Blood Flow In Testis Research Articles

Chronic exercise training attenuates prostate cancer-induced molecular remodelling in the testis.

Prostate cancer is a major cause of cancer-related death in males worldwide and, in addition to impairing prostate function, also causes testicular adaptations. In this study, we aim to investigate the preventive effect of exercise training on PCa-induced testicular dysfunction. As a model, we used fifty Wistar Unilever male rats, randomly divided in four experimental groups. Prostate cancer was chemically and hormonally induced in two groups of animals (PCa groups). One control group and one PCa group was submitted to moderate intensity treadmill exercise training. Fifty weeks after the start of the training the animals were sacrificed and sperm, prostate, testis and serum were collected and analyzed. Sperm concentration and morphology, and testosterone serum levels were determined. In addition, histological analyses of the testes were performed, and testis proteomes and metabolomes were characterized. We found that prostate cancer negatively affected testicular function, manifested as an arrest of spermatogenesis. Oxidative stress-induced DNA damage, arising from reduced testis blood flow, may also contribute to apoptosis of germ cells and consequential spermatogenic impairment. Decreased utilization of the glycolytic pathway, increased metabolism of ketone bodies and the accumulation of branched chain amino acids were also evident in the PCa animals. Conversely, we found that the treadmill training regimen activated DNA repair mechanisms and counteracted several metabolic alterations caused by PCa without impact on oxidative stress. These findings confirm a negative impact of prostate cancer on testis function and suggest a beneficial role for exercise training in the prevention of prostate cancer-induced testis dysfunction.

Testicular blood supply is altered in the 41,XXY* Klinefelter syndrome mouse model

Hypergonadotropic hypogonadism is a major feature of Klinefelter syndrome (KS), assumed to be caused by testicular hormone resistance. It was previously shown that intratesticular testosterone levels in vivo and Leydig cell function in vitro seem to be normal indicating other functional constraints. We hypothesized that impaired testicular vascularization/blood flow could be a co-factor to the observed hypergonadotropic hypogonadism. We evaluated the testicular vascular system by measuring blood vessel sizes during postnatal development and testis blood flow in adult 41,XXY* mice. Proportional distribution and size of blood vessels were analyzed during testicular development (1, 3, 5, 7, 10, 21 dpp, 15 wpp). While ratios of the vessel/testis area were different at 15 wpp only, a lower number of smaller and mid-sized blood vessels were detected in adult KS mice. For testicular blood flow determination we applied contrast enhanced ultrasound. Floating and reperfusion time for testicular blood flow was increased in 41,XXY* mice (floating: XY* 28.8 ± 1.69 s vs XXY* 44.6 ± 5.6 s, p = 0.0192; reperfusion XY* 19.7 ± 2.8 s vs XXY*: 29.9 ± 6.2 s, p = 0.0134), indicating a diminished blood supply. Our data strengthen the concept that an impaired vascularization either in conjunction or as a result of altered KS testicular architecture contributes to hormone resistance.

Hypothyroidism effects on the morpho-histometrical features of testes in adult rats

Background: Up until now, the effect of thyroid hormones on the male reproductive organ, after puberty, is not well understood. OBJECTIVES: In the present study, the morpho-histometrical effects of thyroid hormone deficiency on the adult-male rat reproductive organs were investigated. MATHODS: Thirty adult male rats were randomly divided into three groups (n=10): control, hypothyroid, and hypothyroid which receives Levothyroxine. After 4-months we examined the number of spermatogonia cells, primary spermatocytes, and Sertoli cells, as well as the seminiferous tubules epithelium thickness, area of seminiferous tubules, and the diameter and thickness of testis artery walls. RESULTS: No significant difference was observed between the hypothyroid and control rats in terms of the area of seminiferous tubules, the number of spermatogonia cells, primary spermatocytes, and Sertoli cells. Moreover, the epithelium thickness of seminiferous tubules and the diameter and thickness of artery walls were significantly decreased in hypothyroid group compared with the control rats. CONCLUSIONS: These observations are consistent with the hypothesis that hypothyroidism can affect the male fertility and declare that it may influence male reproduction by reducing the testis blood flow.

