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Colloids Surf B Biointerfaces. 2004 Mar 15;34(2):95-104.

Interactions between hematological derivatives and dipalmitoyl phosphatidyl choline: implications for adult respiratory distress syndrome.

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School of Biosciences and Bioengineering, Indian Institute of Technology, Mumbai 400076, India.


Blood and its components flood the alveoli in adult respiratory distress syndrome (ARDS) and may be responsible for the inhibition of lung surfactant in this syndrome. We have evaluated the surface properties of dipalmitoyl phosphatidylcholine (DPPC) monolayers-the main component of lung surfactant, in the presence of blood and its components. Experiments were performed using a Langmuir-Blodgett trough at physiological temperature (37 degrees C), pH 7.0 and using 0.9% saline as the sub-phase. Whole blood (WB), membranes obtained from whole blood cells (Mem), lysed blood (LB), homogenized blood clot (CLOT), serum (SER), platelet rich plasma (PRP), platelet poor plasma (PPP) and individual plasma proteins (albumin, fibrinogen) were added to the sub-phase in the equivalent proportion of 10 parts of DPPC per million parts (w/v) of hematological inhibitor. Cell membranes were found to be the most inhibitory agent for DPPC surface activity as evidenced by an increase in the minimum surface tension (from 0.818 +/- 0.219 to 7.373 +/- 0.854 mN/m) and percentage area change required to reduce the surface tension from 30 to 10 mN/m (from 21.24 +/- 0.99 to 66.83 +/- 4.44). The inhibitory potential of pure plasma proteins differed from those of more complex blood derivatives like platelet rich plasma and serum. Whole blood and platelet poor plasma were non-inhibitory, but serum, platelet rich plasma and clot significantly increased the minimum surface tension of DPPC to 6.819 +/- 0.925, 6.625 +/- 2.261 and 6.060 +/- 0.640 mN/m, respectively. These results were statistically significant with one-way analysis of variance and Newman-Keul's test (P < 0.05). The present study suggests that, not only the presence of the individual blood component(s) in the lung alveoli but also their interactions decide their inhibitory capability. Pure plasma proteins are not representative of the inhibitory effects of blood derivatives like serum, platelet rich plasma and blood cell membranes which would be more relevant for inhibitory models of ARDS.

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