[Urinary elimination of 3-methoxy-4-hydroxymandelic acid in hyperpressure].
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This study describes an occupational health survey carried out in the polyester industry in order to investigate the hepatic effects caused by exposure to styrene. Fifty-seven workers underwent a medical examination. They were submitted to blood and urine sampling for the determination of the degree of exposure, by the analysis of urinary mandelic and phenylglyoxylic acids (styrene metabolites), and the intensity of induction and/or hepatic effects, by the analysis of urinary glucaric acid and plasma enzyme activities (gamma glutamyl transferase, ornithine carbamoyl transferase, alanine aminotransferase, and aspartate aminotransferase). The results showed that styrene does not give rise to measurable autoinduction. With regard to the hepatic tests, exposure to styrene caused an increase in the plasma enzyme activities, a phenomenon illustrating a possible damaging effect on liver cells. This effect appears with exposure below 100 ppm (time-weighted average).
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Pre-synaptic endings of the sympathetic nervous fibers control the metabolism of catecholamines, particularly inactivating norepinephrine after its neuronal recapture. The present study was carried out to investigate this segment of the metabolism of catecholamines through measurements of DHPG, DOMA and DOPAC concentrations in plasma. A sensitive and specific radio-enzymatic assay was developed of which the major characteristic is to include the plasma sample in the incubation mixture without initial extraction of the deaminated metabolites. In the rat, there was a statistically significant correlation between norepinephrine and DHPG in both anesthetized and conscious conditions and after clonidine or guanethidine induced reduction of sympathetic activity; thus it can be suggested that plasma DHPG is a good index of neuronal metabolism of norepinephrine in this animal. In humans, our data indicate an interesting correlation between norepinephrine and DOMA concentrations in plasma in resting conditions and within three hours after clonidine. Further studies need to be carried out to establish whether DOMA is a better index of neuronal metabolism of norepinephrine than DHPG.
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To determine the physiology of acid secretion after gastrocystoplasty with the body of the stomach we performed a prospective standardized 3-day study in 13 children (median age 12.5 years) who had undergone bladder augmentation/replacement (median postoperative period 2 years). Urinary pH and titratable acid, and serum gastrin levels were measured after gastric distention with a meal and bladder distention with urethral filling at baseline and after medication with a histamine-2 receptor antagonist or an anticholinergic agent. Five children underwent cystoscopy and biopsy of the gastric and native segments of the gastrocystoplasty. In the fasting state pH was neutral, there was no titratable acid in the urine and serum gastrin level was normal in all cases. After a meal urinary acid secretion and serum gastrin level increased markedly. After each medication half of the patients demonstrated marked inhibition of urinary acid secretion after a meal while response was partial in the remainder. In none of the patients was there significant alteration in the pattern of gastrin secretion. Bladder distention did not result in urinary acid secretion or gastrin secretion. The cystoscopic and histological appearance of the native bladder and stomach segment of the gastrocystoplasty in the 5 patients was normal. We conclude that the gastric body segment used in gastrocystoplasty continues to secrete acid as though it were part of the stomach. The secretion of acid in the urine can be decreased with histamine-2 receptor antagonist or anticholinergic medication.
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