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Recognition and Alleviation of Pain and Distress in Laboratory Animals
can influence the stress response include age, sex, physical fitness, experience, disease, and medication.
Neural and endocrine substances are released in response to a stressor and play an important role in the initiation and coordination of the behavioral, cardiovascular, and immunologic responses to stress. The site of origin of those substances influences the physiologic stress response, which has two categories of duration: a rapid increase in circulating neurally derived substances with a short duration of action and a slower increase in endocrine-derived substances with a longer duration of action.
Acute stress—surgery, postoperative pain, burns, anesthesia, cardiac arrest, exercise, and sometimes headache—results in the hypothalamic secretion of corticotropin-releasing factor (CRF). CRF then stimulates the pituitary to cosecrete adrenocorticotropic hormone (ACTH), which promptly stimulates the release of corticosteroids from the adrenal cortex and the opioid peptides β-lipotropin and β-endorphin. In humans, plasma concentrations of these hormones can increase by a factor of 2–5 during stress. The roles of β-lipotropin and β-endorphin in the stress response are poorly understood. β-Endorphin might play a role in pain modulation (Hargreaves et al., 1983, 1987; Pickar et al., 1983; Szyfelbein et al., 1985). A potential target of circulating β-endorphin could be inflamed tissue (Joris et al., 1987).
The major example of neurally derived responses to acute stress is the activation of the sympathoadrenal system. The pituitary-adrenal axis responds with a prompt increase in catecholamines from the adrenal medulla, which is usually followed by an increase in corticosteroids. Plasma concentrations of catecholamines increase considerably after surgery or postoperative pain, because of increased circulating concentrations of epinephrine, primarily from the adrenal medulla, and norepinephrine, primarily from sympathetic nerve terminal activation (Goldstein, 1987). Those different components of the sympathoadrenal system can be regulated separately. The sympathoneural release of norepinephrine evokes a regionally selective effect, whereas the adrenal medulla produces an increase in systemic plasma concentrations of epinephrine. The physiologic consequences of activation of those systems include increased cardiac output, increased skeletal muscle blood flow, cutaneous vasoconstriction, reduced gut motility, and increased glucose availability.
Hormonally derived responses to stress result from changes in concentrations of growth hormone, prolactin, glucagon, insulin, vasopressin, neuropeptides, and other hormones. Acute stress causes increased secretion of growth hormone and prolactin, both from the anterior pituitary. Prolactin participates in metabolic processes and might modify nociception, but concentrations remain in the normal range in the presence of chronic stress. The significance of the short-lasting growth hormone increase is not known. Glucagon increases in response to acute stress, and insulin decreases. The decrease in insulin—in combination with increased prolactin, growth hormone, glucagon, and epinephrine—contributes to the development of hyperglycemia.