Fredholm B B, Farnebo L O, Hamberger B
Acta Physiol Scand. 1979 Apr;105(4):481-95. doi: 10.1111/j.1748-1716.1979.tb00113.x.
Plasma catecholamines, cyclic AMP and metabolic substrates in hemorrhagic shock of rats was studied in 4 groups of animals: 1) Control rats, 2) rats with adrenal demedullation, 3) rats with 6-OH-dopamine induced chemical sympathectomy, and 4) rats with combined demedullation and sympathectomy. The rats were bled to a systemic blood pressure of 35 mmHg. The basal plasma level of noradrenaline (NA), adrenaline (A) and dopamine (DA) in control animals was each about 1 nmol/1. After hemorrhage for 1 h the A levels had reached 50 nmol/l and there was little further rise after 4 h. The rise was eliminated by demedullation but unaffected by sympathectomy. NA levels rose continuously in the control and in the sympathectomized rats. At 1 h the level was about 4 nmol/l and at 4 h about 20 nmol/l. The demedullated rats showed a 3-fold increase in circulating NA, while little or no change was seen in the combined demedullated and sympathectomized rats. DA levels did not change in any of the groups during the first hour, but were markedly elevated after 4 h of hypotension. Cyclic AMP and glucose levels in plasma showed a rapid increase 1 h after hemorrhage and thereafter returned to or below basal values. Demedullation largely prevented the increase, while sympathectomy had no effect. The increase in lactate and pyruvate levels were diminished but not eliminated by either sympathectomy or demedullation. Glycerol levels were unchanged and FFA decreased in all groups of rats. The results show that the adrenal medulla is the dominating source of plasma catecholamines in hemorrhagic shock in rats. The initial increase in plasma glucose and cyclic AMP appear to be largely mediated by adrenal A. The subsequent fall in these parameters and derangement of circulatory homeostasis are not, in the present shock model, primarily due to a failure of catecholamine secretion, but rather to a decreased responsiveness of peripheral tissues to catecholamine stimulation.
对4组大鼠进行了研究，观察失血性休克大鼠血浆儿茶酚胺、环磷酸腺苷（cAMP）和代谢底物的变化情况：1）对照大鼠；2）肾上腺髓质切除大鼠；3）用6-羟基多巴胺诱导化学性交感神经切除术的大鼠；4）肾上腺髓质切除合并交感神经切除术的大鼠。将大鼠放血至全身血压为35 mmHg。对照动物血浆中去甲肾上腺素（NA）、肾上腺素（A）和多巴胺（DA）的基础水平均约为1 nmol/L。出血1小时后，A水平达到50 nmol/L，4小时后几乎不再进一步升高。这种升高可通过肾上腺髓质切除消除，但不受交感神经切除术的影响。对照大鼠和交感神经切除大鼠的NA水平持续升高。1小时时水平约为4 nmol/L，4小时时约为20 nmol/L。肾上腺髓质切除大鼠循环中的NA增加了3倍，而肾上腺髓质切除合并交感神经切除大鼠几乎没有变化或变化不明显。在最初1小时内，所有组的DA水平均无变化，但低血压4小时后显著升高。血浆中的环磷酸腺苷和葡萄糖水平在出血1小时后迅速升高，此后恢复到基础值或低于基础值。肾上腺髓质切除在很大程度上阻止了这种升高，而交感神经切除术则没有影响。乳酸和丙酮酸水平的升高通过交感神经切除术或肾上腺髓质切除术均有所减轻，但未消除。甘油水平未发生变化，所有组大鼠的游离脂肪酸（FFA）均下降。结果表明，肾上腺髓质是大鼠失血性休克时血浆儿茶酚胺的主要来源。血浆葡萄糖和环磷酸腺苷的最初升高似乎主要由肾上腺A介导。在当前的休克模型中，这些参数随后的下降以及循环稳态的紊乱，主要不是由于儿茶酚胺分泌不足，而是由于外周组织对儿茶酚胺刺激的反应性降低。
