Plasma catecholamines, cyclic AMP and metabolic substrates in hemorrhagic shock of the rat. The effect of adrenal demedullation and 6-OH-dopamine treatment.

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.