Cerebral vasoreactivity to acetazolamide is not impaired in patients with severe sepsis

B. Fülesdi, Szilárd Szatmári, Csaba Antek, Zoltán Fülep, Péter Sárkány, L. Csiba, Csilla Molnár

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Introduction: The pathophysiology of sepsis-associated encephalopathy (SAE) is not entirely clear, but one of the possible underlying mechanisms is the alteration of the cerebral microvascular function. The aim of the present work was to test whether cerebral vasomotor reactivity is impaired in patients with severe sepsis. Methods: Patients fulfilling the criteria of clinical sepsis and showing at least 2 organ dysfunctions were included (n = 16). Nonseptic healthy persons without previous diseases affecting cerebral vasoreactivity served as controls (n = 16). Transcranial Doppler blood flow velocities were measured at rest and at 5, 10, 15, and 20 minutes after intravenous administration of 15 mg/kg 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 did not differ between control and septic patients. Assessment of the time course of the vasomotor reaction showed that patients with sepsis reacted in a similar fashion 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 there was no difference in vasodilatory ability between septic and healthy subjects (CRC controls, 54.8% ± 11.1%; CRC sepsis-associated encephalopathy, 61.1% ± 34.4%; P = .49). Conclusions: We conclude that cerebrovascular reactivity is not impaired in patients with severe sepsis. It is conceivable that cerebral vasoreactivity may be differently involved at different severity stages of the septic process.

Original languageEnglish
Pages (from-to)337-343
Number of pages7
JournalJournal of Critical Care
Volume27
Issue number4
DOIs
Publication statusPublished - Aug 2012

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Acetazolamide
Sepsis
Blood Flow Velocity
Cerebrovascular Circulation
Arterioles
Vasodilator Agents
Intravenous Administration
Healthy Volunteers

Keywords

  • Acetazolamide
  • Cerebral vasoreactivity
  • Septic encephalopathy

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

Cerebral vasoreactivity to acetazolamide is not impaired in patients with severe sepsis. / Fülesdi, B.; Szatmári, Szilárd; Antek, Csaba; Fülep, Zoltán; Sárkány, Péter; Csiba, L.; Molnár, Csilla.

In: Journal of Critical Care, Vol. 27, No. 4, 08.2012, p. 337-343.

Research output: Contribution to journalArticle

Fülesdi, B. ; Szatmári, Szilárd ; Antek, Csaba ; Fülep, Zoltán ; Sárkány, Péter ; Csiba, L. ; Molnár, Csilla. / Cerebral vasoreactivity to acetazolamide is not impaired in patients with severe sepsis. In: Journal of Critical Care. 2012 ; Vol. 27, No. 4. pp. 337-343.
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AB - Introduction: The pathophysiology of sepsis-associated encephalopathy (SAE) is not entirely clear, but one of the possible underlying mechanisms is the alteration of the cerebral microvascular function. The aim of the present work was to test whether cerebral vasomotor reactivity is impaired in patients with severe sepsis. Methods: Patients fulfilling the criteria of clinical sepsis and showing at least 2 organ dysfunctions were included (n = 16). Nonseptic healthy persons without previous diseases affecting cerebral vasoreactivity served as controls (n = 16). Transcranial Doppler blood flow velocities were measured at rest and at 5, 10, 15, and 20 minutes after intravenous administration of 15 mg/kg 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 did not differ between control and septic patients. Assessment of the time course of the vasomotor reaction showed that patients with sepsis reacted in a similar fashion 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 there was no difference in vasodilatory ability between septic and healthy subjects (CRC controls, 54.8% ± 11.1%; CRC sepsis-associated encephalopathy, 61.1% ± 34.4%; P = .49). Conclusions: We conclude that cerebrovascular reactivity is not impaired in patients with severe sepsis. It is conceivable that cerebral vasoreactivity may be differently involved at different severity stages of the septic process.

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