Although interruption of the vessels supplying the testis is a common practice in urologic surgery, little attention has been called to its acute effects on the hemodynamics of the testis. The present communication is concerned first with an experimental study of the effects on the dog testis of interruption of the testicular, vasal and cremasteric arteries, and second with that in man as demonstrated by polarographic monitoring of tissue oxygen tension.
The animals used for these experiments comprised forty-one mongrel dogs weighing 10-36kg. Under i. v. thiamylal-Na anesthesia, the testis, vas deferens and spermatic cord were exposed by a median incision in the scrotum. Clamping of the testicular artery was made transperitoneally through an median incision in the lower abdomen.
Testicular tissue oxygen tension, an index of testicular blood flow, was continuously monitored by using the Yagi's polarographic oxygen electrode, an enameled copper wire 300μ in diameter. The electrode was thrust into the substance of the upper pole of the testis in to the depth of 5mm. Oxygen tension measurements were made in these animals after occluding the vasal artery, cremasteric artery, testicular artery and spermatic cord. The effects of occluding blood supply to the testis by rotating the spermatic cord 180-360 degrees on its axis were also studied. Measurements were also made after removal of the occlusion. After starting every experiment, the animals were given pure oxygen to breath for a short period in order to determine the post-occlusion PO
2 response time and increment. The changes in the polarographic amplitude were expressed as percent of the pre-occlusion level (100).
Similar experiments were also performed on 5 patients with prostatic carcinoma. Statistical analysis was made by using the Student T test.
1) On occlusion of the vasal artery the testicular PO
2 was 98.1±13.4 (mean±1S. D.) which did not significantly differ from that of the control. This findings suggest that the vasal artery contributes only a small amount of blood to the testis, or that the other two vessels sufffice in perfusing it.
2) Occlusion of the cremasteric artery produced a significant reduction in the testicular PO
2 (85.3±11.7). However, 4 out of 10 testes were able to restore the ability to increase their PO
2, with the increment of 13. 9±4. 8. This increment could be due to some collateral circulation from the testicular artery.
3) Occlusion of the testicular artery produced a drastic reduction of PO
2 (34.2±17.9). Four out of 10 testes showed only a small restoration of the PO
2 (11.1±5.2), which suggests that the other two vessels are insufficient to compensate for the deficit.
These results suggest that the magnitude of contribution of blood supply to the testis by the vasall artery, cremasteric artery and testicular artery is in the order of 1:8:35.
4) Occlusion of the spermatic cord produced a profound reduction in the testicular PO
2 (41.1±
13.8). Four out of 11 testes were able to increase the PO
2 (14.7±10.6) afterward, the amount of which approximated that of the fall in the PO
2 produced by the cremasteric artery occlusion alone, suggesting that the cremasteric artery is able to compensate for the deficit in the testis in the absence of the testicular and vasal blood flow.
There was no significant difference in the reduction of PO
2 between the occlusion of the testicular artery and the spermatic cord. This suggests that no serious congestion would occur in the testis even when the testicular veins were occluded.
5) In 180 degree-rotation of the spermatic cord the PO
2 was 81.5±14.2, which was significantly lower than the control. The testicular PO
2 showed a good response to the inhalation of pure oxygen, but the PO
2
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