title: Adrenal insufficiency during the late stage of polymicrobial sepsis.
abstract: OBJECTIVE
  Although studies have indicated that adrenal insufficiency occurs after severe trauma and hemorrhagic shock, it remains controversial whether adrenal function is depressed during the late stage of polymicrobial sepsis.
  
  
  METHODS
  Prospective, controlled animal study.
  
  
  METHODS
  A university research laboratory.
  
  
  METHODS
  Male rats (275-325 g) were subjected to polymicrobial sepsis by cecal ligation and puncture (CLP) or sham operation followed by the administration of normal saline solution.
  
  
  RESULTS
  Systemic blood samples were taken at 20 hrs after CLP (i.e., a late stage of sepsis) or sham operation to measure plasma levels of corticosterone and corticotropin as well as adrenal contents of corticosterone. Additional groups of animals were utilized to examine corticotropin-stimulated plasma corticosterone release as well as adrenal levels of cyclic adenosine monophosphate (cAMP, the second messenger of corticotropin action). The results indicate that despite a 75% (p < .05) higher concentration in plasma corticotropin at 20 hrs after the onset of sepsis, plasma corticosterone levels were similar to those in sham-operated animals. In addition, adrenal contents of corticosterone were reduced by 42% (p < .05) in septic animals. Moreover, the plasma corticosterone and adrenal cAMP responses to corticotropin were reduced by 53% and 27% (p < .05), respectively, at 20 hrs after CLP.
  
  
  CONCLUSIONS
  These findings suggest that, despite high plasma levels of endogenous corticotropin, adrenal dysfunction, as indicated by the reduction of corticotropin-induced plasma corticosterone release and adrenal contents of cAMP as well as the decreased adrenal levels of corticosterone, occurs during the late stage of polymicrobial sepsis. Therefore, the recognition of adrenal insufficiency and interventions to improve adrenal responsiveness may be beneficial in improving the outcome during late sepsis.
authors.affiliation: Department of Surgery, University of Alabama at Birmingham School of Medicine, Birmingham, AL 35294-0019, USA.
authors.forename: D J
authors.initials: DJ
authors.lastname: Koo
authors.forename: D
authors.initials: D
authors.lastname: Jackman
authors.forename: I H
authors.initials: IH
authors.lastname: Chaudry
authors.forename: P
authors.initials: P
authors.lastname: Wang
mesh_terms: D000311:Adrenal Glands / Q000737:chemistry; D000309:Adrenal Insufficiency / Q000097:blood / Q000175:diagnosis / Q000382:microbiology* / Q000628:therapy; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000818:Animals; D001424:Bacterial Infections / Q000150:complications* / Q000382:microbiology* / Q000628:therapy; D002432:Cecum / Q000601:surgery; D003345:Corticosterone / Q000032:analysis / Q000097:blood; D000242:Cyclic AMP / Q000032:analysis; D004195:Disease Models, Animal; D015994:Incidence; D008026:Ligation; D008297:Male; D011379:Prognosis; D011446:Prospective Studies; D011677:Punctures; D051381:Rats; D017207:Rats, Sprague-Dawley; D012307:Risk Factors; D018805:Sepsis / Q000150:complications* / Q000382:microbiology* / Q000628:therapy; D012965:Sodium Chloride; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D012965:Sodium Chloride; D000324:Adrenocorticotropic Hormone; D000242:Cyclic AMP; D003345:Corticosterone