320 



PHYSIOLOGY OF GONADS 



mental temperature (Stein, Bader, Eliot 

 and Bass, 1949). The local application of 

 heat does not markedly suppress the pro- 

 duction of androgens, judging from the older 

 work with rats and guinea pigs. To the 

 contrary, some evidence exists that secretion 

 of androgens may be enhanced. After scro- 

 tal insulation, bulls were more ready to 

 serve and excreted more ''androgenic" ster- 

 oid than normal. The amount of fructose 

 in semen (an indicator of androgen) in- 

 creased after scrotal insulation in the ram 

 (Glover, 1956) . Increased temperature orig- 

 inating locally may affect spermatogene- 

 sis in man. Davidson ( 1954) studied semen 

 in cases of oligospermia before and after re- 

 moval of varicoceles. Removal of the vari- 

 cocele was followed by an increased number 

 of sperm cells and a greater incidence of 

 fertility. Defective fertility presumably was 

 caused by interference with normal heat 

 transfer because of the varicocele. 



Local application of cold to the testis or 

 scrotum also results in testicular degenera- 

 tion (Harris and Harrison, 1955) ; however, 

 testicular tissue can be frozen and stored 

 and still retain transplantability and sub- 

 sequently produce hormones and sperm 

 (Parkes, 1954; Parkes and Smith, 1954; 

 Deanesly, 1954). 



The effects of temperature when the en- 

 tire animal is subjected to thermal changes 

 depend on numerous compensatory altera- 

 tions in testicular circulation. The compen- 

 satory mechanisms differ in both ciuality 

 and degree, depending on the nature of the 

 experimental conditions. The testicular tem- 

 perature of rodents placed in a hot room 

 does not increase to a higher level than 

 that of the general body temperature. This 

 is true also for the ram. Within fairly wide 

 limits of environmental temperature (10 to 

 40°C.), the intratesticular temperature of 

 the bull is constant. However, the tempera- 

 ture of the scrotal surface increases slightly 

 with increases in air temperature, but re- 

 mains below body temperature (Riemer- 

 schmid and Quinlan, 1941). The homeostatic 

 mechanisms for maintaining a constant, 

 optimal testicular temperature are several. 

 With increasing scrotal temperature, the 

 scrotum extends and the testes lie lower. 

 This increases heat exchange, despite ilw 

 absence in certain species (mouse, rat, dog. 



cat, and rabbit) of scrotal sweat glands 

 (Harrison and Harris, 1956). Optimal tes- 

 ticular temperature is also maintained by 

 means of heat exchange between vessels of 

 the pampiniform plexus. Exact data on the 

 transfer of heat are not available, because 

 determinations of the blood ffow have not 

 been done. 



There remains for consideration the ef- 

 fect on the testis of severe alterations in 

 circulation. The histologic changes pro- 

 duced in the rat testis by temporary or 

 permanent occlusion of the testicular artery 

 were studied in great detail (Oettle and 

 Harrison, 1952). Acute temporary ischemia 

 (10 to 20 minutes in duration) produced 

 only hyperchromasia of the spermatogonia. 

 Normality was restored within 2 weeks. 

 Ischemia of increasing duration produced 

 correspondingly increased testicular dam- 

 age. Hyperchromatic changes in the sper- 

 matogonia, loosening and exfoliation of the 

 germinal epithelium, and desquamation of 

 the mesothelium of the tunica occurred. The 

 testis shrunk, the interstitium became edem- 

 atous, and the Leydig cells swollen. A 

 layer of ragged and vacuolated Sertoli cells, 

 a few spermatogonia, and an occasional pri- 

 mary spermatocyte may be the only sur- 

 viving elements. When the damage was ex- 

 treme, the tubule became markedly 

 atrojihic, the lumen disappeared, and the 

 Sertoli cells became embedded in a collage- 

 nous matrix. 



Permanent occlusion of the testicular 

 artery in the rat can be accomplished by 

 removing a segment of the artery within the 

 abdominal cavity proximal to its anastomo- 

 sis with the vasal artery (Fig. 5.7), which 

 results in incomplete ischemia. After 1 

 hour of such occlusion, hyperchromasia of 

 the spermatogonia occurs, with exfoliation 

 of the spermatids. After 6 hours, the sper- 

 matocytes are exfoliated. One day later the 

 testis enlarges considerably owing to edema. 

 Multinucleated cells appear and many show 

 pyknosis. The cytoplasm of the Sertoli cells 

 disintegrates. After 3 days, all tubules are 

 abnormal ; within 1 week, they are necrotic. 

 The damage is restricted at first to the cen- 

 tral jwrtion, but within a week practically 

 all tnbulcs except some near the epididymal 

 pole have been killed. Two weeks later, 

 vacuolation occurs in tlie Leydig cells, with 



