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Biomedical subjects

O Thorlacius-Ussing

Publications and source records attributed to O Thorlacius-Ussing.

At least 37 records · Page 2Linked to original sources

[Laparoscopic cholecystectomy].

Forty-one patients with uncomplicated gall stone disease were laparoscopied with the object of cholecystectomy. The procedure was accomplished in 36 patients, but the operation had to be transformed to a conventional open operation in five: Fibrosis made dissection of the gall bladder hazardous in four and bleeding during the procedure made immediate laparotomy necessary in one patient, whose postoperative course was uneventful. The median operating time was 100 minutes, range was 60-250 minutes. The only operative complication was bleeding from a trocar puncture hole on the first postoperative day which stopped spontaneously in one patient. Eighteen were sent home on the first postoperative day and 12 patients on the second day. Peroperative cholangiography was performed employing the Olsen-Reddick cholangiography forceps. We have designed a special catheter, which greatly facilitates the procedure. The procedure was accomplished in 27 of 32 planned cases. Two patients had common bile duct or common hepatic duct stones. A trans-sphincteric endoprosthesis was applied through the cholangiography forceps in both patients, to prevent postoperative bile duct outlet obstruction. The endoprosthesis made the following endoscopic sphincterotomy, which was performed at a convenient time rapid and safe. The stones were extracted and the prosthesis removed on the same occasion. A reliable flushing system was developed on the basis of the "Kidde" automatic tourniquet frequently used in orthopaedic surgery. All patients were seen in the outpatient clinic 1 month after the operation. Superficial infection in the trocar holes in ten patients were the only problem the patients had encountered and all had returned to their normal work.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Selenium in the central nervous system of rats exposed to 75-Se L-selenomethionine and sodium selenite.

The aim of the present study is to investigate the accumulation and retention of organic and inorganic selenium in the central nervous system (CNS) of the rat. Selenium accumulation was investigated after oral treatment (3.0 mg Se/L drinking water) or ip injection (1.7 mg Se/kg body wt) of rats exposed to 75-Se L-selenomethionine (SeMeth) or sodium selenite (NaSe). Significant higher concentrations were observed after exposure to organic compared to inorganic selenium after oral as well as ip administration. Highest concentrations in both experiments were observed in cerebellum followed by the nearly identical levels in the cerebral hemisphere and spinal cord independent of the chemical form of selenium or the route of administration. The difference in concentrations observed between the different parts of the CNS investigated in each group were, however, not significant. Retention of selenium in the CNS was investigated after a single ip injection (1.7 mg Se/kg body wt) of 75-Se SeMeth or NaSe. In both groups, we observed an initial fast excretion phase followed by a slower excretion phase resembling a first-order reaction. Organic selenium disappeared much slower from all parts of the central nervous system compared to NaSe after a single injection.

Animals↗

Selenium complexes in the anterior pituitary of rats exposed to L-selenomethionine.

Selenium precipitates were demonstrated histochemically by silver amplification at light and electron microscopic levels in the anterior pituitary of rats exposed to L-selenomethionine (SeMeth). By electron microscopy (EM), the silver amplified selenium complexes were identified in somatotrophs, corticotrophs and gonadotrophs. Precipitates were observed mainly in the secretory granules and to a lesser extent in the lysosomes. The staining intensity increased with increasing amounts of SeMeth. Following a single injection of 3.7 mg Se/kg a substantial increase in staining was observed during the first 48 h after injection and precipitates could still be observed in the anterior pituitary after 2 weeks. During a long-term study where the rats were exposed to selenium contained in the drinking water (3.0 mg Se/l drinking water for 1, 2 or 4 weeks) an increasing amount of precipitates were observed during the first 2 weeks followed by a small decrease in staining intensity. Organic selenium, or rather a metabolite, is suggested to form bands with endogenous metal, primarily zinc, as has been suggested in the brain and anterior pituitary after exposure to sodium selenite.