Androgen Action via Testicular Arteriole Smooth Muscle Cells Is Important for Leydig Cell Function, Vasomotion and Testicular Fluid Dynamics

Regulation of blood flow through the testicular microvasculature by vasomotion is thought to be important for normal testis function as it regulates interstitial fluid (IF) dynamics which is an important intra-testicular transport medium. Androgens control vasomotion, but how they exert these effects remains unclear. One possibility is by signalling via androgen receptors (AR) expressed in testicular arteriole smooth muscle cells. To investigate this and determine the overall importance of this mechanism in testis function, we generated a blood vessel smooth muscle cell-specific AR knockout mouse (SMARKO). Gross reproductive development was normal in SMARKO mice but testis weight was reduced in adulthood compared to control littermates; this reduction was not due to any changes in germ cell volume or to deficits in testosterone, LH or FSH concentrations and did not cause infertility. However, seminiferous tubule lumen volume was reduced in adult SMARKO males while interstitial volume was increased, perhaps indicating altered fluid dynamics; this was associated with compensated Leydig cell failure. Vasomotion was impaired in adult SMARKO males, though overall testis blood flow was normal and there was an increase in the overall blood vessel volume per testis in adult SMARKOs. In conclusion, these results indicate that ablating arteriole smooth muscle AR does not grossly alter spermatogenesis or affect male fertility but does subtly impair Leydig cell function and testicular fluid exchange, possibly by locally regulating microvascular blood flow within the testis.

Rosuvastatin Prevents No-Reflow Phenomenon Due to Detorsion of Testicular Torsion

PURPOSE Treatment of testicular torsion by detorsion may further damage the testis due to ischemia/reperfusion (I/R) injury. After reestablishment of blood flow, the blood flow diminishes after a while, which is called as the no-reflow phenomenon. Rosuvastatin, a HMG-CoA reductase inhibitor, has “pleiotropic” vasculoprotective effects that include anti-inflammatory and antioxidant effects. This study was designed to determine the effect of rosuvastatin pretreatment on the I/R injury induced no-reflow phenomenon encountered after detorsion of testicular torsion. MATERIAL AND METHODS Wistar albino rats were used in the study. Blood flow of testis were measured before the torsion (baseline value), before the detorsion and 1 hour after detorsion using Laser Doppler flowmetry. Rats were divided into three groups. Sham group (n = 5): Basal blood flow, flow before detorsion, and flow after detorsion of the testis was determined. Torsion/detorsion group (n = 8): After 2 hours torsion of the testis, blood flow before and after detorsion was determined. Torsion/detorsion + rosuvastatin group (n = 8): After measurement of the basal blood flow, Rosuvastatin (10 mg/kg) was injected intraperitoneally 30 minutes before the detorsion of 2 hour torsion and blood flow before and after detorsion was determined. RESULTS There was no significant difference between the the baseline blood flow values of the groups. Blood flow decreased significantly after the torsion. One hour after the detorsion, mean blood flow of the torsion/detorsion + Rosuvastatin group was found significantly higher than the torsion/detorsion group. CONCLUSIONS Pretreatment with Rosuvastatin before detorsion prevents reperfusion injury induced no-reflow phenomenon after detorsion of testicular torsion.

Effect of active immunization against testosterone on plasma gonadotrophin concentrations, spermatogenic function, testicular blood flow, epididymis mass and mating behaviour in adult rams.

The long-term effects of active immunization against testosterone were studied in rams, with particular reference to blood concentrations of gonadotrophin and testosterone, spermatogenesis, testis blood flow and mating behaviour. Ten 18-month-old Merino rams, kept on pasture, were studied for 1 year. Every 2 months, five rams received injections of BSA in Freund's adjuvant and five other rams were treated with testosterone-3(o-carboxymethyl)oxime-BSA as immunogen. Anti-testosterone antibodies (mean titre: 1:4484 +/- 582, after boosters) were maintained in the circulation, with the help of regular booster injections. In time, immunization reduced live mass in testosterone-immunized rams; however, there was no effect on testicular volume throughout the whole study. In testosterone-immunized rams, significantly higher concentrations of gonadotrophins were found in jugular venous plasma, as well as increased concentrations of total plasma testosterone. LH pulse frequency, amplitude and nadir were increased significantly in testosterone-immunized rams. After 12 months of immunization, no differences were found in the number of spermatozoa per ejaculate, in daily sperm production or in testis mass between the two groups of rams; however, testicular blood flow (per testis) and epididymis mass were significantly reduced in testosterone-immunized rams. Testosterone immuno-neutralization also resulted in a significant reduction in the number of mounts culminating in ejaculation performed during a 10 min trial carried out on a number of occasions during the experiment. Additional information on these rams was collected 3 months after castration. However, there were no significant differences in mean plasma LH and FSH concentrations, either before, or after, a single GnRH injection between the two groups of rams at this time.

