were investigated after oral and intravenous (i.v.) administration. Although after i.v. administration with 1.2 mg [14C]DOTC/kg body weight the tissue radioactivity was about 3-4 times higher than after oral administration with 6.3 mg [14C]DOTC/kg body weight, the relative tissue accumulation was found to be the same after the oral and i.v. dosage. The highest amount of radioactivity was found in liver and kidney, and to a lesser degree in adrenal, pituitary and thyroid glands. The lowest activity was recovered from blood and brain. No selective accumulation was observed in thymus, although it has been reported that thymus atrophy is the most sensitive parameter of DOTC toxicity in rats. For all tissues a time dependent decrease in radioactivity was found, except for kidney. The excretion of radioactivity in feces and urine was determined after a single i.v. or oral dose of 1.2 and 2 mg [14C]DOTC, respectively. After i.v. administration most of the radioactivity was excreted in the feces which was characterized by a biphasic excretion pattern. In orally treated rats more than 80% of the radioactivity was already excreted in the feces during the first day after administration. This indicated that only a small part of the DOTC was absorbed, which was calculated to be approximately 20% of the dose. Similar half-life values of 8.3 and 8.9 days were obtained from the fecal excretion of radioactivity after the i.v. and oral administration, respectively. The urinary excretion of radioactivity appeared to be independent of the body burden, since the daily amount of radioactivity excreted in urine was nearly the same independent of the route of administration as well as the time after administration.

Absorption↗
PubMed1994

Comparative effects of chelating agents on distribution, excretion, and renal toxicity of gold sodium thiomalate in rats.

The effects of various chelating agents, such as (2S)-1-(3-mercaptopropionyl)-L-proline (captopril), N-(2-mercaptopropionyl)-glycine (tiopronin), L-cysteine (L-Cys), D-cysteine (D-Cys), N-acetyl-L-cysteine (L-NAC), N-benzyl-D-glucamine dithiocarbamate (BGD), and ethylenediaminetetraacetate (EDTA), on the distribution, excretion, and renal toxicity of gold sodium thiomalate (AuTM) in rats were investigated. Rats were intraperitoneally injected with the chelating agents (1.2 mmol/kg each) immediately after intravenous injection of AuTM (0.026 mmol/kg). Treatment with captopril or tiopronin significantly prevented increases in the urinary excretion of protein, aspartate aminotransferase (AST), and glucose and the blood urea nitrogen (BUN) level after AuTM injection. L-NAC and D-Cys significantly prevented increases in the urinary excretion of protein, AST, and glucose after AuTM injection, but did not reduce to control levels. Treatment with BGD, EDTA, or L-Cys did not prevent AuTM-induced increases in the urinary excretion of protein, AST, and glucose and BUN level. Tiopronin significantly increased the urinary excretion of gold. Captopril slightly promoted both the urinary and fecal excretion of gold, resulting in the significant increase in the total excretion of the metal. Tiopronin and captopril significantly decreased the gold concentration in the kidney and liver. L-Cys, D-Cys, L-NAC, BGD, and EDTA had no significant effect on the excretion or distribution of gold at 7 days after AuTM injection. These results indicate that tiopronin and captopril can ameliorate the renal toxicity induced by AuTM. In addition, the comparative effects of 2,3-dimercaptopropane sulfonate (DMPS), N-(2-mercapto-2-methylpropanoyl)-L-cysteine (bucillamine), captopril, and tiopronin at various dose levels (1.2, 0.4 or 0.2 mmol/kg) on the distribution and renal toxicity of gold were studied. DMPS was effective in removing gold from the kidney and in protecting against the renal toxicity after AuTM injection at the even lower dose level (0.2 mmol/kg). Bucillamine and tiopronin protected against the renal toxicity of gold at dose levels of 0.4 and 1.2 mmol/kg and captopril ameliorated the gold toxicity only at higher dose level (1.2 mmol/kg).

