Hormonal and morphologic evaluation of the effects of antiandrogens on the blood supply of the rat prostate.
OBJECTIVE
To clarify the basic aspects of the regulation of the prostatic blood supply by antiandrogens, their effect on the prostatic blood supply was studied for both androgen content and morphology of true capillaries in the rat ventral prostate. The effectiveness of antiandrogens on the control of hemorrhagic status in prostatic diseases has been previously reported.


METHODS
Androgen concentrations in the prostate were quantified after administration of chlormadinone acetate (CMA), finasteride, or flutamide. The prostatic blood supplies were measured after administration of CMA, finasteride, flutamide, or bicalutamide. The alpha-blockers, terazosin and tamsulosin, were included in the study as negative controls. The histologic changes in the capillaries of the ventral prostate were observed, and the luminal area was measured.


RESULTS
The prostate dihydrotestosterone concentrations were decreased by the administration of all antiandrogens. Treatment with CMA, finasteride, flutamide, or bicalutamide reduced the prostatic blood supply by 50% to 65%. The parallel reduction in luminal areas of the true capillaries was observed in rats treated with CMA. Treatment with alpha-blockers did not affect the prostate androgen content, prostatic blood supply, or capillary luminal area.


CONCLUSIONS
The reduction of the prostatic blood supply was suggested to be the result of a decrease in dihydrotestosterone content and the reduction in the luminal area of capillaries. The early reductive effect of antiandrogens on the prostatic blood supply suggests an alternative use for antiandrogens independent of their typical use for prostate volume regression. The results support the basic aspects of the advantage of preoperative treatment with CMA, flutamide, and bicalutamide, similar to finasteride, in reducing perioperative hemorrhage.
Shibata
Yasuhiro
Y
Department of Urology, Gunma University School of Medicine, Maebashi, Gunma, Japan.
Ono
Yoshihiro
Y
Kashiwagi
Bunzo
B
Suzuki
Kazuhiro
K
Fukabori
Yoshitatsu
Y
Honma
Seijiro
S
Yamanaka
Hidetoshi
H
D058891:5-alpha Reductase Inhibitors; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000726:Androgen Antagonists / Q000494:pharmacology*; D000813:Anilides / Q000494:pharmacology; D000818:Animals; D002196:Capillaries / Q000737:chemistry / Q000187:drug effects; D002715:Chlormadinone Acetate / Q000494:pharmacology; D013196:Dihydrotestosterone / Q000032:analysis*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D018120:Finasteride / Q000494:pharmacology; D005485:Flutamide / Q000494:pharmacology; D007987:Gonadotropin-Releasing Hormone / Q000037:antagonists & inhibitors; D006727:Hormone Antagonists / Q000494:pharmacology; D008297:Male; D008833:Microcirculation / Q000187:drug effects; D009570:Nitriles; D011224:Prazosin / Q000031:analogs & derivatives* / Q000494:pharmacology; D011467:Prostate / Q000098:blood supply* / Q000737:chemistry / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D013449:Sulfonamides / Q000494:pharmacology; D000077409:Tamsulosin; D013739:Testosterone / Q000032:analysis*; D014105:Tosyl Compounds
D058891:5-alpha Reductase Inhibitors; D000317:Adrenergic alpha-Antagonists; D000726:Androgen Antagonists; D000813:Anilides; D004791:Enzyme Inhibitors; D006727:Hormone Antagonists; D009570:Nitriles; D013449:Sulfonamides; D014105:Tosyl Compounds; D013196:Dihydrotestosterone; D002715:Chlormadinone Acetate; D007987:Gonadotropin-Releasing Hormone; D013739:Testosterone; D018120:Finasteride; D005485:Flutamide; C041226:Terazosin; C053541:bicalutamide; D000077409:Tamsulosin; D011224:Prazosin