Abstract
IntroductionSepsis may be associated with disturbances in cerebral oxygen transport and cerebral haemodynamic function, thus rendering the brain particularly susceptible to hypoxia. The purpose of this study was to assess the impact of isocapnic hypoxia and hyperoxia on dynamic cerebral autoregulation in a human-experimental model of the systemic inflammatory response during the early stages of sepsis.MethodsA total of ten healthy volunteers were exposed to acute isocapnic inspiratory hyperoxia (FIO2 = 40%) and hypoxia (FIO2 = 12%) before and after a 4-hour lipopolysaccharide (LPS) infusion (2 ng kg-1). Middle cerebral artery blood follow velocity was assessed using transcranial Doppler ultrasound, and dynamic autoregulation was evaluated by transfer function analysis.ResultsTransfer function analysis revealed an increase in the phase difference between mean arterial blood pressure and middle cerebral artery blood flow velocity in the low frequency range (0.07–0.20 Hz) after LPS (P<0.01). In contrast, there were no effects of either isocapnic hyperoxia or hypoxia on dynamic autoregulation, and the cerebral oxygen vasoreactivity to both hyperoxia and hypoxia was unaffected by LPS.ConclusionsThe observed increase in phase suggests that dynamic cerebral autoregulation is enhanced after LPS infusion and resistant to any effects of acute hypoxia; this may protect the brain from ischaemia and/or blood–brain barrier damage during the early stages of sepsis.
Highlights
Sepsis may be associated with disturbances in cerebral oxygen transport and cerebral haemodynamic function, rendering the brain susceptible to hypoxia
End-tidal CO2 tension (PETCO2) was kept constant during the interventions, and apart from a small decrease during inspiratory hypoxia after LPS, values of PETCO2 were similar at baseline and after LPS; the corresponding PaCO2 levels were consistently lower after LPS, none of the subjects were hypocapnic (PaCO2
In the present study we found that LPS infusion was associated with enhanced dynamic cerebral autoregulation in healthy volunteers, as indicated by an increased mean arterial blood pressure (MAP)-to-middle cerebral artery blood flow velocity (MCAv) phase difference in the low frequency range
Summary
Sepsis may be associated with disturbances in cerebral oxygen transport and cerebral haemodynamic function, rendering the brain susceptible to hypoxia. Dynamic cerebral autoregulation has been found to be improved after lipopolysaccharide (LPS) administration in healthy volunteers [4,10], a human-experimental model of the systemic inflammatory response during early sepsis [11] This discrepancy suggests that dynamic autoregulation is maintained during the early stages of sepsis but becomes ‘indolent’ during the clinical course of disease, in the sense that the magnitude of the cerebrovascular response to a given change in MAP is preserved, while the response time of the cerebrovasculature becomes progressively prolonged [4]. The presence of systemic inflammation may render the cerebral circulation more susceptible to hypoxia by facilitating the formation of reactive oxygen-nitrogen species [15] As of it is unknown whether systemic inflammation enhances the effects of acute hypoxia on dynamic cerebral autoregulation
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