STEROID-HORMONE ALTERATIONS FOLLOWING INDUCTION OF CHRONIC INTRAPERITONEAL SEPSIS IN MALE-RATS

The influence of sepsis on male reproductive function in chronic anima l models has not been extensively investigated. On the basis of earlie r clinical studies, it was hypothesized that chronic intraperitoneal ( i.p.) sepsis in rats would modulate the circulating levels of steroid reproductive hormones. Male Sprague-Dawley rats (300-375 g) were rando mized to septic and nonseptic groups. Sepsis was induced with cecal sl urry (200 mg/kg/5 mL 5% dextrose in water (D5W); i.p.) in septic rats, while nonseptic rats received only sterile D5W. The rats (n = 8-12) w ere catheterized to measure systemic hemodynamics and to collect blood at 0, 12, 24, and 48 h after induction of sepsis/sham sepsis. A separ ate group of normal rats was included to serve as an unoperated contro l group. The plasma concentration of corticosterone, progesterone, and testosterone in serum was determined using radioimmunoassay. The hear t rate was significantly increased at t = 12, 24, and 48 h following i nduction of sepsis. However, septic rats did not display any significa nt alterations in the mean arterial pressure and pulse pressure. Basal circulating concentrations of serum corticosterone, progesterone, and testosterone were 356 +/- 124 ng/mL, 2.37 +/- 1.03 ng/mL, and 1.88 +/ - .29 ng/mL, respectively, in the unoperated rats. At t = 0 h there wa s a significant increase in the levels of corticosterone in septic rat s and in the levels of progesterone in both septic and nonseptic rats. The elevations in the concentrations of corticosterone and progestero ne returned to basal values after 24 and 48 h. The septic animals had significantly decreased levels of testosterone at t = 24 and 48 h as c ompared with basal values and nonseptic groups. Our model of sepsis pr oduced a time-dependent decrease in levels of testosterone, an end pro duct of male steroidogenesis. This, along with unchanged levels of cor ticosterone and progesterone at 24 and 48 h following sepsis, indicate s that separate mechanisms for steroidogenesis regulating synthesis of these steroid hormones (progesterone and testosterone) occur with sep sis. It is concluded that in our chronic septic rat model, induction o f i.p. sepsis produced dysfunction in steroidogenesis, which selective ly affected the synthesis of testosterone.