M. Huribal et al., ENDOTHELIN-1 AND PROSTAGLANDIN E(2) LEVELS INCREASE IN PATIENTS WITH BURNS, Journal of the American College of Surgeons, 180(3), 1995, pp. 318-322
BACKGROUND: Endothelin-1 (ET-1), a powerful vasoconstrictor, is a 21 a
mino acid peptide produced by endothelium. It negatively affects pulmo
nary, cardiac, hepatic, and renal function. It also constricts bronchi
al and gut smooth muscle. This peptide also stimulates monocytes to pr
oduce prostaglandin E(2) (PGE(2)), tumor necrosis factor, interleukin-
6 and 8, and substances that stimulate neutrophil superoxide productio
n. Plasma levels of ET-1 also increase in shock, low flow states, isch
emia, and sepsis. STUDY DESIGN: Fourteen patients between the ages of
seven and 72 years were admitted to the Bridgeport Hospital Burn Unit
and resuscitated with a modified Parkland formula. Plasma was drawn on
admission, at 12, 24, and 48 hours. Endothelin-1 and PGE(2) were meas
ured by radioimmunoassay. RESULTS: Endothelin-1 levels increased ten-
to 20-fold in all patients. Prostaglandin E(2) levels increased five-t
o 40-fold in all patients. There was no correlation between plasma ET-
1 or PGE(2) levels with either size of burn, inhalation injury, patien
t age, organ dysfunction, or survival in this small study of early bur
n injury. CONCLUSIONS: The increased plasma ET-1 response in patients
with burns may have a role in the genesis of the systemic response to
burns. This peptide may also activate monocyte production of PGE(2) an
d other mediators of the systemic inflammatory response syndrome. This
study was done to measure ET-1 and PGE(2) levels in patients with bur
ns greater than 20 percent of the body surface area on admission, at 1
2, 24, and 48 hours. The correlations between severity of burn, ET-1 l
evels, and PGE(2) production were also assessed.