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

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