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Endotoxemia reduces cerebral perfusion but enhances dynamic cerebrovascular autoregulation at reduced arterial carbon dioxide tension.

Abstract：

OBJECTIVE:The administration of endotoxin to healthy humans reduces cerebral blood flow but its influence on dynamic cerebral autoregulation remains unknown. We considered that a reduction in arterial carbon dioxide tension would attenuate cerebral perfusion and improve dynamic cerebral autoregulation in healthy subjects exposed to endotoxemia. DESIGN:Prospective descriptive study. SETTING:Hospital research laboratory. SUBJECTS:Ten healthy young subjects (age: 32 ± 8 yrs [mean ± SD]; weight: 84 ± 10 kg; weight: 184 ± 5 cm; body mass index: 25 ± 2 kg/m2) participated in the study. INTERVENTIONS:Systemic hemodynamics, middle cerebral artery mean flow velocity, and dynamic cerebral autoregulation evaluated by transfer function analysis in the very low (<0.07 Hz), low (0.07-0.15 Hz), and high (>0.15 Hz) frequency ranges were monitored in these volunteers before and after an endotoxin bolus (2 ng/kg; Escherichia coli). MEASUREMENTS AND MAIN RESULTS:Endotoxin increased body temperature of the subjects from 36.8 ± 0.4°C to 38.6 ± 0.5°C (p < .001) and plasma tumor necrosis factor-α from 5.6 (2.8-6.7) pg/mL to 392 (128-2258) pg/mL (p < .02). Endotoxemia had no influence on mean arterial pressure (95 [74-103] mm Hg vs. 92 [78-104] mm Hg; p = .75), but increased cardiac output (8.3 [6.1-9.5] L·min(-1) vs. 6.0 [4.5-8.2] L·min(-1); p = .02) through an elevation in heart rate (82 ± 9 beats·min(-1) vs. 63 ± 10 beats·min(-1); p < .001), whereas arterial carbon dioxide tension (37 ± 5 mm Hg vs. 41 ± 2 mm Hg; p < .05) and middle cerebral artery mean flow velocity (37 ± 9 cm·sec(-1) vs. 47 ± 10 cm·sec(-1); p < .01) were reduced. In regard to dynamic cerebral autoregulation, endotoxemia was associated with lower middle cerebral artery mean flow velocity variability (1.0 ± 1.0 [cm·sec(-1)] Hz vs. 2.8 ± 1.5 [cm·sec(-1)] Hz; p < .001), reduced gain (0.52 ± 0.11 cm·sec(-1) x mm Hg(-1) vs. 0.74 ± 0.17 cm·sec(-1) x mm Hg(-1); p < .05), normalized gain (0.22 ± 0.05 vs. 0.40 ± 0.17%·%; p < .05), and higher mean arterial pressure-to-middle cerebral artery mean flow velocity phase difference (p < .05) in the low frequency range (0.07-0.15 Hz). CONCLUSIONS:These data support that the reduction in arterial carbon dioxide tension explains the improved dynamic cerebral autoregulation and the reduced cerebral perfusion encountered in healthy subjects during endotoxemia.

journal_name

Crit Care Med

journal_title

Critical care medicine

authors

Brassard P,Kim YS,van Lieshout J,Secher NH,Rosenmeier JB

doi

10.1097/CCM.0b013e3182474ca7

subject

Has Abstract

pub_date

2012-06-01 00:00:00

pages

1873-8

issue

eissn

0090-3493

issn

1530-0293

pii

00003246-201206000-00025

journal_volume

pub_type

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Endotoxemia reduces cerebral perfusion but enhances dynamic cerebrovascular autoregulation at reduced arterial carbon dioxide tension.