title: Impaired cerebrovascular reactivity in sepsis-associated encephalopathy studied by acetazolamide test.
abstract: BACKGROUND
  The pathophysiology of sepsis-associated encephalopathy (SAE) is not entirely clear. One of the possible underlying mechanisms is the alteration of the cerebral microvascular function induced by the systemic inflammation. The aim of the present work was to test whether cerebral vasomotor-reactivity is impaired in patients with SAE.
  
  
  METHODS
  Patients fulfilling the criteria of clinical sepsis and showing disturbance of consciousness of any severity were included (n = 14). Non-septic persons without previous diseases affecting cerebral vasoreactivity served as controls (n = 20). Transcranial Doppler blood flow velocities were measured at rest and at 5, 10, 15 and 20 minutes after intravenous administration of 15 mg/kgBW acetazolamide. The time course of the acetazolamide effect on cerebral blood flow velocity (cerebrovascular reactivity, CVR) and the maximal vasodilatory effect of acetazolemide (cerebrovascular reserve capacity, CRC) were compared among the groups.
  
  
  RESULTS
  Absolute blood flow velocities after administration of the vasodilator drug were higher among control subjects than in SAE. Assessment of the time-course of the vasomotor reaction showed that patients with SAE reacted slower to the vasodilatory stimulus than control persons. When assessing the maximal vasodilatory ability of the cerebral arterioles to acetazolamide during vasomotor testing, we found that patients with SAE reacted to a lesser extent to the drug than did control subjects (CRC controls:46.2 +/- 15.9%, CRC SAE: 31,5 +/- 15.8%, P < 0.01).
  
  
  CONCLUSIONS
  We conclude that cerebrovascular reactivity is impaired in patients with SAE. The clinical significance of this pathophysiological finding has to be assessed in further studies.
authors.affiliation: Department of Anesthesiology and Intensive Care, University of Debrecen, Health and Medical Science Center, Debrecen, Nagyerdei krt, Hungary. szatmari@freemail.hu
authors.forename: Szilárd
authors.initials: S
authors.lastname: Szatmári
authors.forename: Tamás
authors.initials: T
authors.lastname: Végh
authors.forename: Akos
authors.initials: A
authors.lastname: Csomós
authors.forename: Judit
authors.initials: J
authors.lastname: Hallay
authors.forename: István
authors.initials: I
authors.lastname: Takács
authors.forename: Csilla
authors.initials: C
authors.lastname: Molnár
authors.forename: Béla
authors.initials: B
authors.lastname: Fülesdi
mesh_terms: D000086:Acetazolamide / Q000008:administration & dosage / Q000494:pharmacology*; D000927:Anticonvulsants / Q000008:administration & dosage / Q000494:pharmacology*; D001783:Blood Flow Velocity / Q000187:drug effects; D001927:Brain Diseases / Q000097:blood / Q000000981:diagnostic imaging / Q000209:etiology* / Q000503:physiopathology*; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D006801:Humans; D018805:Sepsis / Q000150:complications*; D017585:Ultrasonography, Doppler, Transcranial
chemical_list: D000927:Anticonvulsants; D000086:Acetazolamide