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The dynamic cerebral autoregulatory adaptive response to noradrenaline is attenuated during systemic inflammation in humans
Author(s) -
Berg Ronan MG,
Plovsing Ronni R,
Bailey Damian M,
HolsteinRathlou NielsHenrik,
Møller Kirsten
Publication year - 2015
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12421
Subject(s) - medicine , septic shock , sepsis , blood pressure , mean arterial pressure , cerebral autoregulation , lipopolysaccharide , anesthesia , perfusion , transcranial doppler , middle cerebral artery , cerebral blood flow , shock (circulatory) , cerebral perfusion pressure , autoregulation , heart rate , ischemia
Summary Vasopressor support is used widely for maintaining vital organ perfusion pressure in septic shock, with implications for dynamic cerebral autoregulation ( dCA ). This study investigated whether a noradrenaline‐induced steady state increase in mean arterial blood pressure ( MAP ) would enhance dCA following lipopolysaccharide ( LPS ) infusion, a human‐experimental model of the systemic inflammatory response during early sepsis. The dCA in eight healthy males was examined prior to and during an intended noradrenaline‐induced MAP increase of approximately 30 mmHg. This was performed at baseline and repeated after a 4‐h intravenous LPS infusion. The assessments of dCA were based on transfer function analysis of spontaneous oscillations between MAP and middle cerebral artery blood flow velocity measured by transcranial D oppler ultrasound in the low frequency range (0.07–0.20 Hz). Prior to LPS , noradrenaline administration was associated with a decrease in gain (1.18 (1.12–1.35) vs 0.93 (0.87–0.97) cm/mmHg per s; P  <   0.05) with no effect on phase (0.71 (0.93–0.66) vs 0.94 (0.81–1.10) radians; P  = 0.58). After LPS , noradrenaline administration changed neither gain (0.91 (0.85–1.01) vs 0.87 (0.81–0.97) cm/mmHg per s; P  = 0.46) nor phase (1.10 (1.04–1.30) vs 1.37 (1.23–1.51) radians; P  = 0.64). The improvement of dCA to a steady state increase in MAP is attenuated during an LPS ‐induced systemic inflammatory response. This may suggest that vasopressor treatment with noradrenaline offers no additional neuroprotective effect by enhancing dCA in patients with early sepsis.

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