Animals↗
PubMed1991

Level of virulent virus excreted by infected pigs previously vaccinated with different glycoprotein deleted Aujeszky's disease vaccines.

Seven deleted Aujeszky's disease vaccines were compared for their ability to induce an immunity which suppresses virus excretion. For each vaccine, the levels of clinical protection and viral excretion were compared. Groups of eight pigs were vaccinated twice with attenuated deleted Aujeszky's disease vaccines (which do not express certain glycoproteins: gI, gX or gp63). Pigs were vaccinated at the beginning of the fattening period and challenge took place at the end of it when the pigs were 18-19 weeks old. Live virus vaccines were suspended in water or in an oil-in-water emulsion. The experiment was performed in three successive assays of two groups of eight pigs (except three groups for the first assay). At each assay, a control unvaccinated group of eight pigs was added to compare the effects of challenge between vaccinated and unvaccinated animals. In total, 80 pigs were involved in this experiment. All the vaccinated pigs excreted virus from 3 to 9 d after challenge. However the level of viral excretion and the duration of the period of excretion were reduced after vaccination and especially, when oil-in-water emulsion was used. There were obvious differences between vaccines. With some vaccines, when the level of viral excretion was low, the level of clinical protection was high. However, in other cases, the level of clinical protection could be good despite a higher level of viral excretion. The seroneutralizing titres were significantly and inversely related to a low level of viral excretion but not to the level of clinical protection.

Animals↗
PubMed1992

Bromobenzene-glutathione excretion into bile reflects toxic activation of bromobenzene in rats.

This investigation was designed to determine whether biliary excretion of bromobenzene(BB)-glutathione(GSH) conjugate can be used as an index of in vivo activation of BB. In order to test this hypothesis, the effect of chemicals known to alter the toxicity and biotransformation of BB (i.e., cytochrome P-450 inducers and inhibitors) on the biliary excretion of BB-GSH was studied in rats. BB-GSH was the major BB metabolite in bile. A linear relationship was observed between the dosage of BB administered and BB-GSH excreted into bile, up to a dosage of 250 mumol/kg of BB. Of the inducers tested, phenobarbital, which is known to increase the toxicity of BB, dramatically increased (700%) the rate of biliary excretion of BB-GSH over that in control animals. In contrast, 3-methylcholanthrene, which is known to decrease the hepatotoxicity of BB, decreased the biliary excretion of BB-GSH (56%). Inhibitors of P-450, such as SKF 525-A and piperonyl butoxide which are known to decrease the activation and hepatotoxicity of BB, also decreased the biliary excretion of BB-GSH. These findings are in agreement with the hypothesis that the biliary excretion of BB-GSH reflects the formation of the reactive BB metabolite in liver and the rate of biliary excretion can be used to determine factors that are important in determining the toxicity of BB.

Animals↗
PubMed1995

Interindividual variability in the urinary excretion of inorganic arsenic metabolites by C57 BL/6J mice: possible involvement of a thiol/disulfide exchange mechanism.

