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Whether RRI reflects the systemic circulation or renal microcirculation is not well known.
Patients whose microcirculation is not responsive to such resuscitation, however, have a poor prognosis [ 2].
The impact of sepsis on the brain microcirculation is not well defined.
However, the CSF microcirculation is not a quantitatively important pathway for drug distribution into the brain from the CSF compartment.
The fact that the mitoPO2 more or less restores to baseline values suggests that in our model the autoregulation in the cutaneous microcirculation is not (yet) severely compromised.
In shock profiles other than sepsis where the microcirculation is not affected to such an extent, correction of global hemodynamic parameters would likely ensure adequate oxygenation of tissues.
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Markers of the microcirculation were not.
However, as the relationship between systemic hemodynamics and microcirculation are not straightforward [25, 26], the assessment of microcirculation might also improve our understanding of the effects of passive mobilization beyond changes to systemic hemodynamics.
Also the beneficial effects of citrulline supplementation during LPS infusion on the microcirculation were not present in eNOS-/ or double KO mice, although citrulline significantly enhanced the plasma arginine availability in all mouse strains.
Regrettably, despite both groups were managed using the same clinical protocols, as far as other interventions that might affect the microcirculation were not computed (such as red blood cell transfusion), we cannot attribute this improvement to DrotAA therapy.
The mechanisms by which fluids may improve the microcirculation are not well understood but may be related to a decrease in viscosity, to a decrease in white blood cell adhesion and rolling, or, indirectly, to a decrease in endogenous vasoconstrictive substances.
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