The Prostate · 2007
Urodynamic changes in a noble rat model for nonbacterial prostatic inflammation.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Bernoulli Jenni, Yatkin Emrah, Talvitie Eva-Maria, Santti Risto, Streng Tomi
Аннотация
BACKGROUND: Chronic nonbacterial prostatitis (CP) associated with voiding dysfunction is a poorly understood clinical phenomenon. The goal of the present study was to induce prostatic inflammation with estrogen and androgen treatment and to record associated urodynamic changes in Noble rats.
METHODS: Rats were treated with estradiol and testosterone implants to increase estradiol concentration in serum while testosterone concentration was maintained at or slightly above the control level. The urodynamical recordings were performed under anesthesia after the hormone treatments for 3 and 6 weeks. The dorsolateral lobes of the prostates were removed for histopathological analysis after recordings.
RESULTS: After the 3-week treatment, lymphocytes, mainly T-cells, were located around the capillaries. During the following 3 weeks lymphocytes migrated into stroma and acini. Cytotoxic T-cells were seen intraepithelially, and neutrophiles inside the acini. Removal of estrogen implant or treatment with anti-estrogen diminished inflammation. No changes in voiding pattern were seen after the 3-week treatment. Three weeks later, bladder weight and capacity were increased, and the micturition time was prolonged.
CONCLUSIONS: Elevated estrogen concentration was essential for the gradual development of prostatic inflammation. The profile and location of inflammatory cells suggest that prostatic vasculature is one of the sites of estrogen action. Urodynamic changes which developed in association with glandular inflammation indicated abnormal bladder function, reflecting an incipient obstruction.
METHODS: Rats were treated with estradiol and testosterone implants to increase estradiol concentration in serum while testosterone concentration was maintained at or slightly above the control level. The urodynamical recordings were performed under anesthesia after the hormone treatments for 3 and 6 weeks. The dorsolateral lobes of the prostates were removed for histopathological analysis after recordings.
RESULTS: After the 3-week treatment, lymphocytes, mainly T-cells, were located around the capillaries. During the following 3 weeks lymphocytes migrated into stroma and acini. Cytotoxic T-cells were seen intraepithelially, and neutrophiles inside the acini. Removal of estrogen implant or treatment with anti-estrogen diminished inflammation. No changes in voiding pattern were seen after the 3-week treatment. Three weeks later, bladder weight and capacity were increased, and the micturition time was prolonged.
CONCLUSIONS: Elevated estrogen concentration was essential for the gradual development of prostatic inflammation. The profile and location of inflammatory cells suggest that prostatic vasculature is one of the sites of estrogen action. Urodynamic changes which developed in association with glandular inflammation indicated abnormal bladder function, reflecting an incipient obstruction.