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Biomedical subjects

A Bergh

Publications and source records attributed to A Bergh.

At least 145 records · Page 8Linked to original sources

Age-related differences in testicular microcirculation.

Different aspects of testicular microcirculation were studied in rats aged 20, 24 or 90 days, in order to determine if maturational changes in the testis could influence its vasculature. Using laser Doppler flowmetry, it was found that vasomotion was not present in 20-day-old rats, but it could be induced by hCG-treatment given 32 h prior to flow measurements. In rats aged 24 days vasomotion was present in the testis but it was not influenced by hCG treatment, in contrast to adult rats in which testicular vasomotion disappeared after hCG treatment. In all age-groups, hCG treatment induced an increase in testicular interstitial fluid (IF) volume, which was most pronounced in young rats. In young rats, as in adults, there was an increase in the volume density of polymorphonuclear (PMN) leucocytes in testicular blood vessels after hCG treatment. However, rats aged 20 or 24 days did not exhibit any significant extravascular migration of leucocytes as occurred in adult rat testis after hCG injection. The deposition of colloidal carbon particles observed in adult rats after hCG-treatment was also not seen in young rats. It is concluded that the vasculature of the immature rat testis responds to hCG stimulation with an increase in IF volume. However, when compared to adult rats, different mechanisms may be operating because no evidence for opening of inter-endothelial cell gaps was observed in the testis of young rats.

Aging↗

Immunohistochemical localization of inhibin-alpha in the testes of normal men and in men with testicular disorders.

Testicular biopsies from normal men and from men with testicular disorders were examined by immunohistochemistry for the presence of the inhibin-alpha subunit using two different antisera. Immunoreactive inhibin-alpha (irI-alpha) was found in Leydig cells in normal, oligospermic, and azoospermic men and in men with Klinefelter's syndrome, and it was also found in a Leydig cell tumour. hCG-treatment apparently increased the amount of immunoreactive inhibin-alpha, particularly in Leydig cells. Sertoli cells also contained irI-alpha but the staining intensity was considerably stronger in testes with impaired spermatogenesis or Sertoli-cell-only syndrome than in normal testes. It is suggested that the serum concentration of irI-alpha and inhibin in humans may, in a complex way, be related to both Leydig and Sertoli cell function, and that the relative contribution from these cells may change in cases of testicular malfunction.

Humans↗

A physiological increase in LH may influence vascular permeability in the rat testis.

Adult male rats were injected with different doses of hCG, or with 2.5 micrograms ovine LH subcutaneously, and other rats were mated with oestrous females. The animals were examined 4 h after treatments. Treatment with hCG resulted in a dose-dependent increase in leucocyte concentration in testicular blood vessels and in the number of blood vessels which could be labelled with intravenously injected carbon particles. Carbon leakage was not observed in control testes. Treatment with a low dose of ovine LH or inducing an endogenous LH peak by mating also resulted in leucocyte accumulation and vascular leakage of carbon in the testis. The magnitude of the response was considerably lower than after high doses of hCG. The physiological relevance of the discrete response observed after physiological LH stimulation is unknown but LH-induced changes in testicular microcirculation could be of interest for the understanding of the physiology and pathophysiology of the testis.

Animals↗

Bronchial epithelium in humans recently recovering from respiratory infections caused by influenza or mycoplasma.

Sixty three bronchial mucosal biopsies were collected from 12 patients recovering from respiratory infections with influenza virus (n = 8) and Mycoplasma (n = 4). The bronchoscopy was performed within 1-6 wks from the onset of symptoms. Of the 63 biopsies prepared for light microscopy, 27 biopsies from the influenza patients and 10 from the Mycoplasia patients were further analysed at the light and electron microscope level. The epithelium and the underlying stroma was analysed morphometrically and the results were compared to those of 39 biopsies from 27 healthy subjects. A slightly raised bronchial reactivity was noted in two patients. In the influenza patients the epithelial height was greater compared to that of the healthy subjects and subepithelial lymphocytosis was noted. Areas with damaged epithelium, epithelium shedding, and occasionally a thickened basement membrane, considered typical for asthma, occurred in both infected groups, and in the biopsies of the healthy subjects.

