Since nitric oxide (NO) contributes to both circulatory disorders and
host defense, we analyzed the NO production in (poly)trauma patients (
pts) in a prospective (pre)clinical study starting as early as at the
scene of accident. Upon approval of the local IRB/EC, 85 multiple inju
red pts were enrolled. Subsets were performed according to trauma seve
rity (ISS) and injury pattern, and between survivors versus nonsurvivo
rs. The first blood sample was collected at the scene of accident, the
n in hourly to daily intervals. NO production was assessed by measurin
g nitrate+nitrite plasma levels. To estimate dilution effects, all val
ues were calculated according to the actual plasma protein content. Th
e extent of trauma was appraised by C-reactive protein (CRP) levels. I
mmediately after trauma, NO2-+NO3- plasma levels were always elevated.
This was most pronounced in thoracic injury, irrespective of whether
it was combined with multiple trauma. Nitrate+nitrite levels returned
to normal within 24 h, CRP generation increased during 12 h following
trauma and was most marked in severest trauma (ISS >50). For the first
time, we show very early data following major trauma that demonstrate
that NO overproduction starts immediately after trauma. However, syst
emic NO2-+NO3- levels actually reflect the severity of injury only dur
ing the first 2 h. Thereafter, NO generation is rather related to the
individual trauma pattern, e.g., chest trauma. Nonetheless, the role o
f NO after severe trauma and especially in thoracic injury remains unc
lear and should further be elucidated in a specific study.