Intratesticular testosterone levels in Klinefelter syndrome (KS) are comparable to controls and Leydig cell function was proven to be normal at least in vitro, testicular vascularization changes came into focus as a potential factor contributing to hypogonadism. We performed enhanced ultrasound based analysis of the testicular blood support in our 41,XXY* mice. Adult male 41,XXY* (n=5) and control mice (n=6) underwent ultrasound analyses with the Non-Targeted Contrast Agent Vevo MicroMarker. The agent containing gas filled micro-bubbles was administered intravenously (lower body perfusion). After initial perfusion, micro-bubbles were destroyed by high ultrasound pressure and the reperfusion period was analysed. In parallel, electrocardiograms (ECGs) were taken. Afterwards mice were sacrificed and testes removed for histological analysis of vascularization. Whilst ECGs did not reveal differences in heart function, the reperfusion time for testes was significantly increased in 41,XXY* mice (XXY* 28.8±1.7 s; XY* 19.9±2.8 s). Testes of 41,XXY* mice (XXY* 4.6±0.10 mm2; XY* 11.1±0.34 mm2) and the area covered by blood vessels (XXY* 0.025±0.003 mm2; XY* 0.040±0.002 mm2) were significantly smaller. Testicular bIood vessel areas of adult males were assigned to four categories (I=<80 μm2, II=801000 μm2, III=10005062 μm2, IV=>5062 μm2). The blood vessel area of categories I and II was significantly decreased in 41,XXY* mice (P<0.0001). Taking the testis area into account, the area covered by vessels of category II and III is significantly elevated in KS mice. Blood vessels of category IV were missing in KS testes. These functional and morphological data strengthen the assumption that the observation made previously contributes to the endocrine phenotype seen in KS pointing to an affected vascular system in the disturbed testicular tissue of males with supernumerary X.
28 - 31 May 2016
European Society of Endocrinology