These results help to explain the dynamics of the development, clinical relevance, and negative prognostic value of hypocholesterolemia in critical illness.

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Although reports of decreased plasma taurine in trauma, sepsis and critical illness are available, very little is known about the relationships among changes in plasma taurine, other amino acid levels and metabolic variables. We analyzed a large series of plasma amino acid profiles obtained in trauma patients with sepsis who were undergoing total parenteral nutrition. The correlations between plasma taurine, other amino acid levels, parenteral substrate doses and metabolic and cardiorespiratory variables were assessed by regression analysis. Post-traumatic hypotaurinemia was followed by partial recovery toward less abnormal values when sepsis developed. Levels of taurine were directly and significantly related to levels of glutamate, aspartate, ␤-alanine and phosphoethanolamine (and unrelated to other amino acids). Levels of these amino acids increased simultaneously with increasing doses of leucine, isoleucine and valine in total parenteral nutrition. Decreasing taurine was associated with increasing lactate, arteriovenous O 2 concentration difference and respiratory index, and with decreasing cholesterol and cardiac index. These results characterize the relationships between plasma taurine and other amino acid levels in sepsis, provide evidence of amino acid interactions that may support taurine availability and show more severe decreases in plasma taurine with the worsening of metabolic and cardiorespiratory patterns.

Quantitative relationships in CO2 transport and exchange processes were combined for use as the basic components of an original mathematical model for the calculation of venoarterial blood CO2 concentration difference (v-aDCO2). This is calculated as the sum of the increment in CO2 concentration (CCO2) related to the increase in CO2 tension (delta P) from arterial to venous value at constant O2 saturation (delta CCO2/delta P) and of the increment in CO2 concentration related to the decrease in O2 saturation (delta S) from arterial to venous value at constant CO2 tension (delta CCO2/delta S). The newly developed relationships correlated well with the experimental data from which they were derived (r2 = 0.94-0.99). The results provided by the model compared remarkably well with the results of previously published measurements (r2 = 0.96-0.99). This new model allows one to overcome some of the limitations implicit in previously available methods and provides a useful tool for the assessment and monitoring of hemodynamic, metabolic, and O2-CO2 exchange patterns in whole body and regional vascular beds.