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Biomedical subjects

A Bergh

Publications and source records attributed to A Bergh.

At least 163 records · Page 9Linked to original sources

Intratesticular steroids and gonadotrophin receptor concentrations in the testes of immature unilaterally cryptorchid rats.

Testicular descent was prevented unilaterally in newborn rats. In this experimental model of cryptorchidism the first morphological changes are noted in the abdominal testis at 16 days of age. Testicular weight was increased in the abdominal testis at 16 days of age, was unaffected at 20 days but was decreased at 30 days of age. The concentrations of LH and FSH receptors, and the hCG-stimulated progesterone and testosterone secretion in vivo were analysed in scrotal and abdominal testes at different ages. LH- and FSH-receptor content per testis were unaffected by cryptorchidism at 12, 16 and 20 days of age but were depressed markedly at 30 days of age. At 20 days of age (but not earlier) hCG-stimulated progesterone was reduced while testosterone secretion remained unchanged. It is concluded that the early functional changes in abdominal testes are not related to changes in gonadotrophin receptor content.

Animals↗

Treatment of rats with hCG induces inflammation-like changes in the testicular microcirculation.

Adult rats were injected subcutaneously with 50 i.u. hCG and vascular permeability was compared to that in saline-treated control rats by two independent methods. At 4 h after hCG treatment the rats were injected intra-arterially (i.a.) with FITC-labelled macromolecular dextran (Mr 150,000) and the testicular microcirculation was studied in vivo by using a fluorescence microscope. Other rats were injected i.a. with a suspension of colloidal carbon and the location of leaking blood vessels was recorded in sections from the testes by light and electron microscopy. In hCG-treated animals leucocytes were found adhering to the endothelium in post-capillary venules and in these venular segments dextran was leaking into the interstitium. Carbon particles were deposited in the walls of post-capillary venules and leucocytes migrated through open interendothelial cell gaps in hCG-treated animals. In control animals leucocyte adhesion and migration were not observed, the injected dextran remained in the circulation and the blood vessels were not labelled by carbon. It is suggested that the hCG-induced increase in testicular interstitial fluid volume, like the tissue oedema in inflammation, is caused by a leucocyte-mediated increase in venular permeability.

Animals↗

Terbutaline treatment inhibits the hCG-induced increase in venular permeability in the rat testis.

Treatment with hCG results in an increase in venular permeability in the rat testis. This change in vascular permeability can be detected by the carbon-labelling technique, by measurement of the volume of interstitial fluid and by quantification of the leucocyte migration into the interstitial space. Carbon-labelling, interstitial fluid volume and leucocyte migration were all reduced in rats treated with hCG+ terbutaline compared to the values in animals given hCG only. However, terbutaline treatment did not influence the hCG-induced increase in testosterone secretion. These observations suggest that the hCG-induced increase in vascular permeability in the testis can be reduced by a beta-adrenergic agonist.

Animals↗

Effects of oestradiol-17 beta on testicular microcirculation in rats.

The effect of oestradiol-17 beta on testicular microcirculation in intact and hypophysectomized rats was studied before and after treatment with human chorionic gonadotrophin (hCG). Treatment of intact rats with oestradiol-17 beta for 5 days did not influence vasomotion but decreased testicular interstitial fluid volume (IFV). Treatment of intact rats with 50 IU hCG 8 h before the experiment began induced an increase in testicular IFV, abolished vasomotion and increased the accumulation of polymorphonuclear leucocytes in the testicular venules and interstitium. These changes were unaffected by pretreatment with oestradiol-17 beta, despite the decreased testosterone production. However, pretreatment with oestradiol-17 beta potentiated the hCG-induced migration of polymorphonuclear leucocytes to the interstitium. The interstitial fluid volume and number of polymorphonuclear leucocytes in blood vessels were decreased in hypophysectomized rats, and vasomotion was abolished. Daily treatment with 5 IU hCG increased the IFV and the number of polymorphonuclear leucocytes in blood vessels, and preserved vasomotion. Treatment of hypophysectomized rats with oestradiol-17 beta decreased testosterone production but did not influence basal IFV, vasomotion or the changes in IFV and vasomotion induced by 5 IU hCG. The present study shows that the regulation of testicular vascular permeability and vasomotion may not be directly related to testicular steroidogenesis, and that oestrogens are probably not involved as a mediator of the hCG-induced changes in testicular microcirculation.

