Gann D S, Cryer G L, Pirkle J C
Am J Physiol. 1977 Jan;232(1):R5-9. doi: 10.1152/ajpregu.1977.232.1.R5.
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.
为了寻找生理反馈抑制，在连续出血前后测量了完整犬的皮质醇分泌率。两次连续出血，每次10ml/kg，间隔90分钟，第二次出血引起的皮质醇分泌率增加明显低于第一次。这一结果不能用不同的血流动力学效应来解释。垂体或肾上腺功能耗竭被排除，因为犬对第二次更大出血量的出血反应正常。然而，在第一次20ml/kg的大出血后，未观察到对第二次10ml/kg出血的衰减反应。这进而促使人们寻找一种可能抵消反馈效应的生理促进机制。在血浆容量预扩张后，两次快速连续出血至等容状态，第二次出血引起的皮质醇分泌率增加明显大于第一次。这一结果同样不能用不同的血流动力学效应来解释。这些结果支持这样一种假说，即出血引发生理反馈和促进效应，二者相互作用，且是刺激强度的（不同）函数。
