Critical care : the official journal of the Critical Care Forum
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Healthy piglets ventilated with no positive end-expiratory pressure (PEEP) and with tidal volume (VT) close to inspiratory capacity (IC) develop fatal pulmonary oedema within 36 h. In contrast, those ventilated with high PEEP and low VT, resulting in the same volume of gas inflated (close to IC), do not. If the real threat to the blood-gas barrier is lung overinflation, then a similar damage will occur with the two settings. If PEEP only hydrostatically counteracts fluid filtration, then its removal will lead to oedema formation, thus revealing the deleterious effects of overinflation. ⋯ High PEEP (and low VT) do not merely impede fluid extravasation but rather preserve the integrity of the blood-gas barrier in healthy lungs.
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Editorial Comment
Measuring glomerular filtration rate in the intensive care unit: no substitutes please.
Acute kidney injury (AKI), due to its increasing incidence, associated morbidity and mortality, and potential for development of chronic kidney disease with acceleration to end-stage renal disease, has become of major interest to nephrologists and critical care physicians. The development of biomarkers to diagnose AKI, quantify risk and predict prognosis is receiving considerable attention. Yet techniques to accurately assess functional changes within patients still rely on the use of an insensitive marker (creatinine), creatinine-based estimating equations and unreliable urinary tests. Therefore, it is critical that functional tests be developed and used in combination with biomarkers, thus allowing improved care in AKI and chronic kidney disease patient populations.
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Intestinal ischemia is a critical problem resulting in multiple organ failure and high mortality of 60 to 80%. Acute lung injury (ALI) is a common complication after intestinal ischemia/reperfusion (I/R) injuries and contributes to the high mortality rate. Moreover, activated neutrophil infiltration into the lungs is known to play a significant role in the progression of ALI. Integrin-mediated interaction is involved in neutrophil transmigration. Synthetic peptides containing an arginine-glycine-aspartate sequence compete with adhesive proteins and inhibit integrin-mediated interaction and signaling. Thus, we hypothesized that the administration of a cyclic arginine-glycine-aspartate peptide (cRGD) inhibited neutrophil infiltration and provided protection against ALI induced by intestinal I/R. ⋯ Treatment with cRGD effectively protected ALI and gut injury, lowered neutrophil infiltration, suppressed inflammation, and inhibited lung apoptosis after intestinal I/R. Thus, there is potential for developing cRGD as a treatment for patients suffering from ALI caused by intestinal I/R.