The aim of this study was to determine the effect of weight loss induced by 6 weeks very-low-calorie-diet (VLCD) and behavioural intervention on pulmonary gas exchange during exercise in non-smoking morbid obese (BMI>40 kg/m2) otherwise healthy patients. Seven obese patients underwent a maximal bicycle ergometer test with continuous analysis of expired air and arterial blood sampling before and after a mean weight loss of 18% (25.7 kg, range: 10-50 kg). Body mass index (BMI) decreased with weight loss from 46.6 (6.3) kg/m2 to 38.0 (4.7) kg/m2 (P<0.01). Oxygen consumption (VO2) at low and submaximal exercise levels decreased after weight reduction, but the change was not statistically significant. The peak oxygen consumption related to body weight (VO2/kg) increased 22% from the initial 16.2 (3.6) ml/min/kg to 19.8 (3.1) ml/min/kg (P<0.05). Decrease in VCO2 was significant at submaximal exercise level. Ventilatory equivalent for CO2 increased significantly after weight reduction (P<0.05). Standing up and light exercise resulted in a significant increase in the mean arterial oxygen tension (PaO2) (P<0.05) and a significant decrease in the mean alveolar-arterial difference P(A-a)O2 (P<0.05) when compared to supine values. The mean increase in PaO2 with weight loss was not significant. The peak P(A-a)O2 decreased significantly after weight reduction. In conclusion, weight reduction induced by VLCD and behavioural intervention without exercise therapy can improve gas exchange during exercise in morbid obesity. Increased wasted ventilation, and a tendency to alveolar hyperventilation, after weight loss may reflect a delay in the adaptation of regulation of breathing to rapid weight loss.

NAC increased tissue capacity against oxidative stress and decreased inflammatory response in CABG patients with normal ejection fraction.

Background. Heparin binding protein (HBP) is released from neutrophilic secretory vesicles upon neutrophil adhesion on the endothelium. HBP mediates capillary hyperpermeability experimentally. In sepsis, HBP predicts organ dysfunction. Cardiopulmonary bypass induces both neutrophil activation and hyperpermeability. We hypothesized that in cardiopulmonary bypass, HBP is released in the reperfused coronary circulation concomitantly with neutrophil adhesion. Methods. In 30 patients undergoing aortic valve replacement, concomitant blood samples were drawn from the coronary sinus and arterial line before aortic crossclamping and 5 min after reperfusion to calculate transcoronary differences. Plasma HBP concentrations, neutrophil markers lactoferrin and myeloperoxidase, myocardial injury marker heart-type fatty acid binding protein (hFABP) and leukocyte differential counts were measured. Results. Arterial HBP was 4.1 (3.6-5.3) ng/ml preoperatively and 150.0 (108.2-188.6) ng/ml after aortic declamping. HBP increased 39-fold, lactoferrin 16-fold and myeloperoxidase 4-fold during cardiopulmonary bypass. Before cardiopulmonary bypass, there were marginal transcoronary differences in HBP [1.4 (-0.4-3.6) ng/ml, p=0.001] and hFABP [0.4 (-0.04-3.5) ng/ml, p=0.001] but not in the other parameters. During reperfusion, transcoronary HBP release [6.4 (1.8-13.7) ng/ml, p<0.001] was observed, concomitantly with transcoronary neutrophil sequestration [-0.14 (-0.28-0.01) x10^9/l, p=0.001] and transcoronary hFABP release [6.9 (3.0-25.8) ng/ml, p<0.001]. There were no transcoronary differences in lactoferrin or myeloperoxidase during reperfusion. Conclusions. CPB results in substantial increase in circulating HBP. HBP is also released from the reperfused coronary circulation, concomitantly with coronary neutrophil adhesion and myocardial injury. HBP may be one candidate for a humoral factor mediating capillary leak in cardiopulmonary bypass.

SummaryWe assessed agreement between measurement of systemic oxygen uptake using the Fick-derived method, and a novel method described by Biro, based on the difference in oxygen concentrations of the delivered fresh gas and the gas circulating in the circle system. Twenty-nine patients undergoing elective cardiac surgery were studied during stable haemodynamic and ventilatory conditions. Systemic oxygen uptake was measured using the two methods in each patient before and after cardiopulmonary bypass. Limits of agreement were found to be wide ()162 to 311 ml.min )1 before bypass, and )257 to 401 ml.min )1 after bypass), indicating poor agreement between the methods. No significant difference was found between the pre-and post cardiopulmonary bypass values for each method. We conclude that the Biro method, although attractive in terms of its simplicity, is an unreliable measure of systemic oxygen uptake under these conditions.