The 24-h urine of 75 C57 BL/6J mice injected s.c. with 0.5 mg/kg arsenic as sodium arsenite were examined for creatinine, S-adenosylmethionine (SAM), urea and inorganic arsenic metabolites including inorganic arsenic (ASi), monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA). There was interindividual variability of about a 10-fold range in the 24-h urinary excretion of creatinine (80-642 micrograms/24 h, variability (cv) of 33%), SAM (7.5-67.2 micrograms/24 h, cv of 38%), urea (9.5-89.7 mg/24 h, cv of 36%), ASi (0.1-1.6 microgram/24 h, cv of 48%), MMA (0.17-2.1 micrograms/24 h, cv of 50%), DMA (0.73-8.13 micrograms/24 h, cv of 32%) and total arsenic metabolites (1.0-10.4 micrograms/24 h, cv of 31%). Interindividual differences, varying by as much as 5-7-fold, were also found in the urinary proportion of ASi (3-23%, cv of 41%) and MMA (5-22%, cv of 37%), but not in the urinary proportion of DMA (64-90%, cv of 7%). The 24-h urinary excretion of all arsenic metabolites correlated with the 24-h urinary excretion of urea (r = 0.81), creatinine (r = 0.88) and SAM (r = 0.83) as did the 24-h urinary excretion of urea with creatinine (r = 0.94) and SAM (r = 0.86), and the 24-h urinary excretion of creatinine with SAM (r = 0.94). Taken together, these results suggest that the overall intracellular glutathione (GSH)-dependent redox state, as reflected by the 24-h urinary excretion of SAM and creatinine, is involved in the interindividual variability in total arsenic metabolite excretion by C57 BL/6J mice. These preliminary results were also discussed with regard to the involvement of intracellular GSH-dependent redox state in the regulation of the reduction and of the methylation steps of arsenic, and to interindividual variability in the urinary excretion of total arsenic metabolites as a possible complicating factor in the biological monitoring of occupational exposure to arsenic.

Animals↗
PubMed1990

Effect of probenecid on the urinary excretion of TXB2 and PGE2 in the anaesthetised rat.

In the anaesthetised rat, probenecid (33 mg/kg) produced a 50% fall in urinary TXB2 excretion indicating that a component of the TXB2 excreted in the urine is secreted by the proximal tubule. At a higher dose of probenecid (100 mg/kg) this effect was overcome, a relative increase in urinary TXB2 excretion being produced. This may provide evidence for the proximal reabsorption or bi-directional transport of TXB2 in the rat. At 100 mg/kg probenecid also produced an 8-fold increase in urinary PGE2 excretion. Although the bi-directional transport of PGE2 is well known, this is the first time urinary PGE2 excretion rate has been shown to be modified by probenecid. The increase in PGE2 excretion could obscure the assessment of any inhibition by probenecid of proximal PGE2 secretion. It could also provide evidence for the proximal reabsorption of PGE2. However the interpretation of probenecid-induced changes in eicosanoid excretion in terms of modified tubular reabsorption must be treated with caution since urinary eicosanoid excretion could be increased by other properties of probenecid including inhibition of either protein binding or the uptake of eicosanoids into the lung.

Animals↗
PubMed2000

Biliary indocyanine green excretion as a predictor of hepatic adenosine triphosphate levels in patients with obstructive jaundice.

BACKGROUND: Correlation of the hepatic adenosine triphosphate (ATP) level with indocyanine green (ICG) excretion into bile was examined in patients with obstructive jaundice after the relief of hyperbilirubinemia by preoperative percutaneous transhepatic biliary drainage (PTBD). METHODS: Patients with complete bile duct obstruction, the mean serum total bilirubin concentration being 13.6 +/- 8.5 (SD) mg/dL, underwent PTBD prior to surgery. Within a few days before surgery when the mean serum total bilirubin level decreased to 1.2 mg/dL, ICG (0.5 mg/kg) was intravenously injected, and the whole bile was collected at 1-hour intervals for 5 hours. The ICG concentration in bile, bile flow rate, amount of ICG excreted in bile, and biliary ICG excretion rate as percentage of the injected dose were determined. At the time of surgery, a small liver tissue sample was obtained immediately after laparotomy without any ischemic procedures, and ATP concentrations were determined. Results of hepatic ATP levels were correlated with laboratory and clinical determinations. RESULTS: The bile flow rate was essentially constant during the 5-hour period, the mean value being 21 mL/hour. The ICG concentrations in bile gradually increased, reached the maximal level in 3 hour, and declined thereafter. The biliary ICG excretion rate for 5 hours was 40% +/- 18% of its injected dose. The biliary ICG excretion rate and amount of ICG excreted in bile for 5 hours significantly (P <0.05) correlated with the hepatic ATP level. The decline index of serum bilirubin during PTBD was also correlated with the hepatic ATP level. The serum ICG retention rate, bile flow rate, maximal ICG concentration in bile, and other liver function tests including serum albumin and cholinesterase levels did not correlate with the hepatic ATP level. CONCLUSIONS: Both the amount of and excretion rate of ICG in bile reflect the hepatic ATP level. Determination of biliary ICG excretion contributes to precise evaluation of hepatic energy status before surgery in patients with obstructive jaundice.

