Physiological inhibition and facilitation of adrenocortical response to hemorrhage.
In a search for physiological feedback inhibition, secretion rates of cortisol were measured in intact dogs before and after sequential hemorrhages. The sucond of two sequential hemorrhages of 10 ml/kg separated by 90 min evoked significantly less increase of secretion rate of cortisol than did the first. This result was not explained by differential hemodynamic effects. Exhaustion of pituitary or adrenal capacities was excluded, since dogs responded normally to a second, larger hemorrhage. However, no attenuation response to a second 10 ml/kg hemorrhage was seen after a larger, 20 ml/kg, first hemorrhage. This led in turn to a search for a physiological facilitatory mechanism which might offset the feedback effect. The second of two rapid sequential hemorrhages to isovolemia following preexpansion of plasma volume evoked significantly greater increase of secretion rate of cortisol than did the first. This result also was not explained by differential hemodynamic effects. The results support the hypothesis that hemorrhage elicits both physiological feedback and facilitatory effects which interact and which are (different) functions of the intensity of stimulus.
D000311:Adrenal Glands / Q000378:metabolism*; D000324:Adrenocorticotropic Hormone / Q000378:metabolism*; D000818:Animals; D004285:Dogs; D005246:Feedback; D006470:Hemorrhage / Q000503:physiopathology*; D006854:Hydrocortisone / Q000378:metabolism; D010902:Pituitary Gland / Q000502:physiology
D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone