Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: Myocardial injury associated with hyperinflation of the lung. | Available online http content 11 2 412 Letter Myocardial injury associated with hyperinflation of the lung Michael Eisenhut Luton and Dunstable Hospital Lewsey Road Luton UK Correspondence Michael Eisenhut michael_eisenhut@ Published 30 April 2007 Critical Care 2007 11 412 doi cc5738 This article is online at http content 11 2 412 2007 BioMed Central Ltd See related research by Kredel et al. http content 11 1 R13 A recent study 1 conducted in an animal model of acute lung injury compared a ventilation strategy in which lungs were inflated by brief application of 50 cmH2O pressure followed by increased positive end-expiratory pressure recruitment strategy versus conventional ventilation. The study identified an increased inflammatory reaction in liver sinusoids and increased serum aspartate aminotransferase AST and hyaluronate levels with the recruitment strategy. The authors speculated that deficient oxygen delivery and increased sinusoidal pressures may have caused liver injury. The findings of the study suggest an origin of AST outside the liver because there was no elevation in alanine aminotransferase levels hepatocellular necrosis or liver dysfunction. Animals in the group receiving the recruitment strategy required volume support and had temporarily reduced cardiac output. This indicated that the origin of AST elevation was a myocardial injury. Previous studies found that patients with acutely elevated intrapulmonary pressure resulting from bronchospasm 2 and severe respiratory syncytial viral lung disease leading to hyperinflation 3 exhibited evidence of myocardial injury such as elevated cardiac troponin levels this was probably due to strain imposed on the right ventricle by pulmonary hypertension. Ventricular strain has previously also been associated with elevated hyaluronate levels 4 . The increase in hepatic neutrophils may be due to a hyperoxia-induced increased inflammatory response found in .
