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L Daehlin

Publications and source records attributed to L Daehlin.

At least 37 records · Page 2Linked to original sources

Effects of 6-methylene progesterone on growth, morphology, and blood flow of the Dunning R3327 prostatic adenocarcinoma.

Copenhagen x Fisher F1 rats were implanted with the androgen-dependent Dunning R3327 prostatic adenocarcinoma. When the tumors had median volumes of ca 470 mm3, the rats were castrated and/or treated with 6-methylene-4-pregnene-3,20-dione (6MP) in different doses. Tumor growth inhibition occurred in all castrated and treated groups, with decrease in volume of the epithelial compartment in the intact group. Tumor volumes at the highest dose level of 6MP equalled those observed in the castrate group. Plasma levels of testosterone were within the normal range. The administration of 6MP surprisingly induced an increment of tumor blood flow in the castrate group. Also in castrated and testosterone-supplemented animals, 6MP induced a reduction of prostatic tumor growth. Through the castration-like effect on tumor growth, the use of 6MP may represent an attractive alternative to castration for treatment of androgen-responsive prostate cancer.

Adenocarcinoma↗

Effects of ethinyl oestradiol/polyoestradiol phosphate and estramustine phosphate on some proteins related to haemostasis in prostatic carcinoma patients.

Twenty-four previously untreated patients with carcinoma of the prostate were prospectively randomized to one of the following treatments: (1) ethinyl oestradiol combined with polyoestradiol phosphate (EE/EP); (2) estramustine phosphate (EM); (3) bilateral orchiectomy. The effects on some plasma proteins related to haemostasis were studied by measuring the concentrations of alpha-1-antitrypsin, orosomucoid, haptoglobin, antithrombin III, C1-inhibitor and von Willebrand's factor before and 3 months after the start of treatment. Orchiectomy induced a reduction of alpha-1-antitrypsin and haptoglobin, while the other studied proteins were unaffected. It was found that both EE/EP and EM treatment induced significant decreases of orosomucoid, haptoglobin, antithrombin III and C1-inhibitor, while the same treatment increased the plasma concentration of alpha-1-antitrypsin. None of these treatments showed any influence on the plasma concentration of the von Willebrand factor. No differences were observed between EE/EP and EM for any of the studied proteins, suggesting comparable oestrogenic effects of these forms of treatment in patients with prostatic carcinoma. The findings are discussed in relation to the proposed difference in thromboembolic complications between EE/EP and EM treatments of prostatic carcinoma patients.

Aged↗

Squamous cell carcinoma of the urinary bladder.

Thirteen patients with squamous cell carcinoma of the bladder were reviewed. All tumours were muscle invasive at the time of diagnosis. One third of the patients were irradiated, either before cystectomy or as a full course radiotherapy. The 1-year and 5-year survivals were 25 and 17%, respectively. Only cystectomized patients were alive after 5 years.

Aged↗

Prostatic abscess: imaging with transrectal ultrasound. Case report.

A 50-year-old man presented with acute urinary retention and urosepsis. Transrectal ultrasonography (TUS) of the prostate demonstrated an abscess. Transperineal US-guided aspiration of pus, urinary bladder catheterization together with systemically administered antibiotics led to an uneventful recovery. TUS was a rapid diagnostic aid for differentiation between prostatitis and prostatic abscess; the appearance of an hypoechoic process within the prostate suggests an abscess.

Abscess↗

Cerebral air embolism after transthoracic aspiration with a 0.6 mm (23 gauge) needle.

A 54 yr old man experienced weakness in his legs, ataxia and subsequent urinary retention after a percutaneous fine-needle aspiration of a tumor in the right lower lobe. Clinical neurological examination and electroencephalography revealed signs of a brain stem lesion, probably due to an air embolism to the basilar artery. The symptoms and signs gradually disappeared prior to, as well as after, hyperbaric oxygen treatment. We believe this to be the first case of air embolism after transthoracic puncture with a 23 gauge needle to be reported in medical literature.

Biopsy, Needle↗

Depressed testosterone release from testicular tissue in vitro after withdrawal of oestrogen treatment in patients with prostatic carcinoma.

