Critical care medicine
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Critical care medicine · Nov 2013
Complement C5A Antagonist Treatment Improves the Acute Circulatory and Inflammatory Consequences of Experimental Cardiac Tamponade.
Cardiogenic shock often leads to splanchnic macro- and microcirculatory complications, and these events are linked to local and systemic inflammatory activation. Our aim was to investigate the consequences of complement C5a antagonist treatment on the early circulatory and inflammatory changes in a clinically relevant large animal model of cardiac tamponade. ⋯ These results provide evidence that blockade of the C5a effects significantly influences the acute splanchnic macro- and microhemodynamic complications and decreases the potentially harmful inflammatory consequences of experimental cardiogenic shock.
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Critical care medicine · Nov 2013
Prevention of Hemolysis-Induced Organ Damage by Nutritional Activation of the Vagal Anti-Inflammatory Reflex.
Acute hemolysis is associated with organ damage, inflammation, and impaired vascular function. Stimulation of the cholecystokinin-1 receptor-dependent vagal anti-inflammatory reflex with lipid-rich enteral nutrition was demonstrated to prevent tissue damage and attenuate inflammation. This study investigates the effects of nutritional activation of the vagal anti-inflammatory reflex on organ integrity, systemic inflammation, and microcirculation during hemolysis. ⋯ Nutritional activation of the vagal anti-inflammatory reflex preserves tissue integrity and attenuates systemic inflammation in a rodent model of acute hemolysis. In addition, lipid-rich nutrition improves renal, hepatic, and intestinal microcirculation. These findings implicate stimulation of the autonomic nervous system by nutritional means as a potential therapy to prevent complications of acute hemolysis. (Crit Care Med 2013; 41:e361-e367).
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Critical care medicine · Nov 2013
Synergistic Deleterious Effect of Hypoxemia and Hypovolemia on Microcirculation in Intestinal Villi.
To investigate the effect of hypoxemia, hemorrhagic shock, and the association of both of these on intestinal microcirculation (microcirculatory perfusion and leukocytes-endothelium interactions in postcapillary venules), as it can be encountered in hemorrhagic shock following trauma. ⋯ During hemorrhagic shock, the occurrence of hypoxemia considerably alters villous intestinal perfusion as it decreases the fraction of perfused villi in a synergistic manner, thereby increasing the risk of villous ischemia. The association of hypoxemia and hemorrhagic shock did not amplify leukocytes adhesion to the endothelium further than either hemorrhagic shock or hypoxemia alone did. As hypoxemia frequently occurs simultaneously with hemorrhagic shock in traumatic conditions, it can worsen gut ischemia leading to the exacerbation of multiple organ failure syndrome.