Adult↗

Structural characterization of bronchial mucosal biopsies from healthy volunteers: a light and electron microscopical study.

Bronchial mucosal biopsies were collected by flexible fibreoptic bronchoscopy (FFB) from normal healthy volunteers. The volunteers were not receiving any medication and had been free from respiratory infection for at least five weeks prior to the bronchoscopy. Biopsies with a minimum of 115 microns of undamaged perpendicularly sectioned epithelium were investigated by light and transmission electron microscopy. The height of the epithelium varied between 22-62.5 microns, with a median value of 41.5 microns. The volume density of the various epithelial cells in relation to the total epithelium was 61% for the ciliated and non-ciliated, non-secretory luminal cells, 6% for the goblet cells and 32% for the basal cells. The width of the lamina reticularis of the basement membrane ranged between 3-17.5 microns, with a median value of 8.5 microns. Blood vessels occupied 2.8% of the subepithelial tissue. Only a few inflammatory cells were seen in the connective tissue, volume density occupied by lymphocytes and polymorphonuclear granulocytes, 0.6% and 0.2% respectively. This study shows that structural damage is a common finding in biopsies collected by FFB. Mechanical damage of bronchial biopsies caused by the forceps should be considered before alterations in the epithelium are attributed to pulmonary disease.

Adult↗

Cryptorchidism: a registry based study in Sweden on some factors of possible aetiological importance.

STUDY OBJECTIVE: To examine the epidemiological characteristics of boys with cryptorchidism. DESIGN: Cohort survey using the Swedish personal identification code and Medical Birth Registry to link cryptorchid boys with their pregnancy and delivery data. They were compared with the total population of male births during the same period. SUBJECTS: 2861 cryptorchid boys born in Sweden between 1973 and 1982 were identified. Of these 437 could not be linked with their Medical Birth Registry information for various reasons, or were excluded because they were under 1 year of age at the end of 1982, leaving 2424 cases for study. The reference population comprised all boys born in Sweden during the same period (n = 458,601). MEASUREMENTS AND MAIN RESULTS: For each study variable, the observed number of cases among boys with cryptorchidism was compared with the expected number calculated from the whole population. A significant increase in intensity ratio for cryptorchidism was found with the first birth, caesarean section, toxaemia of pregnancy, and certain congenital abnormalities (hypospadias and subluxation of the hip). It was also more common in small for dates infants. There was a seasonal variation in cryptorchidism, with increased incidence in January-March. CONCLUSIONS: Cryptorchidism may be caused by hormonal influences during pregnancy, which could be affected by utero-placental factors involving placental dysfunction or by daylight hours, through pineal activity.

Birth Certificates↗

High and low doses of luteinizing hormone induce different changes in testicular microcirculation.

To study the effects of LH on total testicular blood flow and microcirculation, rats were treated with 2.5 or 25 micrograms LH sc and measurements were made on control rats and on LH-treated rats 1, 2, 3, 4, 6 and 12 h, after treatment. After treatment with 25 micrograms LH, total testicular blood flow, as measured with the radioactive microsphere method, was decreased at 6 h and increased at 12 h. Testicular microcirculatory blood flow was recorded with laser Doppler flowmetry and regular oscillations in blood flow, vasomotion, was observed in control rats. Vasomotion was not present 4 and 6 h after treatment with 25 micrograms LH, but returned at 12 h. Prior to and concomitantly with these changes in vasomotion, polymorphonuclear leukocytes accumulated in testicular microvessels and migrated into the interstitial tissue. These changes were followed, 6 h after treatment, by an increased vascular permeability, measured as increased testicular interstitial fluid volume. The lower dose of LH (2.5 micrograms), doubled plasma testosterone concentration and initially decreased interstitial fluid volume, and later induced a slight increase in blood vessel leukocytes. At the times studied, no changes could be observed in the other vascular parameters. In conclusion, it is suggested that LH, probably via some Leydig cell product, promotes regulatory effects on testicular microcirculation, but different magnitudes of LH stimulation induce different responses.

