Manipulations in coronary flow during reperfusion did not affect postischemic cardiac function in control or aortic constriction hearts, suggesting that depressed coronary flow during early reperfusion is not a primary cause of postischemic diastolic dysfunction in the hypertrophied myocardium.

BackgroundAcute kidney injury (AKI) is a prominent problem in hospitalized patients and associated with increased morbidity and mortality. Clinical medicine is currently hampered by the lack of accurate and early biomarkers for diagnosis of AKI and the evaluation of the severity of the disease.In 2010, we established a multivariate peptide marker pattern consisting of 20 naturally occurring urinary peptides to screen patients for early signs of renal failure. The current study now aims to evaluate if, in a different study population and potentially various AKI causes, AKI can be detected early and accurately by proteome analysis.MethodsUrine samples from 60 patients who developed AKI after cardiac surgery were analyzed by capillary electrophoresis-mass spectrometry (CE-MS). The obtained peptide profiles were screened by the AKI peptide marker panel for early signs of AKI. Accuracy of the proteomic model in this patient collective was compared to that based on urinary neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) ELISA levels. Sixty patients who did not develop AKI served as negative controls.ResultsFrom the 120 patients, 110 were successfully analyzed by CE-MS (59 with AKI, 51 controls). Application of the AKI panel demonstrated an AUC in receiver operating characteristics (ROC) analysis of 0.81 (95 % confidence interval: 0.72–0.88). Compared to the proteomic model, ROC analysis revealed poorer classification accuracy of NGAL and KIM-1 with the respective AUC values being outside the statistical significant range (0.63 for NGAL and 0.57 for KIM-1).ConclusionsThis study gives further proof for the general applicability of our proteomic multimarker model for early and accurate prediction of AKI irrespective of its underlying disease cause.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-016-1344-z) contains supplementary material, which is available to authorized users.

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Oesophageal PCO2 is less than gastric PCO2, and the difference is greater when gastric PCO2 levels are greater. Air tonometry may not measure regional PCO2 levels in the oesophagus satisfactorily. Other methods and sites for carbon dioxide tonometry should be examined.