Acute Stress Response

The stress system is characterized by two modes of operation, a fast phase that serves to mobilize and activate, and a slow phase that promotes recovery and adaptation. Each mode is associated with characteristic behavioral changes that are mediated by distinct cellular and molecular mechanisms. 

The slow phase of the stress system is characterized by processes that promote recovery from, and adaptation to, the stressful conditions that prompted the response. At the level of the hypothalamus, this phase is probably mediated by the urocortins acting through CRHR2 receptors (Reul and Holsboer, 2002 de Kloet et al., 2005). In contrast to the fast phase, the slow phase is associated w ith activation of the parasympathetic nervous system, w hich promotes the appetitive and metabolic functions, w hich help to restore homeostasis. As cortisol levels 

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The first suggestion that abnormal noradrenergic transmission was linked with anxiety came from Redmond s laboratory in the 1970s when he drew attention to the similarities in the symptoms and signs of anxiety with those of the acute stress response (Redmond and Huang 1979). He went on to stimulate the locus coeruleus of (chair-restrained) monkeys and showed that this caused behavioural changes, some of which resembled a cluster of behaviours displayed by the animals when under threat. This work led to the proposal that anxiety was due to (or exacerbated by) excessive... 

If there is no improvement in the acute stress response 3 to 4 weeks post trauma, SSRIs should be started in a low dose with slow titration upward toward antidepressant doses. Eight to 12 weeks is an adequate duration of treatment to determine response. 

Koren, D., Arnon, I., and Klein, E. (1999) Acute stress response and posttraumatic stress disorder in traffic accident victims a one-year prospective, follow-up study. Am] Psychiatry 156 367-373. 

Stroke induces an acute stress response—i.e., over-activation of the sympathetic nervous system and increased corticosteroid levels (with resultant neutrophiha and lymphocytopenia). This in turn leads to depressed immunity and altered immune responses during the acute phase of stroke and may predispose patients to infections, particularly pneumonia, which is the commonest cause of mortality after the first few days of stroke (Meisel et al., 2005). In the clinical setting, increased total white cell counts and neutrophilia, which correlate with infarct size, are independently associated with worse outcome after stroke. Recently a massive and early activation of the systemic immnne system has been shown to occur also in experimental stroke (Offner et al., 2006). 

PTSD symptoms respond slowly to pharmacotherapy, and some patients may never experience full resolution. SSRIs should be started 3 to 4 weeks after exposure to a trauma in patients with no improvement in their acute stress response. The initiation of an SSRI should be at a low dose with gradual titration upward toward antidepres-sant doses. Eight to twelve weeks is an appropriate duration of antidepressant therapy to determine response. ... 

Clarke, D.M., Russell, P.A., Polglase, A.L. and McKenzie, D.P. (1997) Psychiatric disturbance and acute stress response in surgical patients. Australia and New Zealand Journal of Surgery, 67, 115-118. 

Adachi N, Tomonaga S, Tachibana T, Denbow DM, Furuse M (2006) (—)-Epigallocatechin gallate attenuates acute stress responses through GABAergic system in the brain. Eur J Pharmacol 531(1-3) 171-175. doi 10.1016/j.ejphar.2005.12.024, S0014-2999(05)01326-9 [pii]... 

Severe depression of both classical and alternative pathway failure of acute stress response Significant inhibition of acute inflammatory response due to lack of complement derived mediators this enhances significance of phagocytic cell defect in vivo... 

Steroid Hormones and Neurosteroids. Steroids (qv) can affect neuroendocrine function, stress responses, and behavioral sexual dimorphism (78,79) (see Steroids). Mineralocorticoid, glucocorticoid, androgen, estrogen, and progesterone receptors are localized in the brain and spinal cord. In addition to genomic actions, the neurosteroid can act more acutely to modulate the actions of other receptors or ion channels (80). Pregnenolone [145-13-17, ( ) dehydroepiandosterone [53-43-0] C H2 02 (319) are excitatory neurosteroids found in rat brain, independent of adrenal... 

Family of transcription factors that modulate the expression of genes which control immune, inflammatory, and acute-phase responses, as well as cell growth, responses to stress, apoptosis, and oncogenesis. All members of this family have a Rel-homology domain that contains sequences responsible for dimerization and DNA binding. In vertebrates, this family includes NF-kB1 (also known as p50), NF-kB2 (also known as p52), Rel (also known as cRel), Rel-A (also known as p65), and Rel-B. 

Hepatic reperfusion injury is not a phenomenon connected solely to liver transplantation but also to situations of prolonged hypoperfusion of the host s own liver. Examples of this occurrence are hypovolemic shock and acute cardiovascular injur) (heart attack). As a result of such cessation and then reintroduction of blood flow, the liver is damaged such that centrilobular necrosis occurs and elevated levels of liver enzymes in the serum can be detected. Particularly because of the involvement of other organs, the interpretation of the role of free radicals in ischaemic hepatitis from this clinical data is very difficult. The involvement of free radicals in the overall phenomenon of hypovolemic shock has been discussed recently by Redl et al. (1993). More specifically. Poll (1993) has reported preliminary data on markers of free-radical production during ischaemic hepatitis. These markers mostly concerned indices of lipid peroxidation in the serum and also in the erythrocytes of affected subjects, and a correlation was seen with the extent of liver injury. The mechanisms of free-radical damage in this model will be difficult to determine in the clinical setting, but the similarity to the situation with transplanted liver surest that the above discussion of the role of XO activation, Kupffer cell activation and induction of an acute inflammatory response would be also relevant here. It will be important to establish whether oxidative stress is important in the pathogenesis of ischaemic hepatitis and in the problems of liver transplantation discussed above, since it would surest that antioxidant therapy could be of real benefit. 

The development of mild forms of anxiety and neuroveg-etative and/or cognitive responses to stress may represent an adaptive evolutionary step against environmentally (external) or self-triggered (internal) threats, but maladaptive reactions have also emerged in human evolution. Thus, anxiety disorders are maladaptive conditions in which disproportionate responses to stress, or even self-evoked responses, are displayed. Anxiety disorders are one of the most frequent psychiatric illnesses, and have a lifetime prevalence of 15- 20% [1, 89]. The most common presentations are generalized anxiety disorder, with a lifetime prevalence rate of close to 5% [1, 89] social anxiety disorder, with very variable lifetime prevalence rates ranging from 2 to 14% [90] panic disorder, with rates from 2 to 4% [1,89] and post-traumatic stress disorder (PTSD), with a prevalence rate close to 8%. Specific phobias, acute stress and obsessive-compulsive behavior are other clinical presentations of anxiety disorders. 

Webb, N.A. and C.M. Wood. 1998. Physiological analysis of the stress response associated with acute silver nitrate exposure in freshwater rainbow trout (Oncorhynchus mykiss). Environ. Toxicol. Chem. 17 579-588. 

Armario A, Marti 0, Molina T, de Pablo J, Valdes M. (1996). Acute stress markers in humans response of plasma glucose, cortisol, and prolactin to two examinations differing in the anxiety they provoke. Psychoneuroendocrinology. 21(1) 17-24. 

Morinobu, S., Nibuya, M., and Duman, R.S. (1995) Chronic antidepressant treatment down-regulates the induction of c-Fos mRNA in response to acute stress in rat frontal cortex. Neuropsychopharmacology 12 221-228. 

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