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A. Bergh, J. E. Damber and A. Widmark

Summary. Adult male rats were injected with different doses of hCG, or with 2·5 μg ovine LH subcutaneously, and other rats were mated with oestrous females. The animals were examined 4 h after treatments. Treatment with hCG resulted in a dose-dependent increase in leucocyte concentration in testicular blood vessels and in the number of blood vessels which could be labelled with intravenously injected carbon particles. Carbon leakage was not observed in control testes. Treatment with a low dose of ovine LH or inducing an endogenous LH peak by mating also resulted in leucocyte accumulation and vascular leakage of carbon in the testis. The magnitude of the response was considerably lower than after high doses of hCG. The physiological relevance of the discrete response observed after physiological LH stimulation is unknown but LH-induced changes in testicular microcirculation could be of interest for the understanding of the physiology and pathophysiology of the testis.

Keywords: testis; LH; hCG; vascular permeability; inflammation

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O. Colin, A. Bergh, J-E. Damber and A. Widmark

Testicular vasomotion (rhythmical variations in testicular blood flow) was studied in adult rats using laser Doppler flowmetry. Vasomotion was not present in testes in which the Leydig cells had been destroyed, but it could be induced by a low dose of testosterone. Transposition of a scrotal testis into the abdominal cavity inhibited vasomotion and this was apparently not caused by Leydig cell malfunction. Depletion of specific germ cells (by unilateral X-irradiation induced killing of spermatogonia and maturation depletion of germ cells) did not abolish vasomotion in the testis. It is suggested that testicular vasomotion is influenced by testosterone and by factors from Sertoli cells.

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A. Bergh, P. Rooth, A. Widmark and J.-E. Damber

Summary. Adult rats were injected subcutaneously with 50 i.u. hCG and vascular permeability was compared to that in saline-treated control rats by two independent methods. At 4 h after hCG treatment the rats were injected intra-arterially (i.a.) with FITC-labelled macromolecular dextran (M r 150 000) and the testicular microcirculation was studied in vivo by using a fluorescence microscope. Other rats were injected i.a. with a suspension of colloidal carbon and the location of leaking blood vessels was recorded in sections from the testes by light and electron microscopy.

In hCG-treated animals leucocytes were found adhering to the endothelium in post-capillary venules and in these venular segments dextran was leaking into the interstitium. Carbon particles were deposited in the walls of post-capillary venules and leucocytes migrated through open interendothelial cell gaps in hCG-treated animals. In control animals leucocyte adhesion and migration were not observed, the injected dextran remained in the circulation and the blood vessels were not labelled by carbon.

It is suggested that the hCG-induced increase in testicular interstitial fluid volume, like the tissue oedema in inflammation, is caused by a leucocyte-mediated increase in venular permeability.