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Trauma, endocrine response

In the ebb phase, there is increased activity of the sympathetic nervous system and increased plasma levels of adrenaline and glucocorticoids but a decreased level of insulin. This results in mobilisation of glycogen in the liver and triacylglycerol in adipose tissue, so that the levels of two major fuels in the blood, glucose and long-chain fatty acids, are increased. This is, effectively, the stress response to trauma. These changes continue and are extended into the flow phase as the immune cells are activated and secrete the proinflammatory cytokines that further stimulate the mobilisation of fuel stores (Table 18.2). Thus the sequence is trauma increased endocrine hormone levels increased immune response increased levels of cytokines metabolic responses. [Pg.418]

Table 18.2 Endocrine hormones and cytokines responsible for metabolic changes in trauma... Table 18.2 Endocrine hormones and cytokines responsible for metabolic changes in trauma...
Observations regarding the cellular immune response in PTSD are also consistent with enhanced GR responsiveness in the periphery. In one study, beclomethasone-induced vasoconstriction was increased in women PTSD subjects compared to healthy, non-trauma-exposed comparison subjects (Coupland et al. 2003). Similarly, an enhanced delayed-type hypersensitivity of skin test responses was observed in women who survived childhood sexual abuse vs those who did not (Altemus et al. 2003). Because immune responses, like endocrine ones, can be multiply regulated, these studies provide only indirect evidence of GR responsiveness. However, when considered in the context of the observation that PTSD patients showed increased expression of the re-... [Pg.382]

Miksche and Caldwell (Mil) have recently reported that after thyroidectomy rats with such injuries show no significant changes in heat production or average body temperature. Caldwell et al. (C4) had earlier reported that thyroidectomy did not prevent the metabolic response to injury in burned rats and an earlier review by Moore (M13) of the literature found the metabolic data on the thyroid in relation to trauma difficult to interpret. He concluded that, on the whole, it would seem that the thyroid partakes in the general alteration in endocrine and metabolic activity but without the early, massive, and systematic nature characteristic of adrenocorticol and antidiuretic alterations. [Pg.22]

In conclusion, injury leads to a blanket stimulation of endocrine secretion. This increased activity, with a few notable exceptions, does not appear to play a causal role in subsequent metabolic responses to trauma... [Pg.40]

The immediately early and later effects of the response to trauma in experimental animals and in patients housed at normal temperatures and which are all part of the inflammatory response, and the relation of these to such changes in the level of endocrine secretions as occur, are described. The time factor in the response to multiple injuries is also considered. [Pg.42]


See other pages where Trauma, endocrine response is mentioned: [Pg.329]    [Pg.255]    [Pg.257]    [Pg.261]    [Pg.265]    [Pg.267]    [Pg.269]    [Pg.273]    [Pg.275]    [Pg.277]    [Pg.281]    [Pg.283]    [Pg.283]    [Pg.285]    [Pg.427]    [Pg.304]    [Pg.49]    [Pg.341]    [Pg.95]    [Pg.288]    [Pg.396]    [Pg.435]    [Pg.19]   


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