Animals↗

Production of lactate and tissue plasminogen activator in vitro by seminiferous tubules obtained from adult unilaterally cryptorchid rats.

Pieces of seminiferous tubules obtained from adult unilaterally cryptorchid rats were incubated in vitro and the effect of FSH on the secretion of lactate and tissue-plasminogen activator (t-PA) was studied. Tubules from abdominal testes secreted less lactate than scrotal tubules. On the other hand, the basal secretion of t-PA was similar but the FSH-stimulated t-PA secretion was larger from abdominal than from scrotal tubules. These results indicate a more specific dysfunction of the Sertoli cells in cryptorchidism than earlier recognized.

Abdomen↗

Testicular vascular resistance in the rat after intratesticular injection of an LRH-agonist.

Testicular vascular resistance (TVR) was estimated 1, 2, 4 and 8 h after unilateral intratesticular injection of 1 or 10 ng of an LRH-agonist (A). The lower dose had no effect on plasma levels of testosterone or LH, but there was a significant increase in TVR 2 h after injection when compared to the vehicle-injected contralateral testis. Injection of 10 ng LRH-A induced an increase in plasma levels of LH at 1 and 2 h after treatment and in the plasma levels of testosterone at 1, 2 and 4 h. In the same rats there was a decrease in TVR at 2, 4 and 8 h after LRH-A treatment compared to the contralateral testis. It is concluded that LRH-A can have both stimulatory and inhibitory effects on TVR in the rat and that the direction of this effect may be related to the ambient level of LH.

Animals↗

Testicular microcirculation in the rat studied by videophotometric capillaroscopy, fluorescence microscopy and laser Doppler flowmetry.

Testicular capillary blood flow was studied in rats using laser Doppler flowmetry, in vivo fluorescence microscopy and videophotometric capillaroscopy. All the methods revealed rhythmical oscillations in testicular microcirculation with a periodicity of 4-10 c.p.m. In arterioles, capillaries and small post-capillary vessels, periods of continuous blood flow alternated with periods of no or very low flow. No visible leakage of dextran-150 was observed from the testicular blood vessels. Four, 8 and 16 h after an s.c. injection of 200 IU hCG the blood flow was continuous and there was leakage of dextran-150 from the microvessels to the interstitial tissue. Twenty-four and 32 h after hCG the blood flow pattern was again rhythmical, and at 32 h there was no leakage of dextran-150. This suggests that hCG induces changes in blood flow and transvascular fluid exchange in the testis, perhaps by altering smooth muscle activity at the arteriolar-level.

Animals↗

Are leukocytes involved in the human chorionic gonadotropin-induced increase in testicular vascular permeability?

Adult male rats were given a single sc injection of human CG (hCG). The volume density of polymorphonuclear leukocytes (PMNs) located in blood vessels or in the interstitial space was determined by morphometry. The volume of testicular interstitial fluid (IF) was also measured. hCG in doses from 50-800 IU increased the IF volume 8 h after treatment and resulted in migration of PMN into the interstitial space. In contrast, treatment with 12.5 IU hCG, although increasing intratesticular testosterone to about 50% of the maximal value, did not increase the volume of IF, and no leukocytes appeared in the interstitial space. Treatment with 50 IU hCG sc increased the volume of IF at 8, 16, and 32 h after treatment. The increase in IF volume, which is a reliable estimator of changes in the vascular permeability, was preceded by an intravascular accumulation of PMNs. Four hours after hCG treatment, there was a 6-fold increase in the volume density of intravascular PMNs. Later, leukocytes migrated into the interstitial space reaching a maximal concentration 8 h after hCG treatment (at that time 6.4 +/- 0.7 X 10(-5) of the total testis volume was composed of leukocytes). The number of interstitial PMNs declined thereafter and by 32 h they were no longer observed. It is suggested that leukocytes could be involved in mediating the hCG-induced increase in vascular permeability in the testis.

