Evaluation of hemostatic capacities among commando candidates: Would their blood suit a hemorrhagic war-injured patient in case of blood donation on the battlefield?

BACKGROUND: In case of a warm fresh whole blood transfusion on the battlefield, the blood donation usually occurs just after a combat phase and often after several days on the fields. To explore the hemostatic capacity of such blood, we analyzed the blood of volunteers attending the commando course of the French Navy, considering this course as an experimental model, placing them into the same physiological conditions as those faced by deployed fighters. METHODS: Venous blood was collected at the beginning of the course, mimicking their baseline status, and a second time 6 weeks later, from the remaining candidates, during the actual commando training, mimicking the stress conditions. For each candidate, we observed the differences between the two blood samples. RESULTS: Of the 112 men that attended the first day of the course, only 17 remained 6 weeks later. In the second blood samples, we noted significant increased leucocytes and platelets counts and significant decreased hematocrit and hemoglobin levels. Thrombin generation assays showed significantly lower normalized peak heights (-31%), lower normalized endogenous thrombin potential values (-29%), and lower velocity index (-35%). Normalized lag time and time to peak did not differ. Viscoelastometric testing revealed a significant increasing in clot firmness as assessed by maximum amplitude and amplitude at 6 minutes. The clot speed was significantly increased. CONCLUSION: This work brings new data on coagulation during prolonged and considerable physical exercise. No obvious deleterious modification of hemostatic properties was observed. The decrease of the endogenous thrombin potentials may reflect a better ability to control the thrombin generation once started. Altogether, these results suggest that this blood could suit well a hemorrhagic war-injured patient. LEVEL OF EVIDENCE: Prospective observational cohort study, Level III.

Increased susceptibility of low-density lipoprotein to ex vivo oxidation in mice transgenic for human apolipoprotein B treated with 1 melatonin-related compound is not associated with atherosclerosis progression.

Considerable evidence supports the hypothesis that LDL oxidation has an important role in atherosclerosis. It has been demonstrated that the feeding of hypercholesterolemic mice on an atherogenic diet supplemented with melatonin highly increases the surface of atherosclerotic lesions in aorta and the sensitivity of atherogenic lipoprotein to ex vivo oxidation even though high melatonin doses inhibit lipoprotein oxidation in vitro. A melatonin-related compound (DTBHB: N-[2-(5-methoxy-1H-indol-3-yl)ethyl]-3,5-di-tert-butyl-4-hydroxybenzamide) has been reported to strongly inhibit lipid peroxidation in vitro. In the present study, DTBHB treatment considerably increased the sensitivity of atherogenic lipoproteins to ex vivo oxidation but did not modify atherosclerotic lesion development in mice. Moreover, DTBHB treatment did not induce detectable lipidic alteration. These data confirm that the capacity of molecules to inhibit atherogenic lipoprotein oxidation in vitro offers no prediction of their capacity to inhibit in vivo atherosclerosis development.

Daily melatonin supplementation in mice increases atherosclerosis in proximal aorta.

Considerable evidence supports the hypothesis that LDL oxidation plays an important role in atherosclerosis. Even though high melatonin doses inhibit LDL oxidation in vitro, the effect of melatonin on atherosclerosis has never been studied. We have demonstrated that the feeding of hypercholesterolemic mice with an atherogenic diet supplemented with melatonin highly increases the surface of atherosclerotic lesions in the proximal aorta. These observations occur without detectable lipidic or glucidic phenotype alteration. Melatonin treatment increased highly the sensitivity of atherogenic lipoprotein to Cu(2+) and gamma-radiolysis generated oxyradical ex vivo oxidation during the fasting period. Moreover, these altered lipoproteins were less recognized by the LDL receptor metabolic pathway of murine fibroblasts while they transferred many more cholesteryl esters to murine macrophages. This study suggests that caution should be taken as regards high melatonin dosage in hypercholesterolemic patients.