Critical care : the official journal of the Critical Care Forum
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Simple methods to predict the effect of lung recruitment maneuvers (LRMs) in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are lacking. It has previously been found that a static pressure-volume (PV) loop could indicate the increase in lung volume induced by positive end-expiratory pressure (PEEP) in ARDS. The purpose of this study was to test the hypothesis that in ALI (1) the difference in lung volume (DeltaV) at a specific airway pressure (10 cmH2O was chosen in this test) obtained from the limbs of a PV loop agree with the increase in end-expiratory lung volume (DeltaEELV) by an LRM at a specific PEEP (10 cmH2O), and (2) the maximal relative vertical (volume) difference between the limbs (maximal hysteresis/total lung capacity (MH/TLC)) could predict the changes in respiratory compliance (Crs), EELV and partial pressures of arterial O2 and CO2 (PaO2 and PaCO2, respectively) by an LRM. ⋯ A PV-loop-derived parameter, MH/TLC of 0.3, predicted changes in lung mechanics better than changes in gas exchange in this lung injury model.
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Editorial Comment
Are platelets a 'forgotten' source of sepsis-induced myocardial depressing factor(s)?
The mechanism of sepsis-induced cardiac failure was initially thought to be related to the presence of 'myocardial depressant' substances that directly alter heart function. Exosomes released by platelets and identified in the plasma are suggested to, at least partially, explain myocardial depression in sepsis. This hypothesis needs to be evaluated by clinical studies.
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Stimulation of beta2-adrenergic receptors (beta2-ARs) inhibits tumor necrosis factor-alpha (TNF-alpha) release in monocytes. In septic shock, endogenous catecholamines induce beta2-AR downregulation, leading to an increased TNF-alpha release. The aims of this study were to analyze the molecular mechanisms of beta-adrenergic downregulation and to explore therapeutic interventions with maintained anti-inflammatory efficacy in septic shock using the inhibition of phosphodiesterase 4 (PDE4). ⋯ In septic shock, the anti-inflammatory effects of catecholamines are blunted by downregulation of beta2-ARs and upregulation of the inhibitory G protein in CD14+ monocytes. Beta-adrenergic downregulation is overcome by inhibitors of PDE4. These results provide a mechanistic rationale for the therapeutic use of selective PDE4 inhibitors in the treatment of septic shock.
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It is suspected that mitochondrial dysfunction is a major cause of organ failure in sepsis and septic shock. A study presented in this issue of Critical Care revealed that liver mitochondria from pigs treated with norepinephrine during endotoxaemia exhibit greater in vitro respiratory activity. The investigators provide an elegant demonstration of how therapeutic interventions in sepsis may profoundly influence mitochondrial respiration, but many aspects of mitochondrial function in sepsis remain to be clarified.
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Editorial Comment
The essential nature of healthcare databases in critical care medicine.
Medical databases serve a critical function in healthcare, including the areas of patient care, administration, research and education. The quality and breadth of information collected into existing databases varies tremendously, between databases, between institutions and between national boundaries. The field of critical care medicine could be advanced substantially by the development of comprehensive and accurate databases.