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Hemorrhagic coagulopathy is involved in the morbidity and mortality of trauma patients. Nonetheless, many aspects of the mechanisms underlying this disorder are poorly understood. We have therefore investigated changes in fibrinogen metabolism and coagulation function after a moderate hemorrhagic shock, using a new stable isotope approach. Twelve pigs were randomly divided into the control (C) and hemorrhage (H) groups. Hemorrhage was induced by bleeding 35% total blood volume over a 30-min period. A primed constant infusion of [1-13C]phenylalanine (Phe), d5-phenylalanine, and α-[1-13C]-ketoisocaproate (KIC) was given to quantify fibrinogen synthesis and breakdown, together with measurements of circulating liver enzyme activities and coagulation function. Mean arterial pressure was decreased by hemorrhage from 89 ± 4 mmHg in C to 47 ± 4 mmHg in H (P « 0.05), followed by a rebound to 68 ± 5 mmHg afterward. Fibrinogen fractional synthesis rate increased from 2.7 ± 0.2%/h in C to 4.2 ± 0.4%/h in H by Phe (P « 0.05) and from 3.1 ± 0.4%/h in C to 4.4 ± 0.5%/h in H by KIC (P « 0.05). Fibrinogen fractional breakdown rate increased from 3.6 ± 1.0%/h in C to 12.9 ± 1.8%/h in H (P « 0.05). The absolute breakdown rate accelerated from 3.0 ± 0.4 mg·kg-1·h-1 in C to 5.4 ± 0.6 mg·kg-1·h-1 in H (P « 0.05), but the absolute synthesis rate remained unchanged. These metabolic changes were accompanied by a reduction in blood clotting time to 92.7 ± 1.6% of the baseline value by hemorrhage (P « 0.05). No changes were found in liver enzyme activities. We conclude that the observed changes in coagulation after hemorrhagic shock are mechanistically related to the acute acceleration of fibrinogen degradation. [ABSTRACT FROM AUTHOR]

Normal cardiac metabolism requires continuous replenishment (anaplerosis) of catalytic intermediates of the citric acid cycle. Little is known about the quantitative aspects of propionate as a substrate of in vivo anaplerosis; therefore, we measured the rate of propionate entry into the citric acid cycle in hearts of anesthetized pigs. [U-[SUP13]C[SUB3]]propionate (0.25 mM) was infused in a coronary artery branch for I h via an extracorporeal perfusion circuit, and cardiac biopsies were analyzed for the mass isotopomer distribution of citric acid cycle intermediates. Infusion of propionate did not affect myocardial oxygen consumption, heart rate, or contractile function. In the infused territory, propionate infusion did not affect uptake of glucose and lactate but decreased free fatty acid uptake by one-half (P < 0.05). Propionate extraction and uptake were 57.4 ± 3.3% and 0.078 ± 0.009 μmol-min[SUP-1]-g[SUP-1]. Anaplerosis from propionate, calculated from the mass isotopomer distribution of succinate, accounted for 8.9 ± 1.3% of the citric acid cycle flux. Propioylcarnitine release accounted for only 0.033 ± 0.002% of propionate uptake. Methylcitrate did not accumulate. Thus administration of a low concentration of propionate appears to be a convenient and safe way to boost anaplerosis in the heart. [ABSTRACT FROM AUTHOR]

Presents information on a study which investigated the effects of glucose infusion on surfactant phosphatidylcholine (PC) metabolic kinetics in the lungs. Fatty acid composition in surfactant PC; Methodology; Results and discussion.

Explores the contributions of plasma free fatty acids (FFA) and de novo synthesized fatty acids (FA) to lung surfactant phosphatidylcholine (PC) synthesis. Isotopic enrichment of substrates; Synthetic rates of FFA and FA; Secretion rate and recycling rate of FFA and FA.