LOWER URINARY TRACT IN AN EXPERIMENTAL MODEL OF HYPOGONADISM

Abstract

Postoperative hypogonadism represents a clinically important condition that arises due to surgical stress, marked by either a temporary or lasting reduction in serum testosterone (T) levels. An observed decline of 30–50% in T concentration during the early postoperative phase serves as an independent risk factor for delayed tissue healing, ongoing pain symptoms, and dysfunction of the lower urinary tract. Objective. This study aimed to assess the impact of experimental hypogonadism and its subsequent correction on the postoperative recovery following cystotomy. Materials and Methods. This experimental study involved 70 mature male Wistar rats, each weighing between 220 and 250 g. The subjects were randomly assigned to three distinct groups: the OG group (n = 30), which underwent cystotomy followed by daily intramuscular administration of T propionate at a dosage of 2 mg/kg for a duration of 14 days; the PC group (n = 30), which underwent cystotomy without any hormonal intervention; and the OK group (n = 10), which comprised intact animals. The cystotomy model was established utilizing a proprietary method (RU Patent No. 2855647). Testosterone levels were measured via ELISA on postoperative days 0, 7, and 14. The function of the lower urinary tract was evaluated by monitoring voiding frequency in metabolic cages over a period of 3 hours, while nociceptive sensitivity was assessed using the electronic von Frey test, which established the threshold for mechanical allodynia on days 0, 1, 4, 7, 10, and 14. Statistical analyses were conducted employing the Mann-Whitney and Kruskal-Wallis tests. Results. In the animals belonging to the PC group, by the third day following the surgical procedure, the testosterone (T) level had diminished to 5.2 ± 1.1 nmol/l, representing 34% of the baseline measurement (15.3 ± 2.8 nmol/l). This reduction was statistically significant when compared to the intact animals and the OK group (p < 0.001). By the fourteenth day, the T concentration in this group continued to show a decrease (8.9 ± 1.8 nmol/l), indicating a state of persistent hypogonadism. In contrast, the OG group, which received T administration, achieved a restoration of androgen levels to 19.2 ± 3.7 nmol/l by the fourteenth day, surpassing the values observed in the PC group by a factor of 2.2 (p < 0.05) and showing no significant difference from the intact animals (p>0.05). Lower urinary tract dysfunction was evidenced by pollakiuria; in the PC group, the frequency of urination was recorded at 9.8 ± 1.4 times per day on day 7, compared to 4.2 ± 0.6 times per day in the OC group (p < 0.01). Following replacement therapy in the MG group, urination frequency normalized by day 14, measuring 5.1 ± 0.8 times per day, with no significant difference compared to the intact group (p > 0.05). Furthermore, androgen deficiency was correlated with pronounced mechanical allodynia, as the nociceptive threshold in the PC group decreased to 10 ± 3 g on day 14, in contrast to 22 ± 2 g in the MG group and 25 ± 3 g in the OC group (p < 0.05). Conclusions. Postoperative hypogonadism is a factor determining the severity of lower urinary tract dysfunction and the persistence of pain after cystotomy. Androgen replacement therapy restores hormonal status, normalizes urodynamic parameters, and eliminates mechanical allodynia within 14 days postoperatively.