Feline testicular ultrasonogram differentiates pre vs. postpubertal and normal vs. disrupted spermatogenesis.

The aims of this study were: to ultrasonograhically describe and compare testicular parenchyma echogenicity and heterogeneity using digital image analysis in: I) prepubertal (PREP), peripubertal (PERI) and mature (MAT) cats; II) Normal and abnormal mature felids. Secondary, the relationships between histomorphological and ultrasonographic attributes of the testes were also determined. I) Fourteen, PREP, PERI and MAT male cats were ultrasonographically examined and then castrated. II) Seven adult cats were ultrasonographically examined before and after a GnRH antagonist administration and then castrated. All the testes were grossly and histomorphometrically assessed. In the frozen digital images of the longitudinal ultrasound sections, 3 regions of interest (ROI, 1 mm2) were selected. Within each ROI the echogenicity and the heterogeneity of the testicular parenchyma were digitally analyzed. In experiment I, testicular volume (0.15 ± 0.0 vs. 0.49 ± 0.1 vs. 1.65 ± 0.1; P < 0.01) and gonadosomatic index (0.04 ± 0.0 vs. 0.05 ± 0.0 vs. 0.08 ± 0.0; P < 0.01), echogenicity (56.54 ± 0.75 vs. 81.87 ± 5.88 vs.94.67 ± 3.62; P < 0.01) and heterogeneity (10.2420 ± 1.3740 vs.13.65 ± 0.65 vs. 14.67 ± 1.49; P < 0.01) augmented throughout PRE, PERI, and MAT. In experiment II, testicular volume (1.00 ± 0.09 vs. 0.85 ± 0.09; P < 0.05), echogenicity (87.74 ± 1.53 vs. 83.32 ± 1.54; P 0.01) but not heterogeneity (14.09 ± 0.26 vs. 14.19 ± 0.29; P > 0.05) decreased in the post GnRH antagonist abnormal testes. For both experiments, testicular volume, seminiferous tubular diameter, percentage of spermatids as the most mature cell type, and luminal/intertubular ratio were highly correlated (P < 0.01) with their echotextural attributes. Computer-assisted image analysis of B mode ultrasonogram appears as a good indicator of pubertal development and mild alterations of spermatogenesis in felids.

Quantitative bidimentional and Doppler ultrasound assessment of the effect of a GnRH antagonist on canine prostatic hyperplasia.

The objectives of this article were: a) To describe the effect of a single administration of the third generation GnRH antagonist, acyline, on canine benign prostatic hyperplasia (BPH) b)To quantitatively compare parenchyma echogenicity, heterogeneity (SD echogenicity) and blood flow in hyperplastic and treated prostate glands. Seven mixed bred dogs, 11.14 ± 0.8 years of age, weighing 8.5 ± 1.4 (3.8-15.6) kg, with BPH were included in this study and administered acyline 330 mg/kg sc (day 0). Then the dogs were examined by B Mode and Doppler ultrasound on days 15, 30 and 60 after treatment. Parenchymal frozen images were digitally analyzed. On day -7, prostatic volume was 1.60-5.36 fold (volume ratio) enlarged in relation to the expected volume. Prostatic volume decreased up to a mean of -38.44% (P < 0.01; range -32.2 to -70.9%) on day 30 to gradually increase towards pretreatment values. A correlation between volume ratio and nadir treatment volume was also found (r = - 0.87; P < 0.05). Mean parenchyma echogenicity (P < 0.01) and heterogeneity (P < 0.01) diminished in all the post treatment evaluations. Pretreatment intraprostatic cysts disappeared at the time point of peak treatment effect. Prostatic arteries RI increased on day 30, being different from day -7 and also from day 60 values (P < 0.05). It was concluded that a single administration of a third generation GnRH antagonist safely decreased prostatic volume and parenchyma and blood flow abnormities associated with canine BPH during 30 days. Monthly administrations of this treatment could represent a rapid, efficient and safe therapeutic option for BPH.

Physical, histological, endocrinological and steroidogenical evaluation of male cats postnatally exposed to sexual steroids.