Adenosine Triphosphate↗
PubMed1998

Role of glutathione and methylation in the biliary excretion of selenium. The paradoxical effect of sulfobromophthalein.

Biotransformation of selenite involves both reactions with GSH and methylations. Therefore, the role of GSH, methylation, and the hepatobiliary GSH transporter was investigated in the biliary excretion of selenium in rats injected with sodium [75Se]selenite (1-10 micromol/kg, i.v.). Biliary output of selenium exhibited an apparent capacity limitation with an approximately 3 nmol/kg x min maximal rate and a dose-related decline in the fractional excretion. HPLC analysis of bile indicated absence of selenite and presence of selenodiglutathione (GS-Se-SG) and/or its hydrolysis products as the major biliary selenite metabolites. Depletion of hepatic glutathione by D,L-buthionine-[S,R]-sulfoximine or diethyl maleate decreased selenium excretion into bile by 60 and 80%, respectively. In contrast, inhibitors of methylation, i.e. periodate-oxidised adenosine or ethionine doubled the rate of biliary selenium excretion. While indocyanine green--an inhibitor of hepatobiliary GSH transport--failed to influence biliary selenium output, sulfobromophthalein (BSP)--another inhibitor of this sort--dramatically enhanced it. This effect was found to be a function of the dose of both selenite and BSP. The degree of BSP-induced enhancement of the selenium excretion rate gradually increased with elevation of the selenite dose, approaching 20-fold at 10 micromol/kg selenite. In contrast, the stimulatory effect of BSP on biliary selenium output was maximal at 50-100 micromol/kg and gradually lessened with elevation of the BSP dose above 100 micromol/kg. In summary, this study revealed that the biliary excretion of selenium depended on availability of hepatic GSH, probably for formation of GS-Se-SG, the putative cholephilic selenite metabolite. Methylation counteracted selenium excretion into bile and thus may contribute to the apparent capacity limitation of biliary selenium excretion. Finally, selenium output into bile was insensitive to inhibitors of the hepatobiliary GSH transporter, and was enhanced, paradoxically, by BSP several-fold. The mechanism of this unexpected effect is explored in the adjoining article.

Animals↗
PubMed2000

Excretion of copper complexed with thiomolybdate into the bile and blood in LEC rats.

Copper (Cu) accumulating in a form bound to metallothionein (MT) in the liver of Long-Evans rats with a cinnamon-like coat color (LEC rats), an animal model of Wilson disease, was removed with ammonium tetrathiomolybdate (TTM), and the fate of the Cu complexed with TTM and mobilized from the liver was determined. TTM was injected intravenously as a single dose of 2, 10 or 50 mg TTM/kg body weight into LEC and Wistar (normal Cu metabolism) rats, and then the concentrations of Cu and molybdenum (Mo) in the bile and plasma were monitored with time after the injection. In Wistar rats, most of the Mo was excreted into the urine, only a small quantity being excreted into the bile, while Cu excreted into the urine decreased. However, in LEC rats, Cu and Mo were excreted into the bile and blood, and the bile is recognized for the first time as the major route of excretion. The Cu excreted into both the bile and plasma was accompanied by an equimolar amount of Mo. The relative ratio of the amounts of Cu excreted into the bile and plasma was 40/60 for the low and high dose groups, and 70/30 for the medium dose group. The systemic dispositions of the Cu mobilized from the liver and the Mo complexed with the Cu were also determined for the kidneys, spleen and brain together with their urinal excretion. Although Mo in the three organs and Cu in the kidneys and spleen were increased or showed a tendency to increase, Cu in the brain was not increased at all doses of TTM.