Animals↗

Somatostatin analogue administration prevents increase in kidney somatomedin C and initial renal growth in diabetic and uninephrectomized rats.

In a previous study we demonstrated that the kidney content of somatomedin C was maximal one to two days after uninephrectomy or induction of diabetes, and that insulin treatment prevented an increase in kidney somatomedin C as well as kidney growth in diabetic animals. In the present study we have examined the effect of a somatostatin analogue on kidney somatomedin C and initial renal growth in the two experimental situations. The kidney hypertrophy in untreated diabetic animals amounted to 23% four days after streptozotocin injection and followed an increase in kidney somatomedin C content of 60% reaching the maximum after 48 h. In young and old uninephrectomized rats kidney growth was 19% and 16% after four days. In young animals a prompt increase of 50% in kidney somatomedin C was seen as reaching the maximum after 24 h, while the somatomedin C content in kidneys from old animals was maximal after 48 h (increase of 58%) in good accordance with the slightly slower kidney growth. The new findings of the present study are that administration of a long-acting somatostatin analogue (Sandostatin) effectively prevented the obligatory increase in kidney somatomedin C content as well as kidney growth both in experimental diabetes and after uninephrectomy. It is noteworthy that Sandostatin administration did not alter the metabolic state in diabetic animals indicating that the inhibition of kidney hypertrophy could not be attributed to improved metabolic control. The results thus support the concept that somatomedin C is involved in initial diabetic and post-nephrectomy renal growth.

Aging↗

Mercury-selenium interactions in relation to histochemical staining of mercury in the rat liver.

Selenium has been suggested to enhance the histochemical staining of mercury when sections of tissue are subjected to the silver-enhancement method. In the present study, histochemical staining patterns of mercury in tissue sections of rat livers were compared with the actual content of organic and inorganic Hg in the livers, in both the presence and the absence of Se. Rats were injected intravenously with 5 micrograms of Hg g-1 body weight as methyl [203Hg] mercury chloride (MeHg) or as [203Hg]mercuric chloride (Hg2+). After 2 h, half the rats received an additional intraperitoneal injection of 2 micrograms of Se g-1 body weight as sodium [75Se]selenite. All the rats were killed 1 h later. Homogenized liver samples were prepared for mercury analysis by two different methods: alkaline digestion and ultrasonic disintegration. Quantitative chemical analysis based on benzene extraction of the radioactively labelled Hg compounds showed that the chemical form of mercury, either organic or inorganic, was preserved from its administration to its deposition in the liver. Light and electron microscopy demonstrated that no silver enhancement of Hg occurred when MeHg alone was present in the sections of tissue, whereas MeHg accompanied by Se induced a moderate deposition of silver grains. In contrast, sections containing Hg2+ alone yielded some staining, and the addition of Se increased the staining dramatically. The results of the present study show that acute selenite pretreatment is a prerequisite for the histochemical demonstration of methyl mercury, and greatly increases the staining of inorganic mercury when applying the silver-enhancement method.

Animals↗

Distribution of dietary mercury in a dog. Quantitation and localization of total mercury in organs and central nervous system.

An Alsatian dog which had been fed fish contaminated with methyl mercury for 7 years was examined after its death at the age of 12, 4 years after the exposure to methyl mercury had ceased. Two dogs of the same age and breed served as controls. In the exposed dog, mercury was found in all of the organs examined; the highest concentrations were found in the kidneys, and the lowest in the gastrointestinal tract and skeletal muscles. In the central nervous system (CNS) the mercury was fairly uniformly distributed, with 93% in the inorganic state, whereas the skeletal muscles contained approximately 30% inorganic mercury. This demonstrates time-dependent demethylation and suggests a variation in the rate from one type of tissue to another. At the time of death, the mercury level in the dog was still falling. In the control dogs, detectable amounts (0.01 mg kg-1) of mercury were only found in the kidney and liver. The distribution of mercury was determined by a histochemical method (autometallography) for locating mercury in tissue sections. Sections from autometallography of the central nervous system showed large deposits of mercury in all areas of the cerebral hemispheres, the brainstem and the spinal cord, including nerve cells, astrocytes, microglial cells and vessel walls. The granular layer of the cerebellar hemispheres was especially loaded, while only a few granules were present in the Purkinje cells. In the leptomeninges the vessels and the macrophages were heavily encrusted. High amounts of histochemically demonstrable mercury were observed in the liver, thyroid gland and kidney. In the control dogs, all the organs examined were practically devoid of deposits.