To test the hypothesis that postnatal sexual steroids induce an impairment of domestic male cat reproductive function, this study describes the physical, endocrine, steroidogenical and histological effects of a single, high dose of a postnatal sexual steroid in this species. Twenty male kittens were randomly assigned within the first 24 h of birth to: Testosterone enanthate 12.5 mg sc (TE; n = 8), medroxyprogesterone acetate 10 mg sc (MA; n = 6), or Placebo sc (PL; n = 6). The cats were followed until puberty when they were castrated. Kittens achieved puberty without age differences among groups (P > 0.05). Two MA cats presented abnormal testicular descent. Histological evaluation of the MA (P < 0.01), but not of TE testes revealed decreased diameter (P < 0.01) and epithelial height (P < 0.01) of the seminiferous tubules. Leydig cell nuclear area was also reduced in this group. Conversely, tubular/intertubular ratio was increased in TE animals (P < 0.01). Quantitative real-time PCR analysis of mRNA expression of testicular tissue revealed no significant differences among groups for StAR, CYP17A1 and androgen receptors. TE animals showed decreased CYP19A1 mRNA expression (P < 0.05). In the first 4 postnatal weeks, fecal testosterone (T) values were high, basal and intermediate in TE, MA and PL (P < 0.05), respectively. These differences progressively diminished and the three groups presented basal T concentrations from the 7th week on (P > 0.05). It was concluded that the postnatal progestagen initially suppressed the gonadal axis and caused an impairment of spermatogenesis and testicular descent at puberty. Androgen treatment caused downregulation of the final steroidogenic cascade.

Effect of the indenopyridine RTI-4587-073 (l) on feline testicle.

The aim of this study was to describe the seminal, histomorphological and hormonal effects of the oral indenopyridine RTI-4587-073(l) on feline testicle. Clinical side effects were also recorded. Sixty testicles of 30 adult cats that had been treated (d 0) with RTI-4587-073(l) 12.5 mg/kg PO and randomly hemiorchiectomized twice on: day -14 (n = 8), 6 h (n = 6), 12 h (n = 8), 24 h (n = 6), day 7 (n = 8), day 14 (n = 6), day 21 (n = 6), day 35 (n = 6) or day 42 (n = 6) were studied. Before each hemiorchiectomy, fecal samples for testosterone (T) measurement were collected and the testes were grossly and ultrasound examined. This indenopyridine did not cause changes in testicular weight (P > 0.1), volume (P > 0.1), echostructure, gonadosomatic index (P > 0.1), fecal T concentrations (P > 0.1), nor clinical side effects. A severe disorganization of the cytoarchitecture of the seminiferous epithelium, sloughed cells and fluid, were observed in the 6 h samples up to a maximum at 24 h. Tubular diameter (P < 0.01) increased twice, during the first 24 h and on d 35. Germinal epithelium achieved its minimum height on d 14 to rapidly recover thereafter. This treatment caused a significant decrease in the volume of all the seminiferous cell components, except spermatogonias. All histotological parameters normalized by the end of the study. It was concluded that RTI-4587-073(l) severely disrupted spermatogenesis during the first 24 h after treatment returning to normality in approximately one spermatic cycle without clinical side effects.

Postponement of canine puberty by neonatal administration of a long term release GnRH superagonist.

The objective of this study was to assess the efficiency and clinical safety of postnatal administration of a GnRH agonist on canine puberty postponement. Sexual steroids and histological gonadal changes were also described. Twenty-four littermate puppies were randomly assigned to: Deslorelin acetate 18.8 mg sc (DESLO; n = 12) or Placebo: sc (PLACE; n = 12) postnatally. The dogs were clinically and endocrinologically followed up until puberty when they were gonadectomized and their gonads histomorphometrically studied. Deslorelin postponed the age of puberty (72.7 ±â€¯4.8 vs. 35.8 ±â€¯1.9 weeks; P < 0.01) in these dogs. At the time of this submission, 3 DESLO dogs (108 weeks old) remain non-pubertal. All dogs concluded growing at a similar age (29.75 ±â€¯2.44 vs. 29.25 ±â€¯0.90 weeks; P > 0.1) independently of their group and pubertal status. None of the females had side effects while the 2 non pubertal DESLO males presented bilateral cryptorchydism. All the bitches ovulated at puberty (P > 0.1) and the 2 DESLO that were mated became pregnant. Deslorelin postponed basal serum sexual steroids up to puberty in both genders (P < 0.01). The histomorphometrical study of the testes revealed that the tubular diameter (P < 0.05), germinal epithelium height and composition (P < 0.01) were decreased in DESLO group. Ovarian structures did not differ between treatments (P > 0.05). It was concluded that postnatal deslorelin decreased sexual steroids reversibly postponing puberty in both genders without side effects in bitches and causing 2/6 of cryptorchydism and impairment of testicular histomorphometry in male dogs.