α2-Agonists to Restore Adrenergic Vasoconstrictor Responsiveness in Septic Shock

Abstract

Editorial atelectrauma from overdistension injury. Bronchiolar damage may well be a histological marker of atelectrauma.What does the study by Park et al (5) teach us? First, it suggests that even transient losses of airway pressure may frustrate valiant attempts at lung recruitment. Whether complete avoidance of transient derecruitment is a valuable or even feasible, clinical goal remains to be seen. The confusing but very interesting issue of injury location highlights the fact that until the day we really understand the fine detail of what does-or does nothappen at the level of the most distal airspaces, lung recruitment should not be globally declared a lung protective strategy. 2. Caironi P, Cressoni M, Chiumello D, et al: Lung opening and closing during ventilation of acute respiratory distress syndrome. Am J Respir Crit Care Med 2010; 181:578-586 3. Briel M, Meade M, Mercat A, et al: Higher vs \ovjer positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome: Systematic review and meta-analysis. JAMA 2010; 303:865-873 4. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The acute respiratory distress syndrome network. N Engl J Med

Effects of dexmedetomidine and esmolol on systemic hemodynamics and exogenous lactate clearance in early experimental septic shock

“…DEX and clonidine might have opposite actions on vasomotor tone, a direct vasopressor, and indirect vasodilatory effects, with variable impact on MAP. When administered in healthy volunteers, DEX exerts a biphasic response, an initial increase in MAP due to stimulation of postsynaptic α 2b receptors followed by a long-lasting fall in MAP due to its central sympatholytic action with a decrease in epinephrine and NE blood levels [ 43 ]. Some investigators have tested the hypothesis that central sympaticolysis might help to restore adrenergic vasoconstrictor responsiveness in septic shock by reversing downregulation of alpha receptors secondary to high endogenous catecholamines, and some experimental data tend to support this as feasible [ 27 , 44 ].…”

Pressor Response to Noradrenaline in the Setting of Septic Shock: Anything New under the Sun—Dexmedetomidine, Clonidine? A Minireview

“…Following immediate resuscitation [ 1 ], the clinician treating septic shock faces different issues including (a) recoupling the peripheral compartment (i.e., the microcirculation) to the “central” compartment (i.e., brain, heart, and lung) and (b) restoring the pressor response to vasopressors, usually noradrenaline (NA). This minireview addresses these issues in the setting of septic shock, given the surge in interest pertaining to the use of α 2 -adrenoceptor agonists in this setting [ 2 , 3 ].…”