Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In several diseases chronic pain is associated with long-lasting pathophysiological responses which differ strongly from those observed in acute situations. When persisting, acute pain often results in physical and psychological stress which may in turn aggravate the initial pathological state. In the present work we examined the secretory patterns of pituitary hormones related to acute stress (growth hormone (GH), prolactin (PRL) and beta-endorphin (beta-END)) in rats during the phase of Freund adjuvant-induced arthritis (AIA, a model used for chronic pain studies) when chronic pain is maximum (14 and 21 days, postinoculation (PI)). Using radio-immunoassay hormones were measured in plasma samples taken every 30 min for 7 h in free-moving rats 14 and 21 days after Freund adjuvant or vehicle injection and in control animals. The total amount of GH secretion was higher at 14 and 21 days PI in AIA rats as compared to vehicle-treated and control animals, and the pulsatility of GH secretory pattern was not modified by AIA. PRL and beta-END secretion were not significantly different in arthritic rats as compared to controls. These results show that GH, PRL and beta-END responses induced by acute stress are not observed during the AIA phase when chronic pain is maximum. Thus, in our experimental conditions, beta-END and PRL do not seem to be good plasma markers of chronic pain.(ABSTRACT TRUNCATED AT 250 WORDS)
Pain 1992 Apr
PMID:Chronic pain induces a paradoxical increase in growth hormone secretion without affecting other hormones related to acute stress in the rat. 159 79

The effect of acute stress, with and without pain, on serum and mononuclear cell cation content was studied in 205 healthy women in their last trimester of pregnancy or during normal labour, in patients with acute medical conditions in which pain was or was not present, in acute surgical conditions, and immediately prior to elective surgery. In all subjects there was a fall in serum sodium, potassium, magnesium and calcium concentrations during stress, with an apparent shift into the intracellular space. An inverse correlation was present between the severity of pain and the fall in serum cations.
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PMID:Serum and intracellular electrolytes in patients with and without pain. 186 34

Chronic treatment with alprazolam reversed the effect of acute stress on the concentration of immunoreactive beta-endorphin (IR-BE) in the anterior pituitary (AP) and increased the amount of beta-endorphin (BE) relative to beta-lipotropin (B-LPH). In chronically stressed animals, administration of alprazolam did not alter the effect of a single stressful episode on the concentration of IR-BE in the AP, the NIL or the plasma, however, the amount of BE relative to B-LPH was increased in the AP and the plasma. Administration of alprazolam resulted in a significant decrease in the perception of pain. A low dose of alprazolam produced the most consistent decrease in nociception over time. The present findings suggest that alprazolam may modify the effects of acute and chronic stress on BE release from the pituitary. Moreover, alprazolam appears to have an antinociceptive effect in addition to its affect as an anxiolytic.
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PMID:Possible opiate action in the anxiolytic and antinociceptive actions of alprazolam. 204 72

Opinions differ as to whether marathon runners have an increased susceptibility to upper respiratory tract (URT) infections after a race. In an attempt to answer this question, we carried out a prospective study of the incidence of symptoms of URT infections in 150 randomly selected runners who took part in the 1982 Two Oceans Marathon in Cape Town, and compared this with the incidence in individually matched controls who did not run. Runners were questioned on the day before and 2 weeks after the race. Symptoms of URT infection occurred in 33.3% of runners compared with 15.3% of controls, and were most common in those who achieved the faster race times. The incidence in slow runners was no greater than that in controls. Faster runners also experienced more musculoskeletal pain during and after the race. These results suggest a relationship between acute stress and susceptibility to URT infections. Impairment of one or more local mucosal or general host defences may account for this effect.
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PMID:Ultramarathon running and upper respiratory tract infections. An epidemiological survey. 662 47

The present paper examines the role of the ventral noradrenergic bundle (VB) in relation to endorphins in the control of nociception in the rat. Selective, bilateral destruction of the VB produced a substantial fall in hypothalamic levels of noradrenaline. On day 4 post-surgery, VB-lesioned rats displayed a pronounced elevation in basal nociceptive threshold. This proved to be reversible by the specific opioid antagonist, naloxone, evidential of its mediation by endorphins. It was, however, unaffected by dexamethasone, a suppressor of corticotrophic secretion of beta-endorphin, indicative that this pituitary pool of beta-endorphin was not responsible. On day 12, at which time the elevation in nociceptive threshold had disappeared, neither the time course nor the intensity of the antinociception elicited by acute stress or various doses of morphine was attenuated in VB-lesioned as compared to sham rats. These data are evidential that the VB may influence nociceptive thresholds via an interaction with a CNS endorphinergic network. They demonstrate, further, that the VB does not mediate a significant component of the antinociception generated by either morphine or stress.
Pain 1982 Sep
PMID:Evidence for an interrelationship between ventral noradrenergic bundle and CNS endorphins in the control of nociception in the rat. 714 37