Bilateral orchiectomy was performed in patients with prostatic carcinoma after oestrogen treatment for different periods of time. Testicular slices were incubated in vitro to examine the effect of previous oestrogen treatment on testosterone production. After short-term treatment, the testicular tissue responded to human chorionic gonadotrophin by testosterone production. This was in contrast to long-term administration of oestrogen which induced arrest of testosterone synthesis. The results suggest irreversible changes of Leydig cell function after long-term oestrogen treatment.

Chorionic Gonadotropin↗

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↗

Blood flow in the Dunning R3327H rat prostatic adenocarcinoma; effects of oestradiol and testosterone.

Copenhagen X Fischer F1 rats were implanted with Dunning R3327H prostatic adenocarcinoma and studied over a period of three weeks. The tumour volumes in intact and testosterone supplemented castrated rats showed parallel increases. After castration alone the tumour volumes decreased. Treatment of castrates with oestradiol and testosterone combined produced an arrest of tumour growth, suggesting that oestradiol had a direct inhibitory effect on tumour growth. Blood flow in tumours was measured using the microsphere technique. In intact rats, tumour blood flow per unit of weight decreased with increasing weight of tumours and blood flow in peripheral parts was higher than in central parts of large tumours. Oestradiol in combination with testosterone increased tumour blood flow.

Adenocarcinoma↗

The oestrogenic effects of ethinyl oestradiol/polyoestradiol phosphate and estramustine phosphate in patients with prostatic carcinoma. A comparative study of oestrogen sensitive liver proteins, gonadotrophins and prolactin.

Thirty previously untreated patients with carcinoma of the prostate were prospectively randomised to one of the following treatments: ethinyl oestradiol (Etivex) combined with polyoestradiol phosphate (Estradurin); estramustine phosphate (Estracyt); bilateral orchiectomy. Oestrogenic effects were measured by blood levels of pregnancy zone protein, sex hormone binding globulin, LH, FSH and prolactin. During a follow-up period of 6 months, estramustine phosphate and ethinyl oestradiol/polyoestradiol phosphate induced comparable changes in these proteins, suggesting comparable oestrogenic effects of these two forms of treatment in patients with prostatic carcinoma.

Aged↗

Relative affinities of estramustine phosphate metabolites to the cytosol oestrogen receptor of rat testis.

A competitive binding assay was used for analysis of the affinities of ethinyl oestradiol, diethylstilboestrol and metabolites of estramustine phosphate to the oestrogen receptor of rat testis. The affinities were ranked as follows: ethinyl oestradiol greater than oestradiol-17 beta greater than diethylstilboestrol much greater than estramustine. Estromustine did not reveal any oestrogen receptor affinity. The results support the concept that estramustine and estromustine do not mediate the oestrogenic effects of estramustine phosphate. The oestrogenicity of estramustine phosphate is suggested to be mainly due to the metabolite oestradiol-17 beta.

Animals↗

Effects of oestradiol-17 beta and ethinyl oestradiol on human testicular steroidogenesis in vitro.

The inhibition of human testicular testosterone production in vitro by oestrogen was studied by measuring effects of oestradiol-17 beta and ethinyl oestradiol on the 3 beta-hydroxysteroid dehydrogenase/isomerase and the delta 4-pathway of testosterone synthesis. Progesterone, 17 alpha-hydroxyprogesterone, androstenedione and testosterone concentrations of incubation media were all depressed after oestrogen addition. To minimize differences in substrate amounts between incubations, 3H-labelled pregnenolone, progesterone, 17 alpha-hydroxyprogesterone or androstenedione was added to the incubation media. The conversion of pregnenolone, progesterone and 17 alpha-hydroxyprogesterone was inhibited by oestrogen. It is concluded that oestrogen inhibits 3 beta-hydroxysteroid dehydrogenase/isomerase, 17 alpha-hydroxylase and C17-20-lyase enzyme activities of human testicular tissue in vitro while 17 beta-ketosteroid reductase activity is unaffected.

17-alpha-Hydroxyprogesterone↗

Testosterone-induced decrement of prostatic vascular resistance in rats is reversed by estrogens.

