| Objective:Septic shock is characterized by altered tissue perfusion associated with persistent arterial hypotension.Vasopressor therapy is the current recommended mainstay of treatment for septic shock,but excessive adrenergic stress has multiple adverse effects. The aim of this study was to assess the effects of reducing excessive sympathetic outflow usinga2-agonists(dexmedetomidine) on hemodynamic and metabolic variables and on microvascular reactivity in patients with septic shock.Design:Prospective, observational clinical study.Setting:Mixed 60-bed intensive care unit (ICU) at a university hospitalMeasurements and Main Results:After initial fluid resuscitation,26 septic shock patients with relatively stable hemodynamics by using norepinephrine were enrolled.The microcirculatory network was evaluated in the ublingual mucosa by the sidestream dark-field imaging device.after administration dexmedetomidine was not associated with any change in Systemic hemodynamic and oxygen metabolism even if the dose of dexmedetomidine doubling. SDF imaging showed an increase in total vessel density from 20.8mm/mm2(18.6-23.4) to 23.1 mm/mm2 (21.2-25.5) (P<0.00) at point 0.3 and 23.6 mm/mm2 (22.3-25.5) (P<0.00) at point 0.6,while stoped infusion of dexmedetomidine for two hours, TVD was significantly decreased to 21.5 mm/mm2 (18.8-24.5) compared to point 0.3(P<0.01) and point 0.6(P<0.001). Similar differences were also seen in the MFI.The MFI significantly increased after dexmedetomidine infusion from 2.0 (1.6-2.5) to 2.6 (2.4-2.9) (P<0.001), MFI was significantly decreased to 14.0(12.4-15.8) compared to point 0.3(P< 0.00) and point 0.6(P<0.00).Conclusions:In adult patients with septic shock, we found that dexmedetomidine administration can augment microcirculatory perfusion, even if blood plasma catecholamine levels decrease. |
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