The central part of the endocrine system is the hypothalamic-pituitary-adrenal axis. This includes the paraventricular nucleus, which secretes corticotropin-releasing hormone (CRH) and arginine vasopressin, and the noradrenergic neurones clustered within the locus ceruleus. CRH stimulates secretion of pro-opiomelanocortin, simultaneously releasing ACTH from the anterior pituitary gland. The CRH and noradrenergic systems are both stimulated by serotoninergic and cholinergic systems and are inhibited by the g-aminobutyric acid (GABA) and opioid-peptide systems.
The best known neuroendocrine response to injury is undoubtedly the increase in ACTH secretion and the resultant increase in adrenocortical secretion of glucocorticoid hormones. It is obvious that this increase is of great importance. In its absence, tolerance to stress is reduced. In critically ill patients cortisol levels are positively correlated with APACHE, TISS (therapeutic intervention scoring system), and ISS (injury severity score). In patients suffering myocardial infarction cortisol levels reflect both infarct size and mortality. There are also significant associations between burn size and cortisol levels.
Recently the hypothalamic-pituitary-adrenal axis was found to undergo a biphasic change during critical illness. In the first phase, lasting a few days, the high cortisol concentrations appear to be induced by augmented ACTH release. In the second phase there is a discrepancy between low ACTH and high cortisol concentrations, suggesting that cortisol release is stimulated through an alternative pathway.
Sympathetic activation also results in the liberation of norepinephrine from postganglionic nerve endings and the adrenal medulla as well as the release of epinephrine from the adrenal medulla (Fig 1). In addition to cardiovascular disturbances, other contributory factors to the secretion of catecholamines cannot be excluded and pulmonary stimuli may be particularly important. Furthermore, many other factors are known to influence catecholamine secretion, including trauma, hypoxia, hypercarbia, hypoglycemia, body temperature, and acid-base status.
Renin secretion from the juxtaglomerular cells is stimulated by catecholamines from the adrenal medulla and the postganglionic renal sympathetic nerves that surround the juxtaglomerular cells (Fig 2). Any decline in blood pressure produced by injury also contributes to the stimulation of renin secretion. The angiotensin generated by the renin secretion helps to maintain tissue perfusion pressure by maintaining blood pressure, increasing aldosterone secretion, increasing vasopressin secretion, and stimulating sodium and water retention.
Fig. 2 The renin-angiotensin system in shock. (Reproduced with permission from HiQds..aQd.Wa.t§oQ i199.6).)
Various other stressful stimuli also increase vasopressin secretion. Decreased extracellular fluid volume is a particularly strong stimulus since vasopressin contributes to the maintenance of extracellular fluid volume by retaining water and causing vascular smooth muscle to contract. Therefore vasopressin may be seen to have a significant role in maintaining blood pressure when blood volume is reduced.
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