Animals↗

Relationship between human chorionic gonadotrophin-induced changes in testicular microcirculation and the formation of testicular interstitial fluid.

The relationship between testicular vascular permeability and testicular microcirculation as measured by laser Doppler flowmetry was studied in adult rats. In untreated control animals there was an oscillatory testicular blood-flow pattern with a frequency of 10.6 +/- 0.8 pulses/min and the amount of testicular interstitial fluid (IF) collected was 61.5 +/- 2.2 microliter/g testis. Treatment of the rats with 25-200 i.u. human chorionic gonadotrophin (hCG) s.c. 8 h before the experiment resulted in a change in the testicular flow pattern from pulsatile to continuous and an increase in IF volume. Treatment with hCG (50 i.u., s.c.) changed the testicular blood-flow pattern from oscillatory to continuous 4, 8 and 16 h after treatment. The flow pattern returned to being pulsatile 32 h after treatment with hCG. The IF information was increased at those times when the blood-flow pattern was continuous. No effects on blood flow or IF formation were observed with 12.5 i.u. hCG s.c. The present study shows a dose- and time-dependent covariation between the increase in testicular IF volume and the disappearance of the pulsatile flow in testicular microcirculation. It appears that a continuous flow pattern favours the transport of fluid from blood vessels to the interstitium.

Animals↗

Development of stage-specific paracrine regulation of Leydig cells by the seminiferous tubules.

The size of peritubular Leydig cells surrounding tubules in different stages of the spermatogenic cycle was determined in 43- and 47-day-old male rats. A stage-dependent variation in the size of peritubular Leydig cells was not present in 43-day-old rats, but by 47 days those Leydig cells closely adjacent to tubules at stages VII-VIII were larger than others. At 43 days of age spermatogenesis had developed up to step 18 spermatids in late stage VI tubules. At 47 days of age the first mature sperm had just been released from the seminiferous epithelium, and consequently the first wave of the spermatogenic cycle was completed. Tubules at stages VII-VIII therefore acquire the ability to influence surrounding Leydig cells when they contain step 19 spermatids. It remains to be shown whether this maturation step is due to inherent maturation of the Sertoli cells or if step 19 spermatids specifically modulate Sertoli cell function.

Aging↗

Effect of cryptorchidism on the morphology of testicular macrophages: evidence for a Leydig cell-macrophage interaction in the rat testis.

Macrophages and Leydig cells in the testes of adult rats which had been made bilaterally or unilaterally cryptorchid at birth were examined by morphometry for total mass, total number, volume density, and individual cell profile area. The total Leydig cell mass and the average size of Leydig cells, as well as the total mass and the average size of macrophages, were reduced in unilateral abdominal testes, but were unchanged in bilateral abdominal testes when compared to scrotal testes. Leydig cell and macrophage morphology were correlated suggesting a functional coupling between these cell types. The physiological significance of this cell interaction remains to be discovered.

Animals↗

Testicular blood flow, vascular permeability, and testosterone production after stimulation of unilaterally cryptorchid adult rats with human chorionic gonadotropin.

