Many of the pathogenic mechanisms of severe sepsis take place in the microcirculatory unit [ 4], which is comprised of the arteriole, the capillary bed, and the postcapillary venule.
Are there surrogate vascular beds that could be used, and what are their relationships to more relevant microcirculatory units like the gut and the brain microcirculations?
In theory, the systemic administration of vasodilator agents in septic shock could recruit microcirculatory units, decrease microcirculatory shunting, and improve regional tissue oxygenation [ 32].
In patients with sepsis, prostacyclin increased both oxygen delivery and oxygen consumption, probably via recruitment of shunted microcirculatory units that lead to improve tissue metabolism and function [ 12].
In perioperative patients mortality is low, and in sepsis and critical illness mortality is affected by various pathomechanisms and interventions other than tissue perfusion and recruitment of weak microcirculatory units.
In this way, an NO donor agent can open the microcirculation and thereby perfuse weak microcirculatory units, while an anti-inflammatory agent or specific iNOS inhibitor can reduce pathological shunting and redirect blood flow to recruit weak microcirculatory units.
Inhomogeneous expression of iNOS interferes with regional blood flow and promotes shunting from vulnerable weak microcirculatory units [ 23].
However, hemodilution-induced hemodynamic effects can cause a redistribution of oxygen delivery away from weak microcirculatory units within organs, as well as between organs [ 14] and sublingual compartments [ 39, 43].
These hypoxic areas are considered to reflect shunting of weak microcirculatory units [31, 32].
Resuscitation following MMDS must include focused recruitment of hypoxic-shunted microcirculatory units and/or resuscitation of the mitochondria.