Animals↗
PubMed1989

Urinary hydroxyproline and hydroxylysine excretions in relation to hepatic hydroxyproline content in chronic liver disease.

In patients with or without various chronic liver diseases, the total urinary excretion of hydroxyproline and hydroxylysine and the hepatic content of hydroxyproline were examined. In 7 patients without liver disease, the urinary excretion of hydroxyproline and hydroxylysine were 10.3 +/- 1.5 and 1.31 +/- 0.21 mmol/mol creatinine, respectively, and the hepatic content of hydroxyproline was 4.9 +/- 0.6 mumol/g of wet liver. In 33 patients with liver disease, the urinary excretion of hydroxyproline and hydroxylysine and the hepatic content of hydroxyproline were increased in proportion to the severity of liver disease. The hepatic content of hydroxyproline showed a significant correlation with the urinary excretion of hydroxyproline and hydroxylysine (r = +0.406 and r = +0.531, respectively). These results suggest that the study of urinary hydroxyproline and hydroxylysine excretion may yield useful information on the metabolism of hepatic collagen in chronic liver disease. Moreover, urinary hydroxylysine excretion seemed to be a better index of hepatic collagen metabolism than urinary hydroxyproline excretion; perhaps urinary hydroxylysine excretion is not much affected by dietary collagen intake.

Adult↗
PubMed1986

Increased urinary excretion of inorganic sulfate in premature infants fed bovine milk protein.

We report measurements of urinary inorganic sulfate (iSO4) in 38 very low birth weight (VLBW) premature infants receiving various protein intakes in the first 2 months of life. The primary source of urinary iSO4 is the metabolism of amino acids containing sulfur (methionine, cysteine, taurine). It was hypothesized that urinary iSO4 excretion would be increased in VLBW infants fed the relatively high concentrations of protein in mother's own milk (HM), mother's own milk fortified with 0.85 gm/dl bovine whey (fortified HM), and a special formula for premature infants (Similac Special Care, 20 cal/oz), and that urinary iSO4 excretion would correlate with calcium excretion. VLBW premature infants fed HM (protein intake 3.3 gm/kg day) excreted very small amounts of urinary iSO4 compared with infants fed fortified HM (4.5 gm/kg/day protein), Similac SC (2.9 gm/kg/day protein), or Similac (2.7 gm/kg/day protein), all three of which contain bovine whey. Unlike the case in adults, there was no correlation between either total protein intake and urinary calcium excretion or urinary iSO4 excretion. There was, however, a significant correlation between methionine intake and urinary iSO4 excretion (r = 0.48). We speculate that increased urinary iSO4 excretion is indicative of an overload of sulfur-containing amino acids, namely methionine, present in bovine whey protein. The data also support the ability of premature infants to catabolize relatively large quantities of sulfur-containing amino acids after 2 weeks of age.

Animals↗
PubMed1988

Dynamic study of nervous control on prostatic contraction and fluid excretion in the dog.

The effect of the section or stimulation of various nerves on prostatic contraction and fluid excretion was investigated dynamically in the dog using an apparatus devised in our laboratory. Prostatic contraction could be classified into two types from the pattern of the contracting wave. One was a prominent tonic contraction, designated as H-type contraction, observed typically after hypogastric nerve stimulation and followed always by prostatic fluid excretion. The other was a weak clonic contraction, designated as P-type contraction, occurring typically after pelvic nerve stimulation and accompanied by no fluid excretion. The periodical contraction of these two types was noticed even at rest. The H-type contraction was associated with fluid excretion with a mean rate of 0.3 ml./hr. The denervation both of the hypogastric and pelvic nerves showed no distinct influence on contraction and excretion in the resting condition. The pudendal nerve was demonstrated to have no significant effect on prostatic contraction and fluid excretion. From these results, it was considered that dynamic fluid excretion followed by prostatic contraction was regulated chiefly by sympathetic fibers from the hypogastric nerve and the physiological role of parasympathetic fibers from the pelvic nerve was something other than fluid excretion.