Testicular blood flow, testosterone production, and the formation of testicular interstitial fluid (IF) were studied in unilaterally cryptorchid rats, basally, 8 h and 24 h after treatment with 200 IU human CG (hCG). Testicular blood flow was lower in the abdominal testis in both control rats and hCG-treated rats than in the scrotal testis within the same treatment group. The scrotal testicular blood flow increased significantly 24 h after hCG treatment, but not after 8 h. In the abdominal testis, there was a significant increase of blood flow 8 h after hCG, but not 24 h after. The formation of IF was subnormal in the abdominal testes of control rats, but this was corrected in hCG-treated rats, where there was a significant increase of IF in both abdominal and scrotal testes. The total endothelial surface of small blood vessels was decreased in abdominal testes. Testosterone concentration in the spermatic vein was significantly lower on the abdominal side than on the scrotal side in both control and hCG-treated rats. The concentration of testosterone was lower in IF on the abdominal side in control rats, but after hCG the testosterone concentration was similar in both scrotal and abdominal testes, indicating a trapping of testosterone in the abdominal testis. The outflow of testosterone in the spermatic vein was significantly increased at both 8 and 24 h after hCG from both the scrotal and abdominal testes, although it was always smaller from the abdominal testis. The lower secretion of testosterone from the abdominal testis after hCG was mainly due to reduced blood flow and not to any disability of the Leydig cells of abdominal testes to produce testosterone.

Animals↗

Altered concentrations of gonadotrophin, prolactin and GnRH receptors, and endogenous steroids in the abdominal testes of adult unilaterally cryptorchid rats.

Testicular descent was prevented unilaterally in newborn rats by cutting the gubernaculum testis. At 100 days of age, the number of Leydig and Sertoli cells per testis, the concentration of receptors for LH, FSH, prolactin and GnRH, and endogenous concentrations of progesterone and testosterone were determined. The weight of the abdominal testes was reduced by 80%, but in spite of this they contained as many Sertoli (32.8 +/- 1.3 X 10(6), mean +/- s.e.m., n = 6) and Leydig (28.2 +/- 1.7 X 10(6) cells as did scrotal testes (32.1 +/- 2.5 X 10(6) and 24.3 +/- 1.2 X 10(6) respectively). The numbers of receptors for LH (3.2 +/- 0.2 and 1.0 +/- 0.2 pmol/testis, mean +/- s.e.m., n = 11), FSH (358 +/- 11.0 and 96.3 +/- 12.6 fmol/testis) and prolactin (535 +/- 32.7 and 92.4 +/- 13.2 fmol/testis) were reduced (P less than 0.001) in abdominal testes, but the number of GnRH receptors was unaffected (8.9 +/- 1.4 and 12.1 +/- 1.8 fmol/testis, n = 6). Testicular testosterone concentration (30.9 +/- 4.4 vs 15.4 +/- 3.2 ng/g, n = 11, P less than 0.001), but not that of progesterone (0.87 +/- 0.10 vs 1.01 +/- 0.21 ng/g), was decreased in abdominal testes. The decreased receptor and androgen values reflect functional disturbances in the abdominal testes. The changed local milieu within abdominal testes may reduce hormone receptor concentrations which are then involved in the observed Leydig cell dysfunction.

Animals↗

Toxic effects of the antifertility agent gossypol in male rats.

In the present investigation the influence of gossypol on the male sex function and toxicology in the rat have been studied. Gossypol was injected daily for 5 weeks to adult male rats of the Sprague-Dawley strain with 1 or 10 mg/kg body wt. The low dose of gossypol (1 mg/kg body wt.) did not have any effect on the following parameters: plasma testosterone concentrations, body growth, kidney weights, sex organ weights (ventral prostate, seminal vesicle, epididymis), testicular weights, blood flow to testes, epididymides and ventral prostate as measured with the microsphere technique, intraarterial blood pressure and morphology of testis and epididymis. The plasma testosterone response to acute LH-injection was not significantly different in gossypol-treated rats when compared to control rats. The high dose of gossypol (10 mg/kg body wt) caused signs of tubular degeneration, retarded body growth, markedly reduced testosterone concentrations, involutions of the ventral prostate and seminal vesicles and gastrointestinal disturbances. After 5 weeks of treatment the mortality rate was 13%. It is concluded that gossypol is a very toxic substance in rats, since only a 10-fold increase of a non-effective dose caused serious side effects in addition to its antifertility effects.