Animals↗

Changes of testicular cholesteryl ester hydrolase activity in experimentally cryptorchid rats.

A simple and reliable method was developed to determine the neutral cholesteryl ester hydrolase (CEH) activity in rat testes, using cholesteryl-[1-14C]-oleate as substrate. The activity was due to a soluble enzyme present in the cytoplasm of predominantly Sertoli cells, which could be shown after depleting the testes of Leydig cells with ethane dimethyl sulphonate. This treatment also revealed that the loss of CEH activity in abdominal testes of experimentally cryptorchid rats takes place in the Sertoli cells. In prepubertal rats made unilaterally cryptorchid at birth, the CEH activity was significantly higher in the abdominal than in the scrotal testes at 16 days of age. This is earlier than any previously described biochemical change and coincides with, or may even precede, the earliest morphological changes which are accumulation of lipid droplets in the Sertoli cells. The testicular CEH activity then decreased to 30 days of age in the abdominal testes, whereas the activity increased in the contralateral, scrotal testes. When adult rats were made unilaterally cryptorchid for 24 h, the CEH activity decreased rapidly in the abdominal testes. These results suggest that a derangement in cholesteryl ester metabolism is an early event in the pathogenesis of testicular degeneration in cryptorchidism.

Animals↗

Antiestrogens do not counteract the inhibitory effect of estradiol-17 beta on the growth of the Dunning R3327 prostatic adenocarcinoma.

The purpose of this study was to investigate if the local effects of estradiol on the Dunning R3327 prostatic adenocarcinoma were estrogen-receptor mediated. All rats with the transplantable Dunning R3327 prostatic adenocarcinoma were castrated on the first day of treatment and were supplemented with daily s.c. injections of testosterone propionate (0.1 mg) during the treatment period, lasting for 6 weeks. The following treatment groups were studied: castration + testosterone supplementation (C + T, control group), C + T and estradiol-17 beta (50 micrograms/daily s.c.), C + T and tamoxifen (1 mg twice a week s.c.), and C + T and estradiol-17 beta in combination with tamoxifen. Tumor volumes were measured every week. At the end of the treatment period, pieces of the tumors were taken for morphological studies and estrogen-receptor analysis. In the groups of rats given tamoxifen treatment no estrogen-receptor binding was detectable in prostatic tumors, but, despite this, tamoxifen did not prevent either the inhibitory effect of estradiol-17 beta on the tumor growth rate or the estrogen-induced decrease of volume density of prostatic glandular epithelium. In contrast, the estrogen-induced increase of volume density of the stroma was abolished by tamoxifen, suggesting that this effect may be mediated by the estrogen receptor. A morphometrical method for estimating the growth of different tumor compartments is presented. Treatment with estradiol-17 beta, both with or without combined treatment with tamoxifen, reduced the growth of both the tumor epithelium and stroma. The direct effect of estradiol-17 beta on the growth and morphology of the Dunning R3327 prostatic adenocarcinoma seemed not to be mediated by the estrogen receptor.

Adenocarcinoma↗

Treatment with an LHRH agonist or hCG increases interstitial fluid volume and permeability to Evans blue in the mouse testis.

Treatment of adult mice with 1 microgram of an LHRH-agonist or with 5 i.u. hCG, subcutaneously, resulted in an increase in the permeability to intravenously injected Evans blue into the testicular interstitial space and in the volume of testicular interstitial fluid. These changes are probably related to an increase in vascular permeability but, in contrast to the situation in rats, this was accompanied neither by an accumulation of polymorphonuclear leucocytes in testicular blood vessels nor by the formation of large inter-endothelial cell gaps in postcapillary venules. The mechanisms mediating the gonadotrophin-induced increase in vascular permeability in the mouse testis thus remain unknown.

Animals↗

Direct effects of oestradiol on growth and morphology of the Dunning R3327H prostatic carcinoma.

