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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The adrenal response to a soluble form of beta1-24-corticotropin (tetracosactrin [ACTH]: 250 microgram administered intramuscularly) was studied in 28 patients with meningitis due to Neisseria meningitidis (21 with petechiae and seven without) and in six patients with Salmonella typhi bacteremia. Six normal subjects also were tested for adrenal responsiveness at four different times of the day (8 A.M., 12 noon, 4 P.M., and 10 P.M.) and served as controls. The results showed that, whatever the time of testing, patients with meningococcal infections and typhoid fever had unstimulated (basal) levels of plasma cortisol above the 99% confidence limits for the mean unstimulated cortisol levels for the normal subjects. Furthermore, although patients with meningitis without petechiae and subjects with S. typhi bacteremia responded to ACTH stimulation in a manner similar to that of the normal subjects, most subjects with meningitis with petechiae did not have increased levels of plasma cortisol after treatment with ACTH. This lack of response could not be ascribed entirely to the higher basal levels of plasma cortisol in these patients. Patients with meningitis associated with petechiae may have a relatively decreased adrenal response to stimulation with exogenous ACTH.
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PMID:The adrenal response to exogenous adrenocorticotrophin in patients with infections due to Neisseria meningitidis. 21 89

Blood was collected at 20-second intervals from the external carotid artery and from the dorsal longitudinal sagittal sinus (sagittal sinus, SS) of ovariectomized sheep. The point of SS catheterization was very near the point at which diencephalic effluent entered the SS. Concentrations of beta-endorphin (beta-EP) immunoreactivity were quantified by radioimmunoassay procedures in blood plasma and in cerebrospinal fluid (CSF) from the cisterna magna. Increases in plasma beta-EP concentration were provoked by intracarotid injection of naloxone and by experimental production of bacteremia (i.e., intravascular bacteria), but these procedures failed to increase beta-EP in CSF. Quantities of beta-EP in plasma samples from the SS were assumed to represent arterial contribution (minus tissue uptake), diencephalic secretion, and retrograde delivery of pituitary beta-EP to the diencephalic effluent. The arterial contribution was removed mathematically by subtracting the arterial plasma beta-EP concentration from the concurrent SS plasma concentration of beta-EP to yield a paired arteriovenous (AV) difference. When this AV difference was consistently positive and satisfied our statistical criterion for being greater than zero, we concluded that either pituitary beta-EP was delivered in a retrograde manner to diencephalon or the diencephalon secreted beta-EP. However, this situation occurred in only 5 of 31 periods examined. Furthermore, only 2 of these 5 periods occurred during times of increasing arterial concentrations of beta-EP. Such concurrence would be expected if both changes were caused by a major discharge of beta-EP from the pituitary gland. Therefore, the present results provide little evidence for retrograde delivery of pituitary beta-EP to the brain without systemic dilution.
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PMID:Continuous measurement of cerebral arteriovenous differences of beta-endorphin in sheep. 315 82

Acute bacteremia in sheep caused a surge of plasma beta-endorphin/beta-lipotropin (beta-EP/beta-LPH) associated with shivering behavior, tachycardia, hyperthermia, hemoconcentration, and decreased respiration rate. The surge of plasma beta-EP/beta-LPH was immediately followed by increases (P less than 0.05) in plasma prolactin and growth hormone (GH) concentrations and a depression (P less than 0.05) of plasma luteinizing hormone. These changes in pituitary hormone release were consistent with opioid-induced changes described in the literature. To examine possible opioid mediation, naloxone (2.5 mg X kg-1 X h-1) was continuously infused intravenously from 3 h before to 3 h after induction of an E. coli bacteremia. With the exception of plasma GH, naloxone failed to alter any of the hormonal or clinical parameters associated with bacteremia. For plasma GH, naloxone delayed (P less than 0.01) the increase but did not attenuate its magnitude, suggesting that an opioid mechanism may influence the timing of the pituitary GH release resulting from bacteremia. In general, opioid mechanisms sensitive to the present dosage of naloxone do not appear to mediate bacteremia-induced changes in hormonal or clinical parameters.
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PMID:Bacteremia-induced changes in pituitary hormone release and effect of naloxone. 609 78

Patients with cirrhosis are susceptible to bacterial infection, which can result in circulatory dysfunction, renal failure, hepatic encephalopathy, and a decreased survival rate. Severe sepsis is frequently associated with adrenal insufficiency, which may lead to hemodynamic instability and a poor prognosis. We evaluated adrenal function using short corticotropin stimulation test (SST) in 101 critically ill patients with cirrhosis and severe sepsis. Adrenal insufficiency occurred in 51.48% of patients. The patients with adrenal insufficiency had a higher hospital mortality rate when compared with those with normal adrenal function (80.76% vs. 36.7%, P < .001). The cumulative rates of survival at 90 days were 15.3% and 63.2% for the adrenal insufficiency and normal adrenal function groups, respectively (P < .0001). The hospital survivors had a higher cortisol response to corticotropin (16.2 +/- 8.0 vs. 8.5 +/- 5.9 microg/dL, P < .001). The cortisol response to corticotropin was inversely correlated with various disease severity, Model for End-Stage Liver Disease, and Child-Pugh scores. Acute physiology, age, chronic health evaluation III score, and cortisol increment were independent factors to predict hospital mortality. Mean arterial pressure on the day of SST was lower in patients with adrenal insufficiency (60 +/- 14 vs. 74.5 +/- 13 mm Hg, P < .001), and a higher proportion of these patients required vasopressors (73% vs. 24.48%, P < .001). Mean arterial pressure, serum bilirubin, vasopressor dependency, and bacteremia were independent factors that predicted adrenal insufficiency. In conclusion, adrenal insufficiency is common in critically ill patients with cirrhosis and severe sepsis. It is related to functional liver reserve and disease severity and is associated with hemodynamic instability, renal dysfunction, and increased mortality.
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PMID:Adrenal insufficiency in patients with cirrhosis, severe sepsis and septic shock. 1655 38