Animals↗

Stimulatory effect of an LHRH-agonist on testicular blood flow in hypophysectomized rats.

UNLABELLED: The effect of an LHRH-agonist (A) on testicular blood flow and plasma testosterone levels was studied in adult hypophysectomized rats. Subcutaneous injection of 1 microgram LHRH-agonist 2 or 4 h prior to experiment induced an increase in testicular blood flow. ( CONTROLS: 21.1 +/- 2.8 ml/100 g X min; LHRH-A + 2 h: 28.9 +/- 3.3 ml/100 g X min; LHRH-A + 4 h: 32.4 +/- 4.1 ml/100 g X min P less than 0.05; all mean +/- SEM). There was also a significant increase in plasma testosterone levels at 2 h (P less than 0.01) and 4 h (P less than 0.01) after treatment with the LHRH-agonist, with a peak at 2 h.

Animals↗

Early signs of Sertoli and Leydig cell dysfunction in the abdominal testes of immature unilaterally cryptorchid rats.

Testicular descent was prevented unilaterally by cutting the gubernaculum testis of newborn rats. When 20 days old unilaterally cryptorchid rats were injected intraperitoneally with 2 micrograms bFSH per gram body weight and killed 6 h later when testicular testosterone (T) and oestradiol (E2) concentrations were determined. The increase in E2 was subnormal in abdominal testes. In 18-day-old unilaterally cryptorchid rats the efferent ducts were ligated bilaterally, and the rats were killed 48 h later. The weight increase, due to accumulation of seminiferous tubule fluid, was significantly greater in the abdominal testes. In contrast, the ABP content of the abdominal epididymis was subnormal in 20-day-old unilaterally cryptorchid rats. Unilateral orchidectomy was performed in 16-day-old unilaterally cryptorchid rats and at 20 days of age intratesticular T and E2, and plasma FSH and LH concentrations were determined and compared to that in 20-day-old control unilaterally cryptorchid rats. Removal of an abdominal testis resulted in increased plasma FSH and intratesticular E2, whereas plasma levels of LH and intratesticular levels of T were unaffected. Removal of a scrotal testis resulted in increased plasma FSH and LH coupled with increased intratesticular T and E2. Rats with a single abdominal testis had higher plasma FSH and LH and intratesticular T, but similar intratesticular E2, than rats with a single scrotal testis. It is concluded that Sertoli and Leydig cell function are influenced by cryptorchidism at a stage when the temperature difference, and the morphological differences between the testes are very discrete.

Androgen-Binding Protein↗

Local regulation of Leydig cells by the seminiferous tubules. Effect of short-term cryptorchidism.

Unilateral cryptorchism was induced in adult rats for 24 h, and its effect on testicular morphology and intratesticular testosterone concentration after hCG-stimulation were studied. In seminiferous, tubules from abdominal testes an increased number of degenerating germ cells was noted in stages XIV-III of the spermatogenic cycle and Sertoli cells contained an increased amount of lipid droplets in stages XIV-VIII. However, germ cells and Sertoli cells from tubules at other stages of the cycle appeared unaffected. In scrotal testes the size of peritubular Leydig cells varied in phase with the spermatogenic cycle. The largest cells were found adjacent to stage VII-VIII and the smallest adjacent to stage XI-XII. In abdominal testes no stage-dependent variation in the size of peritubular Leydig cells was seen. Perivascular Leydig cells were of equal size in abdominal and scrotal testes. The testicular testosterone concentration following stimulation with a low dose of hCG was significantly lower in abdominal testes. It is suggested that the seminiferous tubules locally modulate Leydig cell function and that the stage specific stimulatory influence from stage VII-VIII is rapidly lost during experimental cryptorchidism.

Animals↗