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  • 1
    ISSN: 1432-1238
    Keywords: Key words Oxygen consumption ; Endotoxemia ; Tumor necrosis factor ; Interleukin-6 ; Hypermetabolism ; Post-perfusion syndrome ; Cardiac surgery
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective: The aim of this study was to determine whether the increase in post-operative oxygen consumption (ΔVO2) in cardiac surgery patients is related to endotoxemia and subsequent cytokine release and whether ΔVO2 can be used as a parameter of post-perfusion syndrome. Design: Prospective study. Setting: Operating room and intensive care unit of a university hospital. Patients: Twenty-one consecutive male patients undergoing elective coronary artery bypass surgery without major organ dysfunction and not receiving corticosteroids. Measurements and results: Plasma levels of endotoxin, tumor necrosis factor (TNF) and interleukin-6 (IL-6) were measured before, during and for 18 h after cardiac surgery. Oxygen consumption, haemodynamics, the use of IV fluids and dopamine, body temperature and the time of extubation were also measured. Measurements from patients with high ΔVO2 (≥median value of the entire group) were compared with measurements from patients with low ΔVO2 (〈median). Patients with high ΔVO2 had higher levels of circulating endotoxin (P=0.004), TNF (P=0.04) and IL-6 (P=0.009) received more IV fluids and dopamine while in the ICU, and were extubated later than patients with low ΔVO2. Several hours after ΔVO2 the patient‘s body temperature rose. Forward stepwise regression analysis showed that circulating endotoxin and TNF explained 50% of the variability of ΔVO2. Conclusions: This study demonstrates that patients with high post operative oxygen consumption after elective cardiac surgery have higher circulating levels of endotoxin, TNF and IL-6 and also have more symptoms of post-perfusion syndrome. Early detection of high VO2 might be used as a clinical signal to improve circulation in order to meet the high oxygen demand of inflammation. In addition, continuous measurement of VO2 provides us with a clinical parameter of inflammation in interventional studies aiming at a reduction of endotoxemia or circulating cytokines.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1435-1803
    Keywords: captopril in ischemia ; captopril in cardioplegia ; adenosine triphosphate ; 31-phosphorusnuclear magnetic resonance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of captopril on energy-rich phosphates and pH during normothermic ischemic arrest, hypothermic cardioplegic arrest and subsequent reperfusion was investigated in the isolated rat heart using 31P-nuclear magnetic resonance. The hearts remained in the probe during all perfusion procedures and captopril (80 ml·l−1) treatment was started directly after cannulation. After normothermic ischemic arrest (15 min), the ATP content of captopril-treated hearts was not significantly different from that of untreated hearts (53±9% and 52±8%, respectively). Accumulation of inorganic phosphate at the end of ischemia was significantly less in treated hearts, suggesting a higher end-ischemic nucleotide content in treated hearts. Hypothermic cardioplegic arrest (St. Thomas' Hospital solution, 4°C) lasted for 3 h at 10°C. Adenosine triphosphate in treated hearts was significantly lower at the end of ischemia; 36±6% compared to 53±9% for untreated hearts. Adenosine triphosphate in untreated hearts recovered to 76±9% after normothermic ischemia and to 72±7% after hypothermic ischemia at the end of 30 min reperfusion. Captopril significantly improved adenosine triphosphate recovery in both treated groups; 89±4% after normothermic and 83±4% hypothermic ischemia. We conclude that captopril has a beneficial effect on recovery of adenosine triphosphate both after normothermic and after hypothermic ischemia.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Hoboken, NJ : Wiley-Blackwell
    Journal of Biomedical Materials Research 20 (1986), S. 773-784 
    ISSN: 0021-9304
    Keywords: Chemistry ; Polymer and Materials Science
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine , Technology
    Notes: To determine whether the surface free energy of polymer materials influences the spreading and growth of cells, surface free energies of 13 polymers and glass were related to spreading and growth of human skin fibroblasts. Experiments were performed in both the presence and absence of serum proteins. We calculated the surface free energy from contact angles of phosphate-buffered saline (PBS), n-propanol/PBS mixtures, and α-bromonaphthalene on the polymers, using the concept of polar and dispersion components accounting for spreading pressures. Cell spreading and substratum surface free energy (γs) showed a characteristic sigmoid relationship both in the presence and in the absence of serum proteins; good spreading only occurred when γs was higher than approximately 57 erg · cm-2. In the presence of serum proteins, cell spreading is similar on most materials; only few materials show relatively high cell spreading. Cell growth in the presence of serum proteins did not differ significantly on the various polymers with reference to their γs values. In contrast, two groups of polymers could be distinguished in the absence of serum with respect to cell growth. The first group showed increasing γs, whereas the second group showed consistently low cell growth. The results demonstrate the complex relationship between cell spreading and substratum surface free energy as well as the role of serum proteins in modifying the surface characteristics of polymers in relation to cell spreading and growth.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
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