Animals↗
PubMed1984

Effect of angiotensin, noradrenaline, vasopressin and aldosterone on urinary kallikrein excretion in the rat.

In male Wistar rats, under osmotic diuresis, the effect of angiotensin II, noradrenaline, vasopressin and aldosterone on urinary kallikrein excretion were evaluated. Angiotensin II did not modify but all the others drugs used increased significantly the urinary kallikrein excretion. In all the groups studied the urinary sodium excretion increased. No modifications were observed in urine flow, glomerular filtration rate, urine osmolality and potassium excretion. The urinary kallikrein excretion was always positively correlated with the urinary flow and urinary sodium excretion. No correlation was observed with the other parameters studied. These findings suggest that noradrenaline, vasopressin and aldosterone are important stimulators of the urinary kallikrein excretion. Probably, kallikrein is one of the mechanisms involved in the regulation of urinary sodium excretion.

Aldosterone↗
PubMed1999

Influence of circadian time, ageing, and hypertension on the urinary excretion of nitric oxide metabolites in rats.

Urinary excretion of NO metabolites (NOx) was measured in male spontaneously hypertensive rats (SHR) and their normotensive Wistar-Kyoto controls (WKY) in two age groups: young (11 weeks) and old (58 weeks). Urine was collected every 6 h throughout 24 h with and without injection interperitoneally of N(G)-nitro-L-arginine-methyl-ester (L-NAME), 30 mg/kg, at 7:00 or 19:00 h. In addition, blood pressure changes by L-NAME were evaluated using radiotelemetry. In both strains of rats, injection of L-NAME abolished almost completely the urinary excretion of NOx, indicating that urinary NOx indeed reflect the endogenous rate of NO synthesis. Time-dependent variation in urinary NOx excretion was observed in WKY rats of both ages (analysis of variance, P<0.05), with higher excretion in the dark period. In SHR rats, time-dependent variation in NOx excretion was lost, and the overall amount of NOx excreted within 24 h was significantly lower in young SHR than in age-matched WKY rats. Moreover, blood pressure increases by L-NAME were significantly smaller in SHR than in WKY rats. In old rats of both strains, NOx excretion was reduced, and the difference between the strains disappeared. Our findings demonstrate that ageing is accompanied by a loss in NOx excretion, and suggest that hypertension in SHR leads to a reduction in NO synthesis already at young age.

Aging↗
PubMed1998

Extended excretion of rotavirus after severe diarrhoea in young children.

BACKGROUND: Rotaviruses are the major cause of severe childhood diarrhoea. Knowledge of the natural history of infection, including duration of intestinal virus shedding, is important in the understanding of transmission, sources of infection, and immune responses. METHODS: We carried out a study of rotavirus excretion in 37 children admitted to hospital with severe rotavirus diarrhoea. Sequential faecal specimens were collected from each child during 100 days of surveillance, and screened for rotavirus by EIA and by amplification of genome double-stranded RNA by reverse-transcription PCR. IgA coproantibody was estimated by EIA. FINDINGS: Duration of rotavirus excretion ranged from 4 to 57 days after onset of diarrhoea. Excretion ceased within 10 days in 16 (43%) children, and within 20 days in 26 (70%) children. Extended excretion was detected for 25-57 days in the remaining 11 (30%) children owing mainly to continued excretion of the primary infecting strain. Extended excretion was significantly associated with antirotavirus IgA coproantibody boosts during 100 days of surveillance (p=0.001, log-rank test), and with recurrence of mild diarrhoea symptoms during convalescence (p=0.006, Fisher's exact test). INTERPRETATION: Severe rotavirus disease in young children may be followed by extended excretion of rotavirus. The risk of transmission to others may be greater than previously believed. Extended excretion could also explain some cases of the postgastroenteritis syndrome.

Antibodies, Viral↗