Animals↗

Kidney tissue somatomedin C and initial renal growth in diabetic and uninephrectomized rats.

Kidney growth after induction of experimental diabetes in rats was compared to compensatory renal growth in response to unilateral nephrectomy. After 4 days of diabetes, kidney weight had increased from 816 +/- 21 mg (SEM) to 940 +/- 42 mg (15%). In insulin-treated diabetic rats kidney weight was unchanged at the end of the study, namely 828 +/- 15 mg. In unilaterally nephrectomised rats kidney weight increased from 840 +/- 20 mg (SEM) to 1050 +/- 60 mg during 4 days (24%). We observed increased kidney content of somatomedin C in both diabetic and uninephrectomized rats. In untreated diabetic rats it was maximal after 48 h, with an increase of 77% (3469 +/- 312 ng/g (SEM) versus 1961 +/- 173 ng/g). After 4 days the somatomedin C content had returned to initial levels. In insulin-treated rats somatomedin C content did not increase during the observation period. The somatomedin C content of the remaining kidney after unilateral nephrectomy was maximal after 24 h with an increase of 58% (from 1340 +/- 203 ng/g (SEM) to 2122 +/- 214 ng/g). The somatomedin C content returned to normal at day 4. Serum somatomedin C declined insignificantly in diabetic animals during the experimental period, but a significant decrease (p less than 0.02) was found in uninephrectomized rats. This study demonstrates that kidney somatomedin C peaks during the first or second day after uninephrectomy or induction of diabetes, respectively, and that insulin treatment sufficient to prevent kidney growth abolishes the increase. These similar rapid initial hypertrophies/hyperplasies may thus be dependent on local somatomedin C formation.

Animals↗

The concentration of twelve elements in the anterior pituitary from human subjects and rats as measured by particle induced X-ray emission (PIXE).

The concentration of twelve elements--potassium, calcium, manganese, iron, cobalt, nickel, copper, zinc, arsenic, selenium, bromine, and rubidium--in anterior pituitaries from human subjects and rats was measured using Particle Induced X-ray Emission (PIXE). The human material included anterior pituitaries from 37 normal human subjects, 27 males and 10 females, all of whom died from traumatic lesions. Excluded from the investigations were persons with alcohol abuse, regular use of drugs, and babies younger than 1 year. For selenium, zinc, bromine, and to some extent copper, there was good correlation between the amounts found in anterior pituitaries from rats and human subjects. A significant difference between male and female rat pituitaries was observed for copper, iron, and rubidium, whereas for humans significant difference was only observed for manganese. Anterior pituitaries from human females contained generally more zinc than male glands, but the concentration of zinc in young males was higher than in females. The present study also indicates age related differences in the copper content in anterior pituitaries from human subjects, since pituitaries from humans between 15-45 years contained 25% more copper than those from younger or older persons. The opposite pattern was observed in males. For such elements as Cu, Fe, Mn, and Se, the content in the anterior pituitary from human subjects was 1.6-2 times that stated for other endocrine organs.

Adolescent↗

Growth in young rats after termination of sodium selenite exposure: studies of growth hormone and somatomedin C.

