Summary. Treatment with hCG results in an increase in venular permeability in the rat testis. This change in vascular permeability can be detected by the carbon-labelling technique, by measurement of the volume of interstitial fluid and by quantification of the leucocyte migration into the interstitial space. Carbon-labelling, interstitial fluid volume and leucocyte migration were all reduced in rats treated with hCG + terbutaline compared to the values in animals given hCG only. However, terbutaline treatment did not influence the hCG-induced increase in testosterone secretion. These observations suggest that the hCG-induced increase in vascular permeability in the testis can be reduced by a β-adrenergic agonist.
A. Bergh and J.-E. Damber
J.-E. Damber and P. O. Janson
Summary. Testicular blood flow was measured by a radioactive microsphere technique. A significant correlation, r s = 0·82, was found between testicular blood flow and testosterone outflow in the spermatic venous blood, indicating that factors which affect the testicular circulation may influence testicular endocrine function.
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
O. Collin, J-E. Damber and A. Bergh
The effects of 5-hydroxytryptamine (5-HT), 5-HT2 receptor antagonists (ritanserin and ketanserin), histamine and substance 48/80 on testicular blood flow and microcirculation were studied in adult rats. The substances were administered by topical application on the testicular surface and by intratesticular injections, and blood flow was measured by radioactive microspheres and with a laser Doppler flowmeter. Blood flow was decreased by 5-HT in a dose-dependent manner and vasomotion in the testis was inhibited, suggesting that it could be involved in the physiological regulation of the testicular vasculature. The 5-HT antagonists did not significantly influence flow or vasomotion in intact testes. Histamine did not cause any major effects on testicular blood flow. Substance 48/80 caused degranulation of testicular mast cells, and reduced testicular blood flow and vasomotion suggesting that testicular mast cells, possibly by releasing 5-HT, could be involved in the local control of the testicular vasculature.
G. Selstam, M. Gåfvels, E. Norjavaara and J.-E. Damber
Summary. Noradrenaline infusion for 2 min (0·4 μg/min) in anaesthetized rats increased the vascular resistance in 6-day-old corpora lutea, but had no significant effect on the vascular resistance in young (2-day-old) or old corpora lutea (11 days old). The luteal blood flow of the control rats was higher in 6-day-old corpora lutea than in those of 2 and 11 days. The luteal blood flow apparently lacks autoregulation, since a linear relationship between blood flow and arterial blood pressure was registered. The present study shows that, besides the well known metabolic effects of catecholamines on corpus luteum function, catecholamines can exert acute vascular effects, but only on the corpus luteum of pseudopregnancy in the middle of its life span.
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.
P. O. Janson, J.-E. Damber and C. Axén
Summary. Ovarian and luteal blood flow rates were measured, by means of radioactive microspheres, in anaesthetized rabbits on Day 8 of pseudopregnancy before and after lowering the ovarian perfusion pressure with a sling placed around the aorta. When blood pressure was lowered by 42% luteal flow decreased 9-fold whilst flow to the remaining part of the ovary remained unchanged, indicating the presence of an autoregulatory mechanism in the ovarian interstitital gland.
Ovarian progesterone secretion, assessed from progesterone concentrations in ovarian venous blood, was positively correlated to the blood flow per unit of weight of luteal tissue. These data indicate that a high rate of luteal blood flow may be necessary for an optimal steroid production by the corpus luteum.
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.
A. Bergh, H. Nikula, J.-E. Damber, R. Clayton and I. Huhtaniemi
Summary. Testicular descent was prevented unilaterally in newborn rats by cutting the gubernaculum testis. At 100 days of age, the number of Leydig and Sertoli cells per testis, the concentration of receptors for LH, FSH, prolactin and GnRH, and endogenous concentrations of progesterone and testosterone were determined. The weight of the abdominal testes was reduced by 80%, but in spite of this they contained as many Sertoli (32·8 ± 1·3 × 106, mean ± s.e.m., n = 6) and Leydig (28·2 ± 1·7 × 106) cells as did scrotal testes (32·1 ± 2·5 × 106 and 24·3 ± 1·2 × 106 respectively). The numbers of receptors for LH (3·2 ± 0·2 and 1·0 ± 0·2 pmol/testis, mean ± s.e.m., n = 11), FSH (358 ± 11·0 and 96·3 ± 12·6 fmol/testis) and prolactin (535 ± 32·7 and 92·4 ± 13·2 fmol/testis) were reduced (P < 0·001) in abdominal testes, but the number of GnRH receptors was unaffected (8·9 ± 1·4 and 12·1 ± 1·8 fmol/testis, n = 6). Testicular testosterone concentration (30·9 ± 4·4 vs 15·4 ± 3·2 ng/g, n = 11, P < 0·001), but not that of progesterone (0·87 ± 0·10 vs 1·01 ± 0·21 ng/g), was decreased in abdominal testes. The decreased receptor and androgen values reflect functional disturbances in the abdominal testes. The changed local milieu within abdominal testes may reduce hormone receptor concentrations which are then involved in the observed Leydig cell dysfunction.