It has been suggested that acute stress induces analgesia in rats and mice. However, stress can have a myriad of debilitating effects on organisms, and it is not clear whether stress decreases the perceived intensity of the painful stimulus (i.e., a change in sensitivity) or decreases the willingness or ability of the organism to carry out the appropriate bodily movement (i.e., a change in responsivity). Since traditional animal analgesia tests confound sensitivity with responsivity, we assessed the effects of immobilization stress on rats trained on a two-choice, two-shock discrimination task, in which the dependent measures are presumably less reflective of alterations in pain responsivity. Immobilization stress significantly disrupted shock discrimination performance, with the disruption occurring primarily in choice performance signalled by the higher intensity shock discriminative stimulus. These effects completely dissipated with successive daily exposures to stress. The data suggest that immobilization stress has a specific effect on pain sensitivity which is separate from its possible effects on pain responsivity.
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PMID:Effects of immobilization stress on shock discrimination performance in rats. 716 86

The occurrence of pain after total hip arthroplasty emphasizes the covert nature of acute stress fractures. In a 46-year-old woman, the lesion was not apparent on initial radiograms; cultures as well as gram stain of the joint fluid were also negative, and the initial ESR and white blood count were normal, effectively ruling out infection. An arthrogram, performed to demonstrate possible loosening, revealed stress fracture of the superior pubic ramus. Without evidence of active infection, it may therefore prove wise to postpone revision surgery for several weeks or until diagnosis of an occult fracture becomes radiologically apparent.
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PMID:Stress fracture of the pubis after total hip arthroplasty. 728 57

Early evidence has indicated the presence and involvement of specific neural systems which can inhibit the responses to painful stimuli. More recently, further advances suggest that the opiate system may interact with other systems to modulate the analgesia produced by the opiates or various stressors. Since corticosteroids were found to be elevated under the conditions of different stress-induced analgesia (SIA), there may be interactions between the pain-inhibiting systems and the corticosteroids. Recently it was reported that acute stress or long-term adrenalectomy can result in release of beta-endorphin (beta E) and ACTH from the pituitary gland, which can be blocked by dexamethasone. In our early studies we have shown partial antagonism of the SIA by dexamethasone and complete antagonism after naloxone. In this report it was found that chronic treatment of the rats with 0.02% metyrapone in drinking water for 8 weeks resulted in minor hyperalgesia. The chronic pretreatment with metyrapone resulted in a significant potentiation of the analgesia induced via the cold swim stress model, which was reversed by 1 mg/kg (IP) naloxone. Also, hyperalgesia was noted 18 days after the bilateral adrenalectomy of the rats as measured in our laboratory by the hot plate method and as reported by Heybach and Vernikos-Danellis in 1978. These results suggest that the corticosteroid modulation (pituitary-adrenal axis) may have a role in regulating the SIA, and this may implicate the interactions of the corticosteroids with pain-inhibiting systems.
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PMID:Corticosteroid modulation and stress-induced analgesia in rats. 730 Oct 53

The stress associated with experiencing or witnessing physical trauma can cause abrupt and marked alterations in mental state, including anxiety and transient dissociative symptoms. Intense manifestations of this pattern of response to trauma are described in a new diagnostic category proposed for DSM-IV: acute stress disorder. Severe dissociative symptoms may predict subsequent posttraumatic stress disorder. Persons who experience a series of traumatic events may be especially vulnerable to a variety of dissociative states, including amnesia, fugue, depersonalization, and multiple personality disorder. Treatment for these symptoms emphasizes strengthening supportive interpersonal relationships and developing insight that reduces psychological pain by integrating the trauma into a meaningful, less self-blaming perspective.
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PMID:Trauma and dissociation. 850 55

1. Twenty-four hour ambulatory blood pressure monitoring (ABPM) was used to evaluate the blood pressure (BP) changes in acute stroke. 2. Stroke was categorized according to the probable underlying vascular mechanism into lacunar infarction (L), thrombotic infarction (T) and intracerebral haemorrhage (ICH). A total of 37 stroke patients were studied (T = 21, L = 9, ICH = 7). Control patients (n = 15) were acute medical admissions not severely ill or in significant pain. ABPM was performed on day 1 and day 7 following admission. 3. Day 1 mean +/- s.d. 24 h systolic BP (SBP) were L (159 +/- 15.8), ICH (151 +/- 33.4), T (147 +/- 15.2) and controls (134 +/- 17.8). Day 7 mean 24 h SBP were L (138 +/- 9.8), ICH (143 +/- 26.9), T (138 +/- 19) and controls (134 +/- 14.8). In each stroke group BP fell to levels similar to control on day 7, while control mean SBP remained unchanged between days 1 and 7. The highest day 1 BP and the greatest subsequent fall on day 7 occurred for lacunar infarction. Diastolic BP showed similar changes to SBP. 4. The acute stress of hospitalization does not appear to explain elevated BP in acute stroke. Lacunar infarction appears to be particularly associated with temporary BP elevation.
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PMID:24 hour ambulatory blood pressure profiles in the acute phase of stroke. 857 17


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