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Muscle protein synthesis was measured by infusion of L-[2H(5)]phenylalanine in two groups of anesthetized dogs, before and during infusion of insulin with euaminoacidemia, and with differing concentrations of unlabeled phenylalanine (tracee). With the infusion of insulin, muscle protein synthesis increased 39 +/- 12% based on phenylalanyl-tRNA. Calculation with plasma phenylalanine enrichment overestimated insulin stimulation by 40% (56 +/- 12 vs. 39 +/- 12%). Raising the concentration of plasma phenylalanine twofold during infusion of insulin further increased the apparent stimulation of muscle protein synthesis based on plasma relative to phenylalanyl-tRNA by 225% (65 +/- 19 vs. 20 +/- 14%, P < 0.001). In both experiments, the stimulation of synthesis rates calculated from phenylalanine enrichment within the muscle was closer to that from phenylalanyl-tRNA (48 +/- 19%, experiment 1; 30 +/- 14%, experiment 2). Results indicate that the enrichment of a labeled amino acid within plasma and tissue amino acid pools is affected by the concentration of tracee infused. Increasing the concentration of tracee overestimates the insulin-mediated stimulation of muscle protein synthesis when amino acid pools other than aminoacyl-tRNA are used as the precursor enrichment.

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BACKGROUND: Critically ill trauma patients are often in negative nitrogen balance and demonstrate advanced muscle protein wasting, which is in part due to a decrease in muscle protein synthesis. Previous studies have been performed on the relationship between pH and protein metabolism. Some evidence suggests that alkalosis might enhance protein synthesis. The purpose of the present study is to determine whether protein synthesis is increased in trauma patients who have a respiratory alkalosis from hyperventilation. METHODS: Trauma patients in the intensive care unit (n = 8) who were treated with hyperventilation for elevated intracranial pressures were enrolled. Muscle protein synthesis rates were determined in vivo using the flooding method with l-[(2)H(5)]phenylalanine. Measurements were performed twice on each patient within a 36-h period, first during hyperventilation and then after hyperventilation was discontinued. Hemoglobin oxygen saturation was maintained above 95% for all measurements. RESULTS: Protein synthesis in muscle was 1.38 +/- 0.11%/day during hyperventilation (pH 7.50 +/- 0.02, pCO(2) 27.3 +/- 1.0 mm Hg) and 0.93 +/- 0.15%/day after respiratory parameters were normalized (pH 7.39 +/- 0.01, pCO(2) 39.4 +/- 1.5 mm Hg). The synthesis rate was significantly higher (P < 0.01, paired t test), 0.46 +/- 0.13%/day (32.6%), at the time of hyperventilation. CONCLUSION: Muscle protein synthesis is elevated during hyperventilation in critically ill patients with traumatic brain injury. We believe this preliminary study provides data that warrant confirmation in larger clinical studies. It suggests that this ventilatory therapeutic strategy may have a role in mitigating the negative nitrogen balance and muscle protein wasting that can impair the recovery of these patients.

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BACKGROUND: Reoperations for coronary artery bypass grafting are on the rise. The general rule of replacing all saphenous vein grafts (SVGs) older than 5 years of age at the time of reoperation has recently been challenged on clinical grounds. This study provides functional data of endothelial behavior in long-term vein grafts. METHODS: Previously placed SVGs were removed at the time of redo operations. Nitric oxide (NO) measurements in real time were carried out before and after stimulation with morphine. The measurements were compared to the angiographic appearance of the grafts obtained prior to operation. Grafts were categorized into 3 groups: disease-free, moderately diseased, and severely diseased. RESULTS: Sixteen grafts were analyzed. Five were angiographically disease-free, 4 had moderate, and 7 severe disease. In the disease-free group, peak NO production after 10(-6) mol/L morphine stimulation was 35 mol/L, equivalent to the production of native saphenous vein. The severely diseased group did not demonstrate an increase in NO production, and the moderately diseased group produced a small rise in production. CONCLUSIONS: Measurement of NO release of old SVGs, when angiographically pristine, equals that of native saphenous vein. These findings support the recent clinical observations that long-term angiographically disease-free vein grafts are biologically privileged.

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Torsion of the gallbladder is an unusual cause of necrosis of the gallbladder. Since its first description a century ago, its diagnosis prior to operative exploration has been extremely elusive. The diagnostic value of current radiological imaging is limited. In the present report, we describe a case of torsion of the gallbladder in which laparoscopy was used successfully to identify and treat this condition without the usual requirement of open exploration. Additionally, the etiology, incidence, clinical presentation, radiologic studies, and treatment of the condition are reviewed.

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BACKGROUND: Previous reports of commercial airline disasters have reviewed incidents occurring at takeoff and landing. The purpose of the present study, which represents the first analysis of aviation injuries incurred during a midflight incident, was to examine the injuries sustained by the victims of the TWA Flight 800 disaster and to determine any correlation of injuries with structural damage and seat location. METHODS: Complete autopsy records, toxicology screening, and forensic analysis were reviewed. Injuries were assessed by anatomic region and severity by using the Abbreviated Injury Scale. The National Transportation Safety Board report of the investigation was applied to correlate individual injuries with seat location and structural damage. A comparison was performed against injury data from takeoff and landing incidents. RESULTS: All 230 passengers of TWA Flight 800 were recovered as fatalities. Head, thoracic, and abdominal injuries were multiple and severe, contributing to the mortality of the occupants. Analysis revealed that the severity of injury and anatomic injury pattern did not generally correlate with seating position or structural damage. A comparison of these injuries with those of takeoff and landing crashes showed differences in injury pattern and severity. CONCLUSION: Passengers of Flight 800 sustained instantaneous fatal blunt force injury. Analysis of the data revealed no global correlation between seat position and pattern of injury. In contrast to injuries incurred during crashes at takeoff and landing, these midflight injuries were too extreme to warrant a reappraisal of current passenger protective safety measures or standards.

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