The function and growth of the rat prostate are stimulated by androgens and inhibited by estrogens. To study the influence of these hormones on the prostatic blood flow, prostatic vascular resistance was measured in castrated adult rats, which were testosterone supplemented and treated with different estrogenic substances. Prostatic blood flow was measured using the microsphere technique. Testosterone supplementation for 8-9 days after castration resulted in decreased vascular resistance in both the ventral and dorsolateral prostates. In testosterone-supplemented rats, treatment for the same period of time with estradiol benzoate, ethinyl estradiol, and diethylstilbestrol induced increased vascular resistance in both the ventral and dorsolateral prostates. However, treatment with estromustine or estramustine did not change prostatic vascular resistance significantly. It was concluded that the testosterone-induced decrease of prostatic vascular resistance was reversed by estradiol, ethinyl estradiol, and diethylstilbestrol, possibly by a direct effect on the prostate.

Animals↗

Effects of human chorionic gonadotrophin, oestradiol and estromustine on testicular blood flow in hypophysectomized rats.

The effects of human chorionic gonadotrophin (hCG), eostradiol benzoate (E2) and estromustine (Eo) on testicular and prostatic blood flow and plasma levels of testosterone were studied in hypophysectomized rats. Daily injections of 5 IU hCG induced a significant increase in testicular blood flow when measured after 8-9 days treatment. This stimulatory effect was inhibited by concomitant injection of E2 (50 micrograms/day) but not by Eo. In contrast, the stimulatory effect of hCG on plasma levels of testosterone was inhibited by administration of E2 as well as by Eo. This inhibition was correlated with decreased blood flow to the prostate. The present study gives further support to the hypothesis the oestrogens have direct effects on the testis and prostate.

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↗

Direct inhibitory effects of natural and synthetic oestrogens on testosterone release from human testicular tissue in vitro.

Human testicular slices were incubated in vitro in order to examine the direct effects of natural and synthetic oestrogens on testosterone secretion. In the presence of human chorionic gonadotrophin (10 IU per ml), oestradiol-17 beta (1 or 10 micrograms per ml) and ethinyl oestradiol (0.1, 1 or 10 micrograms per ml) inhibited testosterone release into the media in a dose dependent manner. The addition of estramustine phosphate, estromustine, diethylstilboestrol or diethylstilboestrol diphosphate in comparable concentrations produced no significant effects on testosterone release.

Adenocarcinoma↗

On the effects of oestrogen in the male. Some effects of different oestrogenic substances in rats and men with prostatic carcinoma.

In vitro incubations of human testicular tissue responded to human chorionic gonadotrophin with testosterone release in a dose-dependent manner. The release of testosterone increased with incubation time. The stimulated release of testosterone was inhibited by oestradiol and ethinyl oestradiol in a dose-dependent manner, suggesting that these oestrogens exert direct inhibitory effects on the human Leydig cells. Estramustine phosphate, estromustine, diethylstilboestrol and diethylstilboestrol diphosphate did not inhibit testosterone release. Hypophysectomized rats were treated for 8-9 days with human chorionic gonadotrophin, which maintained testicular blood flow within the physiological range. Some of the animals received additional treatment with oestradiol or estromustine. Oestradiol and estromustine depressed plasma testosterone concentration. In contrast to estromustine, oestradiol inhibited testicular blood flow, as measured by the microsphere technique. Intact rats were castrated, supplemented with testosterone and concomitantly treated with different oestrogenic substances. Testosterone supplementation induced increase of prostatic blood flow, which was inhibited by oestradiol, ethinyl oestradiol or diethylstilboestrol. Estramustine and estromustine had no effect on prostatic blood flow. The growth of a transplantable rat prostatic carcinoma (Dunning R3327H) was studied after castration, testosterone substitution or testosterone substitution in combination with oestradiol treatment. Oestradiol inhibited tumour growth, possibly by direct action. The blood flow in tumours in intact animals decreased with increasing tumour volume. Oestradiol treatment enhanced tumour blood flow. The oestrogenic effects of estramustine phosphate, ethinyl oestradiol/polyoestradiol phosphate or orchiectomy were studied in previously untreated prostatic carcinoma patients by measuring serum levels of liver proteins (pregnancy zone protein and sex hormone binding globulin) and pituitary hormones (luteinizing hormone, follicle stimulating hormone and prolactin) during a 6 month period. Both medical treatments induced marked but quite comparable changes of the proteins. Apart from the increase of follicle stimulating and luteinizing hormones, no changes were observed in these serum proteins after orchiectomy.

Adenocarcinoma↗

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↗