In a previous study we have shown that the growth retarding effect of selenium in infant rats occurs concomitantly with severely reduced growth hormone responses and serum somatomedin C. Furthermore, normal growth may be restored by administration of exogenous growth hormone administration. In the present study we examined the alterations after withdrawal of selenite administration in growth rate, serum growth hormone after GRF 40 injection and serum somatomedin C. Thirty-six rats were divided into 3 groups; i.e. controls, rats on continuous selenite treatment from days 21 to 63 of age and a group where selenium was withdrawn on day 42. The first 2 groups grew linearly during the experimental period, the second at a very significantly lower rate. In the third group after cessation of exposure a brief growth spurt occurred followed by a growth rate significantly different from that of the other 2 groups. The reduced GH response to GRF 40 stimulation was normalized 3 weeks after withdrawal, whereas serum somatomedin C remained at the same low level as in those rats on continuous selenite administration. There were other signs of liver lesion at day 42, i.e. elevated ALAT and reduced serum albumin, changes which became insignificant in all 3 groups at the end of the experiment. These results demonstrate that whereas stimulated growth hormone secretion was reestablished 3 weeks after termination of selenium exposure, severely reduced liver somatomedin C production persisted. An improvement in growth rate was also noted, but normal growth rate was not reached 3 weeks after discontinuation of the selenite treatment.

Age Factors↗

Growth hormone restores normal growth in selenium-treated rats without increase in circulating somatomedin C.

Selenium intake (5.0 ppm) induces growth retardation, accumulation of selenium in somatotrophs, lack of growth hormone response to GHRH and an 80 per cent reduction in serum somatomedin C in infant rats. In addition, it induces a slight reduction in serum albumin and occasionally slight central liver necrosis. In order to determine the role of insufficient growth hormone production, the influence of exogenous growth hormone was studied during selenium intake in groups of rats during 25 to 46 days of age (post-weaning). A dosage of human growth hormone (100 micrograms twice daily) was chosen, this being sufficient to restore normal growth rate and normal serum somatomedin C in hypophysectomized rats of similar age. The weight gain in selenium-treated (3.3 ppm) rats was 46.0 +/- 11.7 g (SD)/21 days, whereas in selenium rats given growth hormone it was 66.6 +/- 8.9 g (P = 0.01), which was similar to the gain in control rats 72.3 +/- 6.9 g. The latter two were less than the weight gain in control rats given growth hormone: 91.5 +/- 11.5 g (P = 0.01 and P less than 0.01). Serum somatomedin C in untreated rats was 151 +/- 66 (SD) micrograms/l (25 days) increasing to 532 +/- 91 micrograms/l (34 days) and 482 +/- 64 micrograms/l (46 days). It did not increase above these levels in control rats given growth hormone. In selenium-treated rats, no increase occurred during growth hormone administration 138 +/- 148 micrograms/l (34 days) and 185 +/- 84 micrograms/l (46 days) (P less than 0.001 and P less than 0.001 vs untreated controls).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Ultrastructural localization of mercury in adrenals from rats exposed to methyl mercury.

Accumulations of mercury have been demonstrated in adrenal glands by light and electron microscopy with a highly sensitive histochemical technique. Rats were exposed to methyl mercury in drinking water (20 mg/l) for 7-180 days, or were given intraperitoneal injections of methyl mercury (daily dose 100 or 200 micrograms). The amount and location of the mercury deposits were dependent upon the exposure time, the method of administration and the amount administered. In rats exposed to methyl mercury in drinking water, accumulations were often observed in both the zona glomerulosa and reticularis. They appeared first in the zona glomerulosa of animals treated for 1 week. In the zona fasciculata, deposits were observed only in the animals treated for 50 to 180 days. In animals treated for 180 days the cytoplasm of the cells in the zona fasciculata was heavily vacuolated and distinct necrotic cells were observed in other cortical zones. In the chromaffin cells, a slight increase in the amount of deposits was observed with increasing exposure time. Both epinephrenic and norepinephrenic cells contained deposits. Only a few deposits were observed in the cortical and chromaffin cells of animals treated with intraperitoneal injections. Ultrastructural deposits were observed in the lysosomes of cortical cells and in both lysosomes and secretory granules of chromaffin cells.

