Intensive care medicine experimental
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Intensive Care Med Exp · Dec 2015
Why do they die? Comparison of selected aspects of organ injury and dysfunction in mice surviving and dying in acute abdominal sepsis.
The mechanisms of sepsis mortality remain undefined. While there is some evidence of organ damage, it is not clear whether this damage alone is sufficient to cause death. Therefore, we aimed to examine contribution of organ injury/dysfunction to early deaths in the mouse abdominal sepsis. ⋯ In CLP-Only mice, although the deregulation of parameters indicative of organ injury/dysfunction was greater in dying versus surviving mice, it never exceeded the changes in surviving CLP-ODam animals, and it was not followed by histopathological damage and/or mitochondrial dysfunction. This shows that interpretation of the contribution of the organ injury/dysfunction to early deaths in the CLP model is not straightforward and depends on the pathophysiological origin of the profiled disturbances.
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Intensive Care Med Exp · Dec 2015
Effects of early hemodynamic resuscitation on left ventricular performance and microcirculatory function during endotoxic shock.
Microcirculation and macrohemodynamics are severely compromised during septic shock. However, the relationship between these two compartments needs to be further investigated. We hypothesized that early resuscitation restores left ventricular (LV) performance and microcirculatory function but fails to prevent metabolic disorders. We studied the effects of an early resuscitation protocol (ERP) on LV pressure/volume loops-derived parameters, sublingual microcirculation, and metabolic alterations during endotoxic shock. ⋯ Early hemodynamic resuscitation was effective to restore macrohemodynamia and myocardial contractility. Despite MAP and MFI were relatively preserved, the persistent microvascular dysfunction could explain metabolic disorders. The relationship between micro- and systemic hemodynamia and their impact on cellular function and metabolism needs to be further studied during endotoxic shock.
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Intensive Care Med Exp · Dec 2015
Alveolar instability (atelectrauma) is not identified by arterial oxygenation predisposing the development of an occult ventilator-induced lung injury.
Improperly set mechanical ventilation (MV) with normal lungs can advance lung injury and increase the incidence of acute respiratory distress syndrome (ARDS). A key mechanism of ventilator-induced lung injury (VILI) is an alteration in alveolar mechanics including alveolar instability or recruitment/derecruitment (R/D). We hypothesize that R/D cannot be identified by PaO2 (masking occult VILI), and if protective ventilation is not applied, ARDS incidence will increase. ⋯ PaO2 remained clinically acceptable while alveolar instability persisted at all levels of PEEP (especially PEEP <9 cmH2O). Therefore, PaO2 levels cannot be used reliably to guide protective MV strategies or infer that VILI is not occurring. Using PaO2 to set a PEEP level necessary to stabilize the alveoli could underestimate the potential for VILI. These findings highlight the need for more accurate marker(s) of alveolar stability to guide protective MV necessary to prevent VILI.
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High tidal volume can cause ventilator-induced lung injury (VILI), but positive end-expiratory pressure (PEEP) is thought to be protective. We aimed to find the volumetric VILI threshold and see whether PEEP is protective per se or indirectly. ⋯ The threshold for VILI is the lower limit of inspiratory capacity. Below this threshold, VILI does not occur. Within these limits, severe/lethal VILI occurs depending on the dynamic component. Above inspiratory capacity stress at rupture may occur. In healthy lungs, PEEP is protective only if associated with a reduced tidal volume; otherwise, it has no effect or is harmful.
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Intensive Care Med Exp · Dec 2015
Mesenchymal stromal cells are more effective than the MSC secretome in diminishing injury and enhancing recovery following ventilator-induced lung injury.
The potential for mesenchymal stem cells (MSCs) to reduce the severity of experimental lung injury has been established in several pre-clinical studies. We have recently demonstrated that MSCs, and MSC-secreted factors (secretome), enhance lung repair and regeneration at 48 h following ventilation-induced lung injury (VILI). We wished to determine the potential for MSC therapy to exert beneficial effects in the early recovery phase following VILI when ongoing injury coexists with processes of repair, and to compare the efficacy of MSC therapy to the use of the secretome alone. ⋯ The immunomodulating and/or reparative effect of MSCs is evident early after VILI in this model. MSC-conditioned medium was not as effective as the cells themselves in diminishing injury and restoring lung structure and function.