Male Copenhagen x Fischer F1 rats were implanted with Dunning R3327H prostatic carcinoma, castrated when the tumours became palpable and were then treated with testosterone, testosterone in combination with oestradiol or oestradiol alone for four weeks. Treatment with oestradiol produced the smallest tumours. The testosterone-stimulated growth of tumours was inhibited by oestradiol. The adenocarcinoma was moderately to well-differentiated. Morphometric analysis of the composition of the tumours showed that oestradiol stimulated tumour stroma and inhibited glandular epithelium. These effects were produced concomitantly with decreased overall tumour growth. Testosterone stimulated all cell types of the tumour.

Animals↗

Leucocytes mediate the hCG-induced increase in testicular venular permeability.

Human chorionic gonadotrophin (hCG) treatment of adult male rats induces microvascular changes in the testis consisting of abolished vasomotion, an accumulation of leucocytes in postcapillary venules and increased vascular permeability. To study the role of leucocytes, rats were made leucopenic with a specific antineutrophil serum (ANS). Testicular interstitial fluid volume was decreased in leucopenic rats. Leucopenic rats also failed to show an hCG-induced increase in venular permeability as in saline-treated rats. The normally pulsatile blood flow pattern (vasomotion) persisted in leucopenic rats but was abolished after hCG treatment both in saline-treated and leucopenic rats. Plasma testosterone concentration after hCG treatment was not affected by elimination of circulating polymorphonuclear (PMN) leucocytes. It is concluded that PMN leucocytes mediate in part the hCG-induced increase in testicular venular permeability but not the hCG-induced inhibition of vasomotion.

Animals↗

Testicular blood flow and microcirculation in rats after treatment with ethane dimethyl sulfonate.

The effects of ethane dimethyl sulfonate (EDS) on total testicular blood flow, microcirculation, and the testicular interstitial fluid volume (IFV) in rats were studied. In agreement with previous studies, treatment of control rats with human chorionic gonadotropin (hCG) induced an increase in IFV and total testicular blood flow as measured with radioactive microspheres. These effects of hCG were completely abolished in rats pretreated with EDS; in EDS-treated rats not receiving any hCG, there were decreases in IFV when compared with untreated control rats. Furthermore, the pulsatile pattern of testicular microcirculation registered with laser-Doppler flowmetry was abolished after EDS treatment, and this effect was not influenced by hCG treatment. The hCG-induced increase in IFV is associated with an increased accumulation of polymorphonuclear leukocytes locally in the testis, but this accumulation of leukocytes was not observed in rats pretreated with EDS. It was concluded from the present study that hCG-induced changes in total testicular blood flow and testicular microcirculation require functionally intact Leydig cells.

Animals↗

Treatment with hCG increases the size of Leydig cells and testicular macrophages in unilaterally cryptorchid rats.

Adult, unilaterally cryptorchid rats were treated with a single injection of 200 i.u. human chorionic gonadotrophin (hCG). The morphological response of Leydig cells and testicular macrophages at 24 and 72 h after treatment was quantified using morphometry. Treatment with hCG induced an increase in the volume density of Leydig cells and macrophages, as well as in the average cell profile area of individual Leydig cells and macrophages in both scrotal and abdominal testes. However, the relative response was considerably larger in abdominal than in scrotal testes, and there was a strong positive correlation between the response of Leydig cells and macrophages. It is suggested that hCG, probably via effects on Leydig cells, also influences the function of testicular macrophages.

Animals↗

Effect of an LHRH-agonist on testicular microcirculation in hypophysectomized rats.

The effect of an LHRH-agonist on testicular vasomotion was studied in adult hypophysectomized rats. At 0.5 and 1 h after injection of 1 microgram LHRH-agonist, no effect on vasomotion was observed, but after 2 h the pulsatile blood flow pattern had changed to continuous flow in 50% of the rats. At 4 h after treatment with LHRH-agonist, vasomotion was not detected in the testis of any rat. In addition, at the latter time an increased number of polymorphonuclear leucocytes (PMNs) were observed in testicular microvessels, and some PMNs had migrated into the interstitial space. These findings are discussed in relation to the well-known stimulatory effect of LHRH-agonists on testicular interstitial fluid volume.

Animals↗