[Receptor mechanisms for realizing the effect of glucocorticoid hormones in traumatic and hemorrhagic shock].
Blood corticosterone concentrations showed a 2-fold increase in traumatic and hemorrhagic shock. Following 4 hours of injury, the rat hepatic cytasol density of glucocorticoidal receptor II and III decreased to 76 and 67% of the level of intact animals, respectively. There were changes in the physicochemical properties of glucocorticoidal receptors: an increase in Ka and a decrease in Kd of the hormone-receptor complexes. A direct relation was found of the glucocorticoid-binding capacity of receptors II to blood pressure (BP) in shock. The most marked suppression of receptors II was noted in hemorrhagic shock, which seems to be due to more profound systemic hemodynamic changes and low BP in this type of shock. There was a concurrent reduction in the density of receptors I and II up to the certain decrease in the levels of receptors II, then was an increase in receptor III binding of [3H]-corticosterone. With the low density of receptors II and with the high concentration of corticosterone, this appears to be aimed at preserving the glucocorticoid-dependent activation of the cell genetic apparatus. Dysfunctions found in the glucocorticoidal receptors are a cause of the development of relative glucocorticoid deficiency in shock.
Golikov
P P
PP
Kozhevnikova
L M
LM
Arkhipenko
Iu V
IuV
Nikolaeva
N Iu
NIu
D000818:Animals; D001794:Blood Pressure; D005938:Glucocorticoids / Q000502:physiology*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D011965:Receptors, Glucocorticoid / Q000502:physiology*; D012771:Shock, Hemorrhagic / Q000503:physiopathology*; D012774:Shock, Traumatic / Q000503:physiopathology*
D005938:Glucocorticoids; D011965:Receptors, Glucocorticoid