Effects of multiple injections of hCG on testis blood flow

In attempting to determine whether or not multiple injections of human chorionic gonadotropin (hCG) augment testis blood flow, adult male rats were injected with three doses of 10 IU of hCG every other day and testis blood flow was determined on day 5, the day of the final injection. Testis blood flow (mL/100 g testis tissue/min ± SEM) as measured by the 133Xe washout method increased from 10.8 ± 1.3 to 20.4 ± 4.5 ( p < 0.05) after the three doses of hCG. These observations suggest that multiple injections of hCG appear to have the same effect as a single dose of hCG in increasing testis blood flow. This supports the hypothesis that hCG should be administered to all patients undergoing orchiopexy in the hope that the increased perfusion of the gonad will make it less susceptible to ischemia during the surgical procedure.

Recovery of Testicular Blood Flow Following Ligation of Testicular Vessels

To determine whether initial ligation of the testicular vessels of the high undescended testis followed by a delayed secondary orchiopexy is a viable alternative to the classical Fowler-Stephens procedure, a series of preliminary experiments were conducted in the rat in which testicular blood flow was measured by the 133xenon washout technique before, and 1 hour and 30 days after ligation of the vessels. In addition, testicular histology, and testis and sex-accessory tissue weights were measured in 6 control, 6 sham operated and 6 testicular vessel ligated rats 54 days after vessel ligation. The data demonstrate that ligation and division of the testicular blood vessels produce an 80 per cent decrease in testicular blood flow 1 hour after ligation of the vessels. However, 30 days later testis blood flow returns to the control and pre-treatment value. There were no significant changes in testis or sex-accessory tissue weights 54 days after vessel ligation. Histologically, 4 of the surgically operated testes demonstrated necrosis of less than 25 per cent of the seminiferous tubules while 1 testis demonstrated more than 75 per cent necrosis. The rest of the tubules in all 6 testes demonstrated normal spermatogenesis.From this study we conclude that initial testicular vessel ligation produces an immediate decrease in testicular blood flow but with time the collateral vessels are able to compensate and return the testis blood flow to its normal pre-treatment value. These preliminary observations lend support for the concept that initial ligation of the testicular vessels followed by a delayed secondary orchiopexy in patients with a high undescended testis may be a possible alternative to the classical Fowler-Stephens approach.

Limitations imposed by testicular blood flow on the function of Leydig cells in rats in vivo.

Testis blood flow per testis closely follows testis weight in rats made aspermatogenic by a single exposure of the testis to 43 degrees C for 30 min or 500 rad (5 Gy) of irradiation from a caesium source, or following ligation of the efferent ducts. Aspermatogenesis following these treatments was associated with only minor changes in the concentrations of testosterone in peripheral blood before stimulation with human chorionic gonadotrophin (hCG), and a reduced responsiveness to hCG when testis weight had fallen after heating. The concentrations of testosterone in testicular venous blood was normal or above normal during aspermatogenesis resulting from heat or irradiation, and only slightly reduced following efferent duct ligation. Consequently testosterone production (defined as the product of plasma flow and the veno-arterial concentration difference for testosterone) was markedly reduced during aspermatogenesis, both before and after stimulation with hCG. It appears that the reduced blood flow limits the amount of testosterone leaving the testis, and while the Leydig cells are capable under some circumstances of compensating partially for this fall by increasing the concentration of testosterone in the testicular venous blood, this compensation is not complete when there are severe reductions in blood flow. Therefore one can conclude that the mass of the tubules is the main determinant of testis blood flow and the Leydig cells must manage with what the tubules require.

Changes in testis blood flow, the spermatic artery and prostaglandin F2alpha content in testis tissue of heat-stressed rams.

Blood flow to the testis, measured by the133-Xenon isotope clearance technique, initially increased after rams were exposed to elevated (32°C) temperature. However, after 5 and 7 days continuous exposure, blood flow decreased significantly. Similar changes in blood flow to the testis were found during whole body exposure to elevated temperature, or when the temperature of the testis was increased by scrotal heating. After one week of heating the wall of the spermatic artery in the middle region of the pampiniform plexus had thickened, and the arterial lumen had decreased significantly. The PGF2α content in the testis of rams exposed to elevated temperature increased significantly. It is tentatively postulated that the higher levels of PGF2α in the testis of rams exposed to elevated temperature may be responsible for impaired spermatogenic function by constricting the spermatic artery in the pampiniform plexus region and thereby reducing blood flow to the testis.