The effects of varicocele and varicocele repair on testicular blood flow, temperature, sperm counts, and sperm motility were assessed in adult male rats. The duration of the experimental varicocele and the varicocele repair were three and two times as long, respectively, as that studied previously. Varicoceles were created by partial ligation of the left renal vein and repairs were accomplished by high ligation of the left spermatic vein. Testicular blood flow was determined by using the radiolabeled microsphere technique. Testicular temperature was taken via needle probe thermometer. Sperm samples were obtained by micropuncture of the cauda epididymidis, and were counted on a hemacytometer and observed for motility under the light microscope. Varicoceles were studied 100 days after their creation. Repairs were performed on varicoceles that had lasted 100 days and the animals were studied 60 days after repair. Mean testicular blood flow (ml/100 g tissue/min) was significantly increased (P less than 0.05) in animals with varicocele (left testis (LT) = 42.2 +/- 1.1, right testis (RT) = 39.1 +/- 1.2) when compared with normal controls (LT = 29.3 +/- 1.6, RT = 29.6 +/- 1.7), animals with varicocele repair (LT = 30.7 +/- 1.3, RT = 30.0 +/- 1.6), or sham-operated animals (LT = 29.7 +/- 1.4, RT = 31.1 +/- 1.4).(ABSTRACT TRUNCATED AT 250 WORDS)
A method is described for the measurement of intratubular hydrostatic pressure in the testis, caput epididymidis, and cauda epididymidis of the golden hamster. Pressures in these locations in normal animals ranged from 3 to 6 cmH2O. Mean pressure in the tubules of the caput was significantly higher than that in the seminiferous tubules (P smaller than 0.05) and in the proximal caudal tubules (P smaller than 0.02). There was a small, significant increase in pressure from the proximal cauda to the distal cauda (P smaller than 0.04). Two weeks after vasectomy, the mean pressure in the seminiferous tubules of 3.3 cmH2O was significantly lower (P smaller than 0.004) than the mean pressure in the normal seminiferous tubules of 4.4 cmH2O. Pressures in the cauda at 2 wk of 10-18 cmH2O were significantly greater than normal (P smaller than 0.0005) and reflected the accumulation of sperm and fluid. The high incidence of spermatic granuloma formation and/or rupture of the epididymis observed after vasectomy emphasized that there are definite limits to both distensibility and reabsorptive capacity of the epididymis in some species. Pressures at 1 mo after vasectomy were similar to those at 2 wk in animals that were still obstructed and comparable to normal in animals with granulomas and/or large epididymal leaks. Testicular weight was slightly but significantly decreased 2 wk after vasectomy. At 4 wk, there was no detectable effect of vasectomy on the weights of the testes.
The occurrence of spermatic granulomas of the vas deferens was studied in Lewis rats at intervals up to 7 months after vasectomy or vasectomy followed 3 months later by vasovasostomy. The incidence of granuloma progressed with time to involve one or both tracts in 100% of vasectomized rats. In addition, the majority of animals developed new granulomas after vasovasostomy, even though fluid flow through the reconnected vas deferens was demonstrated in vitro. When individual tracts were analyzed, the weight of the testis was related to ipsilateral spermatic granuloma formation in both vasectomy and vasovasostomy groups at 3 and 4 months after initial operation. Testes were small in the absence of a granuloma but similar to those of sham‐operated rats if a granuloma was present. The possible protective effect of spermatic granuloma formation on the testis is discussed.
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