CL Robinette, TM Weber
College of Veterinary Medicine,
North Carolina State University, Raleigh, NC
This laboratory has previously shown that a
profound inflammation can be induced in the rat lateral prostate after treatment with estradiol17b (E2) and that this response is mediated by prolactin (PRL) release (Endocrinology 132:24072416, 1993). Since restraint
stress also stimulates PRL release in the rat, the present study was undertaken to determine if this type of stress could sustain prostatitis that was previously established by a short- term treatment with E2.
Prostatitis was induced in castrated, sexually mature, male Wistar rats by placing an E2 implant under the skin for one week. At the beginning of week 2, the E2 implant was removed and a dihydrotestosterone implant was
placed subcutaneously to restore prostate wet weight. Periods of restraint lasting 15 minutes were administered Monday- Friday in the morning and afternoon during weeks 3-6. Control rats were similarly treated except
that they were removed from and immediately returned to their cages instead of being restrained.
Rats subjected to restraint showed more inflammation and a higher level of serum PRL than did the unstressed controls.
The inflammation was characterized by the presence of intraluminal neutrophils and stromal Iymphocytes. Myeloperoxidase, a frequently used biochemical index for the number of neutrophils, was significantly elevated in
the stressed rats compared to the controls and correlated well with our histologic observations.
In contrast, rats that were subjected to restraint stress, but in the absence of previously established E2-induced
prostatitis, showed minimal evidence of inflammation. Therefore, stress was more effective in influencing an already established prostatitis than it was in inducing the process. The rat thus provides a model for further
characterizing the response of prostatitis to stress and its associated increases in serum PRL. Furthermore, these findings also raise interesting questions concerning the relationship between stress, prolactin, and
prostatitis in humans.
(Supported by the State of North Carolina)