compensatory hyperfunction
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2008 ◽  
Vol 179 (4S) ◽  
pp. 697-697
Author(s):  
Mitsuru Saito ◽  
Shigeru Satoh ◽  
Takamitsu Inoue ◽  
Hiroshi Tsuruta ◽  
Takashi Obara ◽  
...  

1980 ◽  
Vol 95 (3) ◽  
pp. 416-421 ◽  
Author(s):  
Jan-Erik Damber ◽  
Anders Bergh

Abstract. Rats were made cryptorchid, bi- or unilaterally, by cutting gubernaculum testis at birth. At 100 days of age the basal plasma testosterone concentration was smaller in bilateral cryptorchid animals as compared to unilateral cryptorchid and control rats. After acute LH-stimulation plasma testosterone concentration increased in all rats, where the highest concentrations were found in the control group. The amount of testosterone in the testis after a 30 min LH-stimulation was lower in both kinds of cryptorchid testes but higher in the scrotal testis of the unilateral cryptorchid rats, all as compared to control testis. This decreased effect of LH observed in cryptorchid animals indicates an impaired Leydig cell function in cryptorchid testis. The results also show a compensatory hyperfunction of Leydig cells in the scrotal testes of unilateral cryptorchid rats. It was also found that the intratesticular concentration of oestradiol-17β was three-fold increased in unilateral cryptorchid testes and even more in bilateral cryptorchid ones.


1977 ◽  
Author(s):  
S.V. Andreev ◽  
A.A. Kubatiev

According to current concepts, pathogenesis of intravascular trombus formation is underlaid by three crucial factors: lesion of the vascular wall, impairment of hemodynamics and hemostatic properties of the blood. While admitting the important role of each of these factors, one should acknowledge that the true nature of thrombosis is much more complicated and does not always fit the framework of this triad. In our experiments on rabbits, it was demonstrated that the thrombotic process in the basin of the pulmonary vessels could be successfully reproduced even in intact animals under conditions of disturbed immune homeostasis. A distinctive feature of immune thrombosis of the pulmonary vessels was a generalized lesion of the microcirculatory bed, gradual increase in the thrombotic masses and involvement of the major branches of the pulmonary vessels (PV). Morphologically, a picture of lymphoid-cellular infiltration and localization of the antigenic complex in the affected PV was revealed. As a result of progressive decrease in the pulmonary arterial blood circulation and increasing resistance in the system of the lesser circulation there were noted, already during the first hours after the onset of the capillary thrombosis, a compensatory hyperfunction of the right ventricle of the heart which was manifested in its highly increased contractility, higher levels of cyclic AMP and phosphorylation potential. At a later period, however, the compensatory possibilities of the right ventricle of the heart failed to overcome this resistance with resulting incompetence of the organ starting to develop within 2-3 days.


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