Administration, Oral↗

Zinc in the anterior pituitary of rat: a histochemical and analytical work.

Recent studies have suggested zinc to be a possible modulator of hormone secretion from the anterior pituitary. The three aims of the present study were: to estimate the total amount of zinc in the gland by instrumental analysis; to visualize the zinc at light and electron microscopical levels, and to estimate the amount of zinc that can be visualized by histochemical techniques. PIXE measurement showed the total amount of zinc to be 74 ng/mg dry weight in males and 100 ng/mg dry weight in females, which is a highly significant difference. Histochemically, the zinc was shown by a modified Timm method and the selenium method to be localized to the secretory granules, and to a smaller extent to the Golgi apparatus of the somatotrophs, corticotrophs and thyrotrophs. Chelation of tissue zinc by intravital dithizone treatment effectively blocked subsequent selenium and Timm staining in the secretory granules, and PIXE assays of the chelated metal (extracted into CCl4) showed it constituted less than 5% of the total zinc in the tissue. It is concluded from the study that zinc is present in the anterior pituitary of rats in rather high amounts and that loosely bound zinc, which is suggested to exert a biological effect by itself, can be located to the parts of the cells responsible for production, storing and release of hormones.

Animals↗

Evidence that selenium induces growth retardation through reduced growth hormone and somatomedin C production.

Growth retardation has long been known to be a major characteristic in selenium-intoxicated animals. As selenium is known to accumulate in the anterior pituitary, especially in the secretory granules of the somatotroph, we have investigated the GH secretion after GH-releasing factor 40 stimulation and the somatomedin C secretion in young male rats exposed to 15 mg sodium selenite/liter drinking water. The immediate output to 900 +/- 120 ng/ml GH in control animals was reduced to 200 +/- 69.4 ng/ml in selenium-treated animals. The somatomedin C level was reduced from 720 +/- 16 ng/ml in control to 119 +/- 17 ng/ml in selenium-treated animals. Both differences were highly significant. These findings suggest that growth retardation in selenium-treated rats could be mediated by reduced GH and somatomedin C production.

Animals↗

Accumulation of mercury in the anterior pituitary of rats following oral or intraperitoneal administration of methyl mercury.

A sensitive histochemical technique has been used to visualize the ultrastructural localization of mercury in the anterior pituitary of rats which have been exposed to methyl mercury. After administration of methyl mercury in the drinking water (20 mg X l-1 methyl mercury in distilled water) or intraperitoneally (daily dose 100 ug or 200 ug methyl mercury) intracellular accumulations of mercury were found in the lysosomes and granules of secretory cells (somatotrophs, thyrotrophs and corticotrophs). In non-secretory cells (follicular cell and marginal layer cells) mercury deposits were found in lysosomes. In orally treated rats, the number of mercury deposits increased significantly with time up to day 21. In rats exposed intraperitoneally, a continuous increase was seen in intracellular mercury accumulation. Apart from vacuolation of lysosomes, no structural damage was observed in the cells containing mercury.

Administration, Oral↗

Light and electron microscopical visualization of selenium in adrenal glands from rats exposed to sodium selenite.

A histochemical study was performed to determine the cellular localization of selenium in the adrenals from rats exposed to sodium selenite, as these organs were known to obtain the highest concentration in the rats. Male rats were treated either with 1-15 mg of sodium selenite for 14 days to 6 months in the drinking water, or with 1-20 mg as intraperitoneal injections. Selenium was shown to accumulate in both norepinephrenic and epinephrenic cells in a dose-dependent fashion. After oral exposure most deposits were found in the epinephrenic cells, whereas the norepinephrenic cells contained most in the injected animals. Fourteen days after a single injection (4 mg/kg), deposits could still be observed in the granules of the chromaffin cells. At the ultrastructural level, accumulations were primarily found in the chromaffin granules and to a lesser extent in the lysosomes. Selenium may possibly form bonds to endogenous zinc in the adrenals as has been suggested for the